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Treatment for chronic diarrhea in elderly: Diarrhea in Seniors | Geriatric Urgent Medical Care

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Microscopic colitis — a common cause of diarrhoea in older adults | Age and Ageing

Abstract

Diarrhoeal diseases are common in older populations and often markedly affect their quality of life. Although there are numerous potential causes, microscopic colitis (MC) is increasingly recognised as a major diagnostic entity in older individuals. MC is comprised of two distinct histological forms — collagenous colitis and lymphocytic colitis, both of which frequently occur in older populations. Recent studies suggest that between 10 and 30% of older patients investigated for chronic diarrhoea with an endoscopically normal appearing colon will have MC. It is unclear why MC is more common in older populations, but it is associated with both autoimmune disorders and several drugs that are commonly used by seniors. A definitive diagnosis can only be made with colonic biopsies. Since MC was first described in 1976 and only recently recognised as a common cause of diarrhoea, many practising physicians may not be aware of this entity. In this review, we outline the epidemiology, risk factors associated with MC, its pathophysiology, the approach to diagnosis and the management of these individuals.

Introduction

At any one point in time, ∼9% of an older out-patient population will be experiencing diarrhoea [1]. While the prevalence of chronic diarrhoea in older patients is unknown, it is a significant cause of morbidity among them — especially in vulnerable populations like those residing in long-term care facilities. In older populations, chronic diarrhoea can arise from a variety of conditions like coeliac disease and inflammatory bowel disease (IBD) [2]. Microscopic colitis (MC) has emerged as a new and common cause of chronic diarrhoea in the general population.

MC is an umbrella term for a group of inflammatory diseases of the colon where the colonic lining appears endoscopically normal, but histologic examination on biopsy reveals increased intraepithelial lymphocytes (IEL) in the colonic mucosa. MC is subgrouped into two different forms that are characterised by histological means – lymphocytic and collagenous colitis. While both subgroups have increased numbers of IELs, a thickened collagen band on the basement membrane of the colonic epithelium is seen in the latter subtype.

MC is frequently associated with systemic disorders (such as hypothyroidism) and the use of certain medications. Not surprisingly, the disorder is being increasingly recognised as a common cause of diarrhoea in middle-aged and older patients. For many of these patients, especially women, the looser and/or more frequent movements may lead to rectal urgency and faecal incontinence or may result in a exacerbation of a previously controlled but latent insufficient anal sphincter [3].

Epidemiology

When first described over 30 years ago, MC was believed to be rare [4, 5]. However, studies have shown that it is a common cause of watery diarrhoea, particularly in older female patients [6]. MC is a disease that predominantly affects older patients, with incidence rates anywhere from 5 to 10 times higher in those over 65.

Some population-based studies have looked at the incidence of MC in European and North American populations [7–12]. The overall total population annual incidence of collagenous colitis has ranged from 1.1 to 5.2 cases per 100,000 (Table 1) while the annual incidence of lymphocytic colitis per 100,000 was reportedly 3.1–5.5 (Table 1). More recent studies suggest an even higher incidence for MC. This is likely because of an increased awareness of the entity with more colonic biopsies being performed. For example, American incidence rates of 7.1 and 12.6 per 100,000 person-years for collagenous and lymphocytic colitis, respectively, were recently reported with a point prevalence for MC of 103.0 (39.3 for collagenous and 63.7 for lymphocytic colitis per 100,000) [11]. Reports suggest that the incidence of MC approaches that of ulcerative colitis and Crohn’s disease [7].

Table 1

Epidemiology of microscopic colitis

Study
Patients (n)
Incidence CC per 105
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.8 N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.2 4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 
Study
Patients (n)
Incidence CC per 105
.  
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.8 N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.2 4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 

Table 1

Epidemiology of microscopic colitis

Study
Patients (n)
Incidence CC per 105
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.2 4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 
Study
Patients (n)
Incidence CC per 105
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.8 N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 

Risk Factors and Disease Associations

Increasing age [7–9], female sex [7–9], autoimmune diseases such as thyroid disease [13] and coeliac disease [14, 15], past or current diagnosis of malignancy [12, 16] and solid organ transplant are identified as risk factors for MC [17].

The incidence of MC increases substantially with advancing age [7–9]. The mean age of diagnosis of the condition is in the fifth and sixth decades. In one Canadian study, patients greater than 65 years of age were more than five times as likely to have developed MC [12]. The reasons for this are unknown. While a genetic or environmental component seems possible since familial cases have also been reported [18–20], MC does appear to be an age-associated condition.

Female sex is also a major risk factor [7–9, 11, 21, 22]. This predisposition is more pronounced for the collagenous colitis subtype. Population-based studies report a female to male ratio of 4.4–7.9:1 for collagenous and 1.8–5.0:1 for lymphocytic colitis [7–12]. The reasons for the higher rate among women are also unknown but might be related to the higher likelihood of autoimmune diseases, hormonal alterations and/or an ascertainment bias as women may be more likely to seek help for intermittent watery diarrhoea.

Autoimmune diseases, particularly thyroid and/or coeliac disease, are associated with MC [8, 11, 13–15, 21–24]. Fifty-three percent of patients with collagenous and 43% of patients with lymphocytic colitis have at least one concomitant autoimmune disease. Thyroid disease is found in 8.6 to 21% of those with MC [7, 13, 14]. A recent epidemiological study of 164 patients with MC found that 18 (11.0%) had a prior diagnosis of hypothyroidism [12]. Several studies have documented an association between coeliac disease and MC. Later studies have supported that coeliac disease is found in 6–15% with lymphocytic [22, 24] and 3–23% in patients with collagenous colitis [14, 22]. In a recent study conducted by our group, 7% of patients with a new diagnosis of MC had a prior diagnosis of coeliac disease, which was nearly eight times higher than the expected rate for the general population [12].

The association of MC with neoplasia is less well studied. Several case reports have linked collagenous colitis with solid tumours [25, 26] and lymphoproliferative disorders [27]. Nearly 12% of patients with MC were found to have either a past or current diagnosis of malignancy [12]. After adjusting for age and sex, the risk was only higher in women over the age of 65. Other studies examining the risk of developing a malignancy after the diagnosis of MC have been unable to document an association [16, 28].

Only one study has looked at solid organ transplant recipients [17]. The authors reported a point prevalence of 8. 8 cases of MC per 1,000 solid organ transplant patients and an annual incidence rate of 5.0 per 1,000 transplant person-years. This incidence rate is ∼50-fold higher than the rate found in the general population.

MC has been associated with the use of several medications including NSAIDs, SSRIs, beta-blockers, statins, biphosphonates, ticlopidine, flutamide and PPIs [23, 29–31]. A recent study showed that those with collagenous colitis more commonly consumed NSAIDs and SSRIs, than controls, while those with lymphocytic colitis more commonly consumed SSRIs, beta-blockers, statins and biphosphonates [30]. Other agents including PPIs [31], ticlopidine [30] and flutamide [29] have been linked in case studies. There have been a few reports of symptom improvement with cessation of NSAIDs [32].

Aetiology

Although MC is technically an IBD and shares a number of parallel etiological aspects with Crohn’s disease and ulcerative colitis (the ‘classical’ IBDs), it is thought to be unrelated to the latter two disorders. The aetiology of MC is likely multi-factorial with a specific mucosal response to various noxious luminal agents occurring in predisposed hosts.

Genetics

Data suggesting a strong genetic contribution are lacking, but as noted familial clusters of MC have been described [20]. In addition, up to 12% of patients with MC have a family history of inflammatory bowel or coeliac disease [24]. Koskela et al. recently reported an association between HLA-DQ2 and MC and also found that MC patients more commonly had an uncommon polymorphism in the tumour necrosis factor alpha (TNFα) gene that results in increased TNFα production [33].

Autoimmunity

There is some evidence of an autoimmune basis to the development of MC. There is a female preponderance and an association of MC with autoimmune-based disorders such as coeliac and thyroid disease. One study found that 40% of patients with Hashimotos’ thyroiditis had histological findings compatible with lymphocytic colitis [13]. Although perinuclear antineutrophil cytoplasmic and antinuclear antibodies are increased in some patients with MC, to date specific autoantibodies for MC have not been defined [34].

Exogenous factors

An increased number of T cells in the epithelium raise the suspicion that MC is the result of a dysfunctional immunological response to a yet undetermined luminal toxin. This theory is supported by the observation that in some patients an elemental diet results in symptom resolution [35]. Further support stems from the observation that diverting the faecal stream with an ileostomy can result in normalisation of histopathological changes in collagenous colitis [36]. After closure, both symptoms and histopathology changes recurred [36]. Proposed luminal/environmental toxins include medications, GI infectious agents and bile salts.

Beaugerie and Pardi [37] have reported that multiple drugs have a high or intermediate probability of causality (Table 2). The mechanism(s) underlying these associations is (are) unknown, but the strong relationship with the use of NSAIDs suggests that prostaglandins may play a role. With the remarkable ORs reported for a variety of medications and the occurrence of MC, which were detailed in the risk factors section, a possible role of these medications has to be considered and the therapeutic approach to MC should include medication withdrawal, if one of the risky medications is to be identified.

Table 2

Drugs associated with microscopic colitis

Strong association
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  
Strong association
.  
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  

Table 2

Drugs associated with microscopic colitis

Strong association
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  
Strong association
.  
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  

Some patients report a preceding gastrointestinal infection, and others with MC exhibit significant improvement with antibiotics [29]. Antibodies to Yesinia are more common in patients with collagenous colitis than in healthy controls [38], and there are case reports linking MC to Clostridium difficile [39] and Campylobacter [40].

Bile acids

Bile acid malabsorption has been documented in 9–60% of patients with lymphocytic and 27–44% of patients with collagenous colitis [41]. Interestingly, bile acid-binding therapy can result in improvement in both those with and those without documented bile acid malabsorption.

Pathophysiology

The precise mechanism of diarrhoea in these patients is not well understood. Factors that may play a role include bile salt induced injury, active chloride excretion, decrease in net sodium absorption, creation of a diffusion barrier by collagen band and increased local inflammatory mediators such as nitric oxide and prostaglandins. It remains unclear which of these results in the symptoms reported by patients.

Two studies have looked at inflammatory cytokines in MC. Patients with MC seem to have a predominantly Th2 type cytokine profile with significant increases in interferon gamma, TNFα and interleukin 15 as well as an increased inducible nitric oxide synthase. Others have found increased levels of TGF-β in patients with collagenous colitis [42].

Clinical Features

The clinical features of collagenous and lymphocytic colitis are similar. The two entities can only be differentiated on histopathological grounds. Both cause chronic (either recurrent or intermittent) watery, non-bloody diarrhoea. Although the clinical course is classically one of the chronic relapsing symptoms, a minority of patients present with an acute onset. Although the diarrhoea may be severe in some patients, complications such as dehydration are rare. Associated symptoms include nocturnal bowel motions, mild abdominal pain, fatigue, slight weight loss, arthralgias and faecal incontinence. Symptoms are often attributed to an irritable bowel syndrome.

The natural history of MC is variable. Many cases are self-limiting, with symptoms lasting a few weeks or months. Others may be symptomatic for years in a relapsing or continuous pattern. Although a small number of case reports have suggested that MC may lead to development of ulcerative colitis, a small case series of patients with MC showed that none developed ulcerative colitis or Crohn’s disease after a follow-up of at least 6 years [28]. Similarly, MC does not appear to affect colorectal cancer risk [16].

Diagnosis/Histopathology

The diagnosis of MC is dependent on (i) a convincing clinical history with other etiologies ruled out, (ii) normal or near normal endoscopic and/or radiographic findings and (iii) endoscopic biopsies with histopathologic findings consistent with MC (Table 3).

Table 3

Histopathological features of collagenous colitis and lymphocytic colitis

Lymphocytic colitis
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 
Lymphocytic colitis
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 

Table 3

Histopathological features of collagenous colitis and lymphocytic colitis

Lymphocytic colitis
.  
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 
Lymphocytic colitis
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 

The first step in the diagnostic process is a thorough history with particular attention paid to risk factors and the disease associated with MC. A complete history helps one to rule out other etiologies that may cause a similar clinical picture such as IBD, coeliac disease, diarrhoea-predominant irritable bowel syndrome or infectious colitis.

Laboratory and radiographic investigations can be employed to help rule out other entities on the differential diagnosis list, but they are typically unremarkable.

Endoscopy with biopsy is necessary to confirm the diagnosis. Colonoscopy generally reveals macroscopically normal mucosa. However, non-specific changes such as erythema, edema, abnormal vascular markings or even tears associated with perforation have been described.

Microscopic evaluation of the colonic mucosa reveals significant inflammatory changes as outlined in Table 3. Both collagenous and lymphocytic colitis demonstrate lymphocytic infiltration of the lamina propria and epithelium. Collagenous is differentiated from lymphocytic colitis by the presence of marked thickening of the subepithelial collagen layer (Table 3). Histological assessment by a pathologist familiar with MC is required.

Since the macroscopic appearance is generally normal and the microscopic lesions can be skipped, random colonic biopsies are recommended. There is currently no consensus whether flexible sigmoidoscopy or colonoscopy is the best initial approach [43]. Flexible sigmoidoscopy is an attractive option due to efficiency (takes less time), cost savings, easier bowel preparation and no requirement for sedation. However, some studies suggest that biopsies of the rectosigmoid colon alone may be insufficient to rule out a diagnosis [44, 45] as up to 40% of cases are missed. Offner et al. reported that the diagnostic yield was highest from biopsies of the transverse colon (83%) and right colon (70%) and lowest from the rectosigmoid (66%) [45]. Other studies have reported lower false-negative rates with left-sided biopsies alone. Tanaka et al. reported that only 10% of patients with MC had isolated right-sided disease [44], and a larger study by Fine et al. reported that all 80 patients evaluated for chronic diarrhoea who were diagnosed with MC had histological evidence of MC in the left colon, whereas biopsies taken from other regions of the colon could be false negative [46].

The practical benefits of flexible sigmoidoscopy must be weighed against the potentially increased diagnostic yield of colonoscopy. The choice of which procedure to perform will depend on the clinical scenario, local expertise and resource constraints. If initial biopsies obtained on flexible sigmoidoscopy do not lead to a diagnosis and the suspicion of MC is high, we recommend a colonoscopy.

Treatment

Treatment recommendations for MC are largely based on case reports and uncontrolled studies, and Table 4 gives a suggested algorithm. Specific agents evaluated include 5-aminosalicylic acid (5-ASA), prednisone, immunomodulators, bismuth, probiotics and Boswellia extract. Small randomised controlled trials have shown that agents such as budesonide offer promise as an effective form of symptomatic therapy for both collagenous and lymphocytic colitis.

Table 4

Suggested treatment algorithm

Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e.g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 
Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e. g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 

Table 4

Suggested treatment algorithm

Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e.g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 
Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e. g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 

As a first step in managing MC, an in depth medication history should be taken with potentially precipitating medications stopped where possible. Associated conditions such as coeliac disease should be appropriately managed. In patients with mild symptoms, dietary restrictions like avoiding caffeine and lactose might be helpful.

Anti-diarrhoeal therapies

Non-specific anti-diarrhoeal therapies such as loperamide are commonly used in the management of MC. Retrospective studies have suggested benefit with doses ranging from 2 to 16 mg per day [29, 47]. Due to the safety of this agent and the possibility of spontaneous remission, we suggest loperamide for first-line therapy for MC. In our experience, however, those with moderate to severe diarrhoea or associated complaints of significant abdominal pain often fail to respond to anti-diarrhoeal therapy alone.

Aminosalicylates

Uncontrolled retrospective series have suggested symptomatic improvement in up to 50% of patients with MC treated with mesalamine (5-ASA) [24, 29, 48]. A recent randomised trial of 64 MC patients compared mesalamine (800 mg tid) to mesalamine (800 mg tid) and cholestyramine (4 g/day) [49]. Treatment resulted in resolution of diarrhoea in 84% overall after 2 weeks. If treatment was continued over 6 months, clinical and histological remission was achieved in 85% of those with lymphocytic and 91% of those with collagenous colitis. The number of relapsing patients after 6 months of treatment was low, and symptomatic relapses could be successfully retreated. Overall, the combination of mesalamine with cholestyramine was slightly superior [48].

Budesonide

Budesonide is currently the most promising treatment for collagenous colitis. Three trials involving 94 patients have shown that budesonide therapy (9 mg daily for 6–8 weeks) compared to placebo resulted in statistically significant improvements in clinical symptoms [50–52] and quality of life [53]. A recent Cochrane database meta-analysis reported pooled odds ratio of 12.3 for clinical response with budesonide with a number needed to treat of two [54]. Although effective in the short-term, all trials showed a high rate (61–80%) of relapse within ∼2 weeks of budesonide cessation. Age <60 was a significant risk factor for relapse. Although, there are no studies to support a tapering course of budesonide, many clinicians employ this in an effort to minimise the likelihood of relapse.

One randomised controlled trial of budesonide for the treatment of lymphocytic colitis has been conducted. When compared to the placebo arm, the patients randomised to budesonide (9 mg daily × 6 weeks) had a statistically significantly higher rate of remission (<3 bowel movements/day) at 3 and 6 weeks [55].

Prednisolone

A double-blind, placebo-controlled randomised trial of oral prednisolone 50 mg daily for 2 weeks for collagenous colitis was inconclusive because of the low number of patients enrolled [56]. Studies examining the effect of prednisone in the treatment of lymphocytic colitis have not been performed.

Immunosuppressive therapy

Immunosuppressive therapy with azathioprine or methotrexate has been utilised in patients either refractory to corticosteroid therapy or corticosteroid dependent, but there are no randomised controlled trials to guide therapy with these medications [57, 58].

Other therapies

Small clinical trials studying bismuth subsalicylate, Boswellia serrata extract, probiotics and empirical antibiotic treatment for collagenous and lymphocytic colitis look promising but cannot be suggested outside of such trials. Finally, case reports suggest that pentoxifylline, verapamil and subcutaneous octreotide might be treatment options, but their use cannot be recommended at this time. When medical therapy was unsuccessful and symptoms were very severe, surgical interventions such as a temporary or permanent loop ileostomy or even a proctocolectomy have been employed in smaller case series.

Recommended approach to treatment

Firstly, the diagnosis must be confirmed and other potential etiologies ruled out. Any complications related to chronic diarrhoea such as dehydration or electrolyte abnormalities must be identified and corrected. Potentially contributing medications such as PPIs or NSAIDs should be discontinued if possible. Depending on symptom severity, non-specific anti-diarrhoeal agents like loperamide, bile salt binding resins or bismuth should be tried. If this fails and the symptoms are sufficiently severe, the patient should be cared for or referred to someone with experience in dealing with this condition. Budesonide, 9 mg daily for at least 6 weeks, could then be used. Some clinical reports suggest a maintenance dose of budesonide 3–6 mg daily may be effective, but this approach has not been studied prospectively. If administration becomes long-term, patients have to be monitored for the development of the complications of chronic steroid therapy. If symptoms fail to improve, clinicians should consider alternative diagnoses. Prednisone, 5-ASA, immunosuppressive therapy or surgery could be cautiously considered for refractory cases.

Prognosis/Outcome

MC has a variable course, but overall, the long-term prognosis is good. Symptoms of diarrhoea and abdominal pain may precede the diagnosis by a number of months. These symptoms are generally mild. With most patients, symptoms resolve spontaneously or with symptomatic therapy. MC has not been associated with an increased risk of colorectal cancer — this information should be conveyed to the patients. There is only limited information about the long-term course and the prognosis of MC. One study followed 81 patients for an average of 37 months. Their initial symptoms were successfully treated with a number of different drugs. Approximately 30% of these patients relapsed with ∼70% remaining symptom free [59]. Prospective observational and clinical trials are warranted to specifically address the issue of prognosis and the durability of the response to initial therapy.

Conclusion

MC is a common cause of diarrhoea in older patients. After ruling our other causes of diarrhoea, flexible sigmoidoscopy (or colonoscopy) with appropriate biopsies allows for the diagnosis of either lymphocytic or collagenous colitis by histological analysis. Based on symptom severity, a stepwise approach to the treatment is suggested.

Key points

  • MC is common in older adults.

  • The incidence of MC is rising.

  • MC is diagnosed in biopsies taken during a colonoscopy.

  • MC is treated using a stepwise approach.

Conflicts of interest

None.

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Oxford University Press

Microscopic colitis — a common cause of diarrhoea in older adults | Age and Ageing

Abstract

Diarrhoeal diseases are common in older populations and often markedly affect their quality of life. Although there are numerous potential causes, microscopic colitis (MC) is increasingly recognised as a major diagnostic entity in older individuals. MC is comprised of two distinct histological forms — collagenous colitis and lymphocytic colitis, both of which frequently occur in older populations. Recent studies suggest that between 10 and 30% of older patients investigated for chronic diarrhoea with an endoscopically normal appearing colon will have MC. It is unclear why MC is more common in older populations, but it is associated with both autoimmune disorders and several drugs that are commonly used by seniors. A definitive diagnosis can only be made with colonic biopsies. Since MC was first described in 1976 and only recently recognised as a common cause of diarrhoea, many practising physicians may not be aware of this entity. In this review, we outline the epidemiology, risk factors associated with MC, its pathophysiology, the approach to diagnosis and the management of these individuals.

Introduction

At any one point in time, ∼9% of an older out-patient population will be experiencing diarrhoea [1]. While the prevalence of chronic diarrhoea in older patients is unknown, it is a significant cause of morbidity among them — especially in vulnerable populations like those residing in long-term care facilities. In older populations, chronic diarrhoea can arise from a variety of conditions like coeliac disease and inflammatory bowel disease (IBD) [2]. Microscopic colitis (MC) has emerged as a new and common cause of chronic diarrhoea in the general population.

MC is an umbrella term for a group of inflammatory diseases of the colon where the colonic lining appears endoscopically normal, but histologic examination on biopsy reveals increased intraepithelial lymphocytes (IEL) in the colonic mucosa. MC is subgrouped into two different forms that are characterised by histological means – lymphocytic and collagenous colitis. While both subgroups have increased numbers of IELs, a thickened collagen band on the basement membrane of the colonic epithelium is seen in the latter subtype.

MC is frequently associated with systemic disorders (such as hypothyroidism) and the use of certain medications. Not surprisingly, the disorder is being increasingly recognised as a common cause of diarrhoea in middle-aged and older patients. For many of these patients, especially women, the looser and/or more frequent movements may lead to rectal urgency and faecal incontinence or may result in a exacerbation of a previously controlled but latent insufficient anal sphincter [3].

Epidemiology

When first described over 30 years ago, MC was believed to be rare [4, 5]. However, studies have shown that it is a common cause of watery diarrhoea, particularly in older female patients [6]. MC is a disease that predominantly affects older patients, with incidence rates anywhere from 5 to 10 times higher in those over 65.

Some population-based studies have looked at the incidence of MC in European and North American populations [7–12]. The overall total population annual incidence of collagenous colitis has ranged from 1.1 to 5.2 cases per 100,000 (Table 1) while the annual incidence of lymphocytic colitis per 100,000 was reportedly 3.1–5.5 (Table 1). More recent studies suggest an even higher incidence for MC. This is likely because of an increased awareness of the entity with more colonic biopsies being performed. For example, American incidence rates of 7.1 and 12.6 per 100,000 person-years for collagenous and lymphocytic colitis, respectively, were recently reported with a point prevalence for MC of 103.0 (39.3 for collagenous and 63.7 for lymphocytic colitis per 100,000) [11]. Reports suggest that the incidence of MC approaches that of ulcerative colitis and Crohn’s disease [7].

Table 1

Epidemiology of microscopic colitis

Study
Patients (n)
Incidence CC per 105
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.8 N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.2 4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 
Study
Patients (n)
Incidence CC per 105
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.8 N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.2 4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 

Table 1

Epidemiology of microscopic colitis

Study
Patients (n)
Incidence CC per 105
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.8 N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.2 4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 
Study
Patients (n)
Incidence CC per 105
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.8 N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.2 4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 

Risk Factors and Disease Associations

Increasing age [7–9], female sex [7–9], autoimmune diseases such as thyroid disease [13] and coeliac disease [14, 15], past or current diagnosis of malignancy [12, 16] and solid organ transplant are identified as risk factors for MC [17].

The incidence of MC increases substantially with advancing age [7–9]. The mean age of diagnosis of the condition is in the fifth and sixth decades. In one Canadian study, patients greater than 65 years of age were more than five times as likely to have developed MC [12]. The reasons for this are unknown. While a genetic or environmental component seems possible since familial cases have also been reported [18–20], MC does appear to be an age-associated condition.

Female sex is also a major risk factor [7–9, 11, 21, 22]. This predisposition is more pronounced for the collagenous colitis subtype. Population-based studies report a female to male ratio of 4.4–7.9:1 for collagenous and 1.8–5.0:1 for lymphocytic colitis [7–12]. The reasons for the higher rate among women are also unknown but might be related to the higher likelihood of autoimmune diseases, hormonal alterations and/or an ascertainment bias as women may be more likely to seek help for intermittent watery diarrhoea.

Autoimmune diseases, particularly thyroid and/or coeliac disease, are associated with MC [8, 11, 13–15, 21–24]. Fifty-three percent of patients with collagenous and 43% of patients with lymphocytic colitis have at least one concomitant autoimmune disease. Thyroid disease is found in 8.6 to 21% of those with MC [7, 13, 14]. A recent epidemiological study of 164 patients with MC found that 18 (11.0%) had a prior diagnosis of hypothyroidism [12]. Several studies have documented an association between coeliac disease and MC. Later studies have supported that coeliac disease is found in 6–15% with lymphocytic [22, 24] and 3–23% in patients with collagenous colitis [14, 22]. In a recent study conducted by our group, 7% of patients with a new diagnosis of MC had a prior diagnosis of coeliac disease, which was nearly eight times higher than the expected rate for the general population [12].

The association of MC with neoplasia is less well studied. Several case reports have linked collagenous colitis with solid tumours [25, 26] and lymphoproliferative disorders [27]. Nearly 12% of patients with MC were found to have either a past or current diagnosis of malignancy [12]. After adjusting for age and sex, the risk was only higher in women over the age of 65. Other studies examining the risk of developing a malignancy after the diagnosis of MC have been unable to document an association [16, 28].

Only one study has looked at solid organ transplant recipients [17]. The authors reported a point prevalence of 8.8 cases of MC per 1,000 solid organ transplant patients and an annual incidence rate of 5.0 per 1,000 transplant person-years. This incidence rate is ∼50-fold higher than the rate found in the general population.

MC has been associated with the use of several medications including NSAIDs, SSRIs, beta-blockers, statins, biphosphonates, ticlopidine, flutamide and PPIs [23, 29–31]. A recent study showed that those with collagenous colitis more commonly consumed NSAIDs and SSRIs, than controls, while those with lymphocytic colitis more commonly consumed SSRIs, beta-blockers, statins and biphosphonates [30]. Other agents including PPIs [31], ticlopidine [30] and flutamide [29] have been linked in case studies. There have been a few reports of symptom improvement with cessation of NSAIDs [32].

Aetiology

Although MC is technically an IBD and shares a number of parallel etiological aspects with Crohn’s disease and ulcerative colitis (the ‘classical’ IBDs), it is thought to be unrelated to the latter two disorders. The aetiology of MC is likely multi-factorial with a specific mucosal response to various noxious luminal agents occurring in predisposed hosts.

Genetics

Data suggesting a strong genetic contribution are lacking, but as noted familial clusters of MC have been described [20]. In addition, up to 12% of patients with MC have a family history of inflammatory bowel or coeliac disease [24]. Koskela et al. recently reported an association between HLA-DQ2 and MC and also found that MC patients more commonly had an uncommon polymorphism in the tumour necrosis factor alpha (TNFα) gene that results in increased TNFα production [33].

Autoimmunity

There is some evidence of an autoimmune basis to the development of MC. There is a female preponderance and an association of MC with autoimmune-based disorders such as coeliac and thyroid disease. One study found that 40% of patients with Hashimotos’ thyroiditis had histological findings compatible with lymphocytic colitis [13]. Although perinuclear antineutrophil cytoplasmic and antinuclear antibodies are increased in some patients with MC, to date specific autoantibodies for MC have not been defined [34].

Exogenous factors

An increased number of T cells in the epithelium raise the suspicion that MC is the result of a dysfunctional immunological response to a yet undetermined luminal toxin. This theory is supported by the observation that in some patients an elemental diet results in symptom resolution [35]. Further support stems from the observation that diverting the faecal stream with an ileostomy can result in normalisation of histopathological changes in collagenous colitis [36]. After closure, both symptoms and histopathology changes recurred [36]. Proposed luminal/environmental toxins include medications, GI infectious agents and bile salts.

Beaugerie and Pardi [37] have reported that multiple drugs have a high or intermediate probability of causality (Table 2). The mechanism(s) underlying these associations is (are) unknown, but the strong relationship with the use of NSAIDs suggests that prostaglandins may play a role. With the remarkable ORs reported for a variety of medications and the occurrence of MC, which were detailed in the risk factors section, a possible role of these medications has to be considered and the therapeutic approach to MC should include medication withdrawal, if one of the risky medications is to be identified.

Table 2

Drugs associated with microscopic colitis

Strong association
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  
Strong association
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  

Table 2

Drugs associated with microscopic colitis

Strong association
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  
Strong association
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  

Some patients report a preceding gastrointestinal infection, and others with MC exhibit significant improvement with antibiotics [29]. Antibodies to Yesinia are more common in patients with collagenous colitis than in healthy controls [38], and there are case reports linking MC to Clostridium difficile [39] and Campylobacter [40].

Bile acids

Bile acid malabsorption has been documented in 9–60% of patients with lymphocytic and 27–44% of patients with collagenous colitis [41]. Interestingly, bile acid-binding therapy can result in improvement in both those with and those without documented bile acid malabsorption.

Pathophysiology

The precise mechanism of diarrhoea in these patients is not well understood. Factors that may play a role include bile salt induced injury, active chloride excretion, decrease in net sodium absorption, creation of a diffusion barrier by collagen band and increased local inflammatory mediators such as nitric oxide and prostaglandins. It remains unclear which of these results in the symptoms reported by patients.

Two studies have looked at inflammatory cytokines in MC. Patients with MC seem to have a predominantly Th2 type cytokine profile with significant increases in interferon gamma, TNFα and interleukin 15 as well as an increased inducible nitric oxide synthase. Others have found increased levels of TGF-β in patients with collagenous colitis [42].

Clinical Features

The clinical features of collagenous and lymphocytic colitis are similar. The two entities can only be differentiated on histopathological grounds. Both cause chronic (either recurrent or intermittent) watery, non-bloody diarrhoea. Although the clinical course is classically one of the chronic relapsing symptoms, a minority of patients present with an acute onset. Although the diarrhoea may be severe in some patients, complications such as dehydration are rare. Associated symptoms include nocturnal bowel motions, mild abdominal pain, fatigue, slight weight loss, arthralgias and faecal incontinence. Symptoms are often attributed to an irritable bowel syndrome.

The natural history of MC is variable. Many cases are self-limiting, with symptoms lasting a few weeks or months. Others may be symptomatic for years in a relapsing or continuous pattern. Although a small number of case reports have suggested that MC may lead to development of ulcerative colitis, a small case series of patients with MC showed that none developed ulcerative colitis or Crohn’s disease after a follow-up of at least 6 years [28]. Similarly, MC does not appear to affect colorectal cancer risk [16].

Diagnosis/Histopathology

The diagnosis of MC is dependent on (i) a convincing clinical history with other etiologies ruled out, (ii) normal or near normal endoscopic and/or radiographic findings and (iii) endoscopic biopsies with histopathologic findings consistent with MC (Table 3).

Table 3

Histopathological features of collagenous colitis and lymphocytic colitis

Lymphocytic colitis
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 
Lymphocytic colitis
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 

Table 3

Histopathological features of collagenous colitis and lymphocytic colitis

Lymphocytic colitis
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 
Lymphocytic colitis
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 

The first step in the diagnostic process is a thorough history with particular attention paid to risk factors and the disease associated with MC. A complete history helps one to rule out other etiologies that may cause a similar clinical picture such as IBD, coeliac disease, diarrhoea-predominant irritable bowel syndrome or infectious colitis.

Laboratory and radiographic investigations can be employed to help rule out other entities on the differential diagnosis list, but they are typically unremarkable.

Endoscopy with biopsy is necessary to confirm the diagnosis. Colonoscopy generally reveals macroscopically normal mucosa. However, non-specific changes such as erythema, edema, abnormal vascular markings or even tears associated with perforation have been described.

Microscopic evaluation of the colonic mucosa reveals significant inflammatory changes as outlined in Table 3. Both collagenous and lymphocytic colitis demonstrate lymphocytic infiltration of the lamina propria and epithelium. Collagenous is differentiated from lymphocytic colitis by the presence of marked thickening of the subepithelial collagen layer (Table 3). Histological assessment by a pathologist familiar with MC is required.

Since the macroscopic appearance is generally normal and the microscopic lesions can be skipped, random colonic biopsies are recommended. There is currently no consensus whether flexible sigmoidoscopy or colonoscopy is the best initial approach [43]. Flexible sigmoidoscopy is an attractive option due to efficiency (takes less time), cost savings, easier bowel preparation and no requirement for sedation. However, some studies suggest that biopsies of the rectosigmoid colon alone may be insufficient to rule out a diagnosis [44, 45] as up to 40% of cases are missed. Offner et al. reported that the diagnostic yield was highest from biopsies of the transverse colon (83%) and right colon (70%) and lowest from the rectosigmoid (66%) [45]. Other studies have reported lower false-negative rates with left-sided biopsies alone. Tanaka et al. reported that only 10% of patients with MC had isolated right-sided disease [44], and a larger study by Fine et al. reported that all 80 patients evaluated for chronic diarrhoea who were diagnosed with MC had histological evidence of MC in the left colon, whereas biopsies taken from other regions of the colon could be false negative [46].

The practical benefits of flexible sigmoidoscopy must be weighed against the potentially increased diagnostic yield of colonoscopy. The choice of which procedure to perform will depend on the clinical scenario, local expertise and resource constraints. If initial biopsies obtained on flexible sigmoidoscopy do not lead to a diagnosis and the suspicion of MC is high, we recommend a colonoscopy.

Treatment

Treatment recommendations for MC are largely based on case reports and uncontrolled studies, and Table 4 gives a suggested algorithm. Specific agents evaluated include 5-aminosalicylic acid (5-ASA), prednisone, immunomodulators, bismuth, probiotics and Boswellia extract. Small randomised controlled trials have shown that agents such as budesonide offer promise as an effective form of symptomatic therapy for both collagenous and lymphocytic colitis.

Table 4

Suggested treatment algorithm

Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e.g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 
Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e.g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 

Table 4

Suggested treatment algorithm

Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e.g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 
Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e.g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 

As a first step in managing MC, an in depth medication history should be taken with potentially precipitating medications stopped where possible. Associated conditions such as coeliac disease should be appropriately managed. In patients with mild symptoms, dietary restrictions like avoiding caffeine and lactose might be helpful.

Anti-diarrhoeal therapies

Non-specific anti-diarrhoeal therapies such as loperamide are commonly used in the management of MC. Retrospective studies have suggested benefit with doses ranging from 2 to 16 mg per day [29, 47]. Due to the safety of this agent and the possibility of spontaneous remission, we suggest loperamide for first-line therapy for MC. In our experience, however, those with moderate to severe diarrhoea or associated complaints of significant abdominal pain often fail to respond to anti-diarrhoeal therapy alone.

Aminosalicylates

Uncontrolled retrospective series have suggested symptomatic improvement in up to 50% of patients with MC treated with mesalamine (5-ASA) [24, 29, 48]. A recent randomised trial of 64 MC patients compared mesalamine (800 mg tid) to mesalamine (800 mg tid) and cholestyramine (4 g/day) [49]. Treatment resulted in resolution of diarrhoea in 84% overall after 2 weeks. If treatment was continued over 6 months, clinical and histological remission was achieved in 85% of those with lymphocytic and 91% of those with collagenous colitis. The number of relapsing patients after 6 months of treatment was low, and symptomatic relapses could be successfully retreated. Overall, the combination of mesalamine with cholestyramine was slightly superior [48].

Budesonide

Budesonide is currently the most promising treatment for collagenous colitis. Three trials involving 94 patients have shown that budesonide therapy (9 mg daily for 6–8 weeks) compared to placebo resulted in statistically significant improvements in clinical symptoms [50–52] and quality of life [53]. A recent Cochrane database meta-analysis reported pooled odds ratio of 12.3 for clinical response with budesonide with a number needed to treat of two [54]. Although effective in the short-term, all trials showed a high rate (61–80%) of relapse within ∼2 weeks of budesonide cessation. Age <60 was a significant risk factor for relapse. Although, there are no studies to support a tapering course of budesonide, many clinicians employ this in an effort to minimise the likelihood of relapse.

One randomised controlled trial of budesonide for the treatment of lymphocytic colitis has been conducted. When compared to the placebo arm, the patients randomised to budesonide (9 mg daily × 6 weeks) had a statistically significantly higher rate of remission (<3 bowel movements/day) at 3 and 6 weeks [55].

Prednisolone

A double-blind, placebo-controlled randomised trial of oral prednisolone 50 mg daily for 2 weeks for collagenous colitis was inconclusive because of the low number of patients enrolled [56]. Studies examining the effect of prednisone in the treatment of lymphocytic colitis have not been performed.

Immunosuppressive therapy

Immunosuppressive therapy with azathioprine or methotrexate has been utilised in patients either refractory to corticosteroid therapy or corticosteroid dependent, but there are no randomised controlled trials to guide therapy with these medications [57, 58].

Other therapies

Small clinical trials studying bismuth subsalicylate, Boswellia serrata extract, probiotics and empirical antibiotic treatment for collagenous and lymphocytic colitis look promising but cannot be suggested outside of such trials. Finally, case reports suggest that pentoxifylline, verapamil and subcutaneous octreotide might be treatment options, but their use cannot be recommended at this time. When medical therapy was unsuccessful and symptoms were very severe, surgical interventions such as a temporary or permanent loop ileostomy or even a proctocolectomy have been employed in smaller case series.

Recommended approach to treatment

Firstly, the diagnosis must be confirmed and other potential etiologies ruled out. Any complications related to chronic diarrhoea such as dehydration or electrolyte abnormalities must be identified and corrected. Potentially contributing medications such as PPIs or NSAIDs should be discontinued if possible. Depending on symptom severity, non-specific anti-diarrhoeal agents like loperamide, bile salt binding resins or bismuth should be tried. If this fails and the symptoms are sufficiently severe, the patient should be cared for or referred to someone with experience in dealing with this condition. Budesonide, 9 mg daily for at least 6 weeks, could then be used. Some clinical reports suggest a maintenance dose of budesonide 3–6 mg daily may be effective, but this approach has not been studied prospectively. If administration becomes long-term, patients have to be monitored for the development of the complications of chronic steroid therapy. If symptoms fail to improve, clinicians should consider alternative diagnoses. Prednisone, 5-ASA, immunosuppressive therapy or surgery could be cautiously considered for refractory cases.

Prognosis/Outcome

MC has a variable course, but overall, the long-term prognosis is good. Symptoms of diarrhoea and abdominal pain may precede the diagnosis by a number of months. These symptoms are generally mild. With most patients, symptoms resolve spontaneously or with symptomatic therapy. MC has not been associated with an increased risk of colorectal cancer — this information should be conveyed to the patients. There is only limited information about the long-term course and the prognosis of MC. One study followed 81 patients for an average of 37 months. Their initial symptoms were successfully treated with a number of different drugs. Approximately 30% of these patients relapsed with ∼70% remaining symptom free [59]. Prospective observational and clinical trials are warranted to specifically address the issue of prognosis and the durability of the response to initial therapy.

Conclusion

MC is a common cause of diarrhoea in older patients. After ruling our other causes of diarrhoea, flexible sigmoidoscopy (or colonoscopy) with appropriate biopsies allows for the diagnosis of either lymphocytic or collagenous colitis by histological analysis. Based on symptom severity, a stepwise approach to the treatment is suggested.

Key points

  • MC is common in older adults.

  • The incidence of MC is rising.

  • MC is diagnosed in biopsies taken during a colonoscopy.

  • MC is treated using a stepwise approach.

Conflicts of interest

None.

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© The Author 2010. Published by Oxford University Press on behalf of the British Geriatrics Society. All rights reserved. For Permissions, please email: [email protected]

Oxford University Press

Microscopic colitis — a common cause of diarrhoea in older adults | Age and Ageing

Abstract

Diarrhoeal diseases are common in older populations and often markedly affect their quality of life. Although there are numerous potential causes, microscopic colitis (MC) is increasingly recognised as a major diagnostic entity in older individuals. MC is comprised of two distinct histological forms — collagenous colitis and lymphocytic colitis, both of which frequently occur in older populations. Recent studies suggest that between 10 and 30% of older patients investigated for chronic diarrhoea with an endoscopically normal appearing colon will have MC. It is unclear why MC is more common in older populations, but it is associated with both autoimmune disorders and several drugs that are commonly used by seniors. A definitive diagnosis can only be made with colonic biopsies. Since MC was first described in 1976 and only recently recognised as a common cause of diarrhoea, many practising physicians may not be aware of this entity. In this review, we outline the epidemiology, risk factors associated with MC, its pathophysiology, the approach to diagnosis and the management of these individuals.

Introduction

At any one point in time, ∼9% of an older out-patient population will be experiencing diarrhoea [1]. While the prevalence of chronic diarrhoea in older patients is unknown, it is a significant cause of morbidity among them — especially in vulnerable populations like those residing in long-term care facilities. In older populations, chronic diarrhoea can arise from a variety of conditions like coeliac disease and inflammatory bowel disease (IBD) [2]. Microscopic colitis (MC) has emerged as a new and common cause of chronic diarrhoea in the general population.

MC is an umbrella term for a group of inflammatory diseases of the colon where the colonic lining appears endoscopically normal, but histologic examination on biopsy reveals increased intraepithelial lymphocytes (IEL) in the colonic mucosa. MC is subgrouped into two different forms that are characterised by histological means – lymphocytic and collagenous colitis. While both subgroups have increased numbers of IELs, a thickened collagen band on the basement membrane of the colonic epithelium is seen in the latter subtype.

MC is frequently associated with systemic disorders (such as hypothyroidism) and the use of certain medications. Not surprisingly, the disorder is being increasingly recognised as a common cause of diarrhoea in middle-aged and older patients. For many of these patients, especially women, the looser and/or more frequent movements may lead to rectal urgency and faecal incontinence or may result in a exacerbation of a previously controlled but latent insufficient anal sphincter [3].

Epidemiology

When first described over 30 years ago, MC was believed to be rare [4, 5]. However, studies have shown that it is a common cause of watery diarrhoea, particularly in older female patients [6]. MC is a disease that predominantly affects older patients, with incidence rates anywhere from 5 to 10 times higher in those over 65.

Some population-based studies have looked at the incidence of MC in European and North American populations [7–12]. The overall total population annual incidence of collagenous colitis has ranged from 1.1 to 5.2 cases per 100,000 (Table 1) while the annual incidence of lymphocytic colitis per 100,000 was reportedly 3.1–5.5 (Table 1). More recent studies suggest an even higher incidence for MC. This is likely because of an increased awareness of the entity with more colonic biopsies being performed. For example, American incidence rates of 7.1 and 12.6 per 100,000 person-years for collagenous and lymphocytic colitis, respectively, were recently reported with a point prevalence for MC of 103.0 (39.3 for collagenous and 63.7 for lymphocytic colitis per 100,000) [11]. Reports suggest that the incidence of MC approaches that of ulcerative colitis and Crohn’s disease [7].

Table 1

Epidemiology of microscopic colitis

Study
Patients (n)
Incidence CC per 105
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.8 N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.2 4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 
Study
Patients (n)
Incidence CC per 105
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.8 N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.2 4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 

Table 1

Epidemiology of microscopic colitis

Study
Patients (n)
Incidence CC per 105
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.8 N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.2 4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 
Study
Patients (n)
Incidence CC per 105
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.8 N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.2 4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 

Risk Factors and Disease Associations

Increasing age [7–9], female sex [7–9], autoimmune diseases such as thyroid disease [13] and coeliac disease [14, 15], past or current diagnosis of malignancy [12, 16] and solid organ transplant are identified as risk factors for MC [17].

The incidence of MC increases substantially with advancing age [7–9]. The mean age of diagnosis of the condition is in the fifth and sixth decades. In one Canadian study, patients greater than 65 years of age were more than five times as likely to have developed MC [12]. The reasons for this are unknown. While a genetic or environmental component seems possible since familial cases have also been reported [18–20], MC does appear to be an age-associated condition.

Female sex is also a major risk factor [7–9, 11, 21, 22]. This predisposition is more pronounced for the collagenous colitis subtype. Population-based studies report a female to male ratio of 4.4–7.9:1 for collagenous and 1.8–5.0:1 for lymphocytic colitis [7–12]. The reasons for the higher rate among women are also unknown but might be related to the higher likelihood of autoimmune diseases, hormonal alterations and/or an ascertainment bias as women may be more likely to seek help for intermittent watery diarrhoea.

Autoimmune diseases, particularly thyroid and/or coeliac disease, are associated with MC [8, 11, 13–15, 21–24]. Fifty-three percent of patients with collagenous and 43% of patients with lymphocytic colitis have at least one concomitant autoimmune disease. Thyroid disease is found in 8.6 to 21% of those with MC [7, 13, 14]. A recent epidemiological study of 164 patients with MC found that 18 (11.0%) had a prior diagnosis of hypothyroidism [12]. Several studies have documented an association between coeliac disease and MC. Later studies have supported that coeliac disease is found in 6–15% with lymphocytic [22, 24] and 3–23% in patients with collagenous colitis [14, 22]. In a recent study conducted by our group, 7% of patients with a new diagnosis of MC had a prior diagnosis of coeliac disease, which was nearly eight times higher than the expected rate for the general population [12].

The association of MC with neoplasia is less well studied. Several case reports have linked collagenous colitis with solid tumours [25, 26] and lymphoproliferative disorders [27]. Nearly 12% of patients with MC were found to have either a past or current diagnosis of malignancy [12]. After adjusting for age and sex, the risk was only higher in women over the age of 65. Other studies examining the risk of developing a malignancy after the diagnosis of MC have been unable to document an association [16, 28].

Only one study has looked at solid organ transplant recipients [17]. The authors reported a point prevalence of 8.8 cases of MC per 1,000 solid organ transplant patients and an annual incidence rate of 5.0 per 1,000 transplant person-years. This incidence rate is ∼50-fold higher than the rate found in the general population.

MC has been associated with the use of several medications including NSAIDs, SSRIs, beta-blockers, statins, biphosphonates, ticlopidine, flutamide and PPIs [23, 29–31]. A recent study showed that those with collagenous colitis more commonly consumed NSAIDs and SSRIs, than controls, while those with lymphocytic colitis more commonly consumed SSRIs, beta-blockers, statins and biphosphonates [30]. Other agents including PPIs [31], ticlopidine [30] and flutamide [29] have been linked in case studies. There have been a few reports of symptom improvement with cessation of NSAIDs [32].

Aetiology

Although MC is technically an IBD and shares a number of parallel etiological aspects with Crohn’s disease and ulcerative colitis (the ‘classical’ IBDs), it is thought to be unrelated to the latter two disorders. The aetiology of MC is likely multi-factorial with a specific mucosal response to various noxious luminal agents occurring in predisposed hosts.

Genetics

Data suggesting a strong genetic contribution are lacking, but as noted familial clusters of MC have been described [20]. In addition, up to 12% of patients with MC have a family history of inflammatory bowel or coeliac disease [24]. Koskela et al. recently reported an association between HLA-DQ2 and MC and also found that MC patients more commonly had an uncommon polymorphism in the tumour necrosis factor alpha (TNFα) gene that results in increased TNFα production [33].

Autoimmunity

There is some evidence of an autoimmune basis to the development of MC. There is a female preponderance and an association of MC with autoimmune-based disorders such as coeliac and thyroid disease. One study found that 40% of patients with Hashimotos’ thyroiditis had histological findings compatible with lymphocytic colitis [13]. Although perinuclear antineutrophil cytoplasmic and antinuclear antibodies are increased in some patients with MC, to date specific autoantibodies for MC have not been defined [34].

Exogenous factors

An increased number of T cells in the epithelium raise the suspicion that MC is the result of a dysfunctional immunological response to a yet undetermined luminal toxin. This theory is supported by the observation that in some patients an elemental diet results in symptom resolution [35]. Further support stems from the observation that diverting the faecal stream with an ileostomy can result in normalisation of histopathological changes in collagenous colitis [36]. After closure, both symptoms and histopathology changes recurred [36]. Proposed luminal/environmental toxins include medications, GI infectious agents and bile salts.

Beaugerie and Pardi [37] have reported that multiple drugs have a high or intermediate probability of causality (Table 2). The mechanism(s) underlying these associations is (are) unknown, but the strong relationship with the use of NSAIDs suggests that prostaglandins may play a role. With the remarkable ORs reported for a variety of medications and the occurrence of MC, which were detailed in the risk factors section, a possible role of these medications has to be considered and the therapeutic approach to MC should include medication withdrawal, if one of the risky medications is to be identified.

Table 2

Drugs associated with microscopic colitis

Strong association
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  
Strong association
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  

Table 2

Drugs associated with microscopic colitis

Strong association
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  
Strong association
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  

Some patients report a preceding gastrointestinal infection, and others with MC exhibit significant improvement with antibiotics [29]. Antibodies to Yesinia are more common in patients with collagenous colitis than in healthy controls [38], and there are case reports linking MC to Clostridium difficile [39] and Campylobacter [40].

Bile acids

Bile acid malabsorption has been documented in 9–60% of patients with lymphocytic and 27–44% of patients with collagenous colitis [41]. Interestingly, bile acid-binding therapy can result in improvement in both those with and those without documented bile acid malabsorption.

Pathophysiology

The precise mechanism of diarrhoea in these patients is not well understood. Factors that may play a role include bile salt induced injury, active chloride excretion, decrease in net sodium absorption, creation of a diffusion barrier by collagen band and increased local inflammatory mediators such as nitric oxide and prostaglandins. It remains unclear which of these results in the symptoms reported by patients.

Two studies have looked at inflammatory cytokines in MC. Patients with MC seem to have a predominantly Th2 type cytokine profile with significant increases in interferon gamma, TNFα and interleukin 15 as well as an increased inducible nitric oxide synthase. Others have found increased levels of TGF-β in patients with collagenous colitis [42].

Clinical Features

The clinical features of collagenous and lymphocytic colitis are similar. The two entities can only be differentiated on histopathological grounds. Both cause chronic (either recurrent or intermittent) watery, non-bloody diarrhoea. Although the clinical course is classically one of the chronic relapsing symptoms, a minority of patients present with an acute onset. Although the diarrhoea may be severe in some patients, complications such as dehydration are rare. Associated symptoms include nocturnal bowel motions, mild abdominal pain, fatigue, slight weight loss, arthralgias and faecal incontinence. Symptoms are often attributed to an irritable bowel syndrome.

The natural history of MC is variable. Many cases are self-limiting, with symptoms lasting a few weeks or months. Others may be symptomatic for years in a relapsing or continuous pattern. Although a small number of case reports have suggested that MC may lead to development of ulcerative colitis, a small case series of patients with MC showed that none developed ulcerative colitis or Crohn’s disease after a follow-up of at least 6 years [28]. Similarly, MC does not appear to affect colorectal cancer risk [16].

Diagnosis/Histopathology

The diagnosis of MC is dependent on (i) a convincing clinical history with other etiologies ruled out, (ii) normal or near normal endoscopic and/or radiographic findings and (iii) endoscopic biopsies with histopathologic findings consistent with MC (Table 3).

Table 3

Histopathological features of collagenous colitis and lymphocytic colitis

Lymphocytic colitis
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 
Lymphocytic colitis
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 

Table 3

Histopathological features of collagenous colitis and lymphocytic colitis

Lymphocytic colitis
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 
Lymphocytic colitis
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 

The first step in the diagnostic process is a thorough history with particular attention paid to risk factors and the disease associated with MC. A complete history helps one to rule out other etiologies that may cause a similar clinical picture such as IBD, coeliac disease, diarrhoea-predominant irritable bowel syndrome or infectious colitis.

Laboratory and radiographic investigations can be employed to help rule out other entities on the differential diagnosis list, but they are typically unremarkable.

Endoscopy with biopsy is necessary to confirm the diagnosis. Colonoscopy generally reveals macroscopically normal mucosa. However, non-specific changes such as erythema, edema, abnormal vascular markings or even tears associated with perforation have been described.

Microscopic evaluation of the colonic mucosa reveals significant inflammatory changes as outlined in Table 3. Both collagenous and lymphocytic colitis demonstrate lymphocytic infiltration of the lamina propria and epithelium. Collagenous is differentiated from lymphocytic colitis by the presence of marked thickening of the subepithelial collagen layer (Table 3). Histological assessment by a pathologist familiar with MC is required.

Since the macroscopic appearance is generally normal and the microscopic lesions can be skipped, random colonic biopsies are recommended. There is currently no consensus whether flexible sigmoidoscopy or colonoscopy is the best initial approach [43]. Flexible sigmoidoscopy is an attractive option due to efficiency (takes less time), cost savings, easier bowel preparation and no requirement for sedation. However, some studies suggest that biopsies of the rectosigmoid colon alone may be insufficient to rule out a diagnosis [44, 45] as up to 40% of cases are missed. Offner et al. reported that the diagnostic yield was highest from biopsies of the transverse colon (83%) and right colon (70%) and lowest from the rectosigmoid (66%) [45]. Other studies have reported lower false-negative rates with left-sided biopsies alone. Tanaka et al. reported that only 10% of patients with MC had isolated right-sided disease [44], and a larger study by Fine et al. reported that all 80 patients evaluated for chronic diarrhoea who were diagnosed with MC had histological evidence of MC in the left colon, whereas biopsies taken from other regions of the colon could be false negative [46].

The practical benefits of flexible sigmoidoscopy must be weighed against the potentially increased diagnostic yield of colonoscopy. The choice of which procedure to perform will depend on the clinical scenario, local expertise and resource constraints. If initial biopsies obtained on flexible sigmoidoscopy do not lead to a diagnosis and the suspicion of MC is high, we recommend a colonoscopy.

Treatment

Treatment recommendations for MC are largely based on case reports and uncontrolled studies, and Table 4 gives a suggested algorithm. Specific agents evaluated include 5-aminosalicylic acid (5-ASA), prednisone, immunomodulators, bismuth, probiotics and Boswellia extract. Small randomised controlled trials have shown that agents such as budesonide offer promise as an effective form of symptomatic therapy for both collagenous and lymphocytic colitis.

Table 4

Suggested treatment algorithm

Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e.g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 
Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e.g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 

Table 4

Suggested treatment algorithm

Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e.g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 
Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e.g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 

As a first step in managing MC, an in depth medication history should be taken with potentially precipitating medications stopped where possible. Associated conditions such as coeliac disease should be appropriately managed. In patients with mild symptoms, dietary restrictions like avoiding caffeine and lactose might be helpful.

Anti-diarrhoeal therapies

Non-specific anti-diarrhoeal therapies such as loperamide are commonly used in the management of MC. Retrospective studies have suggested benefit with doses ranging from 2 to 16 mg per day [29, 47]. Due to the safety of this agent and the possibility of spontaneous remission, we suggest loperamide for first-line therapy for MC. In our experience, however, those with moderate to severe diarrhoea or associated complaints of significant abdominal pain often fail to respond to anti-diarrhoeal therapy alone.

Aminosalicylates

Uncontrolled retrospective series have suggested symptomatic improvement in up to 50% of patients with MC treated with mesalamine (5-ASA) [24, 29, 48]. A recent randomised trial of 64 MC patients compared mesalamine (800 mg tid) to mesalamine (800 mg tid) and cholestyramine (4 g/day) [49]. Treatment resulted in resolution of diarrhoea in 84% overall after 2 weeks. If treatment was continued over 6 months, clinical and histological remission was achieved in 85% of those with lymphocytic and 91% of those with collagenous colitis. The number of relapsing patients after 6 months of treatment was low, and symptomatic relapses could be successfully retreated. Overall, the combination of mesalamine with cholestyramine was slightly superior [48].

Budesonide

Budesonide is currently the most promising treatment for collagenous colitis. Three trials involving 94 patients have shown that budesonide therapy (9 mg daily for 6–8 weeks) compared to placebo resulted in statistically significant improvements in clinical symptoms [50–52] and quality of life [53]. A recent Cochrane database meta-analysis reported pooled odds ratio of 12.3 for clinical response with budesonide with a number needed to treat of two [54]. Although effective in the short-term, all trials showed a high rate (61–80%) of relapse within ∼2 weeks of budesonide cessation. Age <60 was a significant risk factor for relapse. Although, there are no studies to support a tapering course of budesonide, many clinicians employ this in an effort to minimise the likelihood of relapse.

One randomised controlled trial of budesonide for the treatment of lymphocytic colitis has been conducted. When compared to the placebo arm, the patients randomised to budesonide (9 mg daily × 6 weeks) had a statistically significantly higher rate of remission (<3 bowel movements/day) at 3 and 6 weeks [55].

Prednisolone

A double-blind, placebo-controlled randomised trial of oral prednisolone 50 mg daily for 2 weeks for collagenous colitis was inconclusive because of the low number of patients enrolled [56]. Studies examining the effect of prednisone in the treatment of lymphocytic colitis have not been performed.

Immunosuppressive therapy

Immunosuppressive therapy with azathioprine or methotrexate has been utilised in patients either refractory to corticosteroid therapy or corticosteroid dependent, but there are no randomised controlled trials to guide therapy with these medications [57, 58].

Other therapies

Small clinical trials studying bismuth subsalicylate, Boswellia serrata extract, probiotics and empirical antibiotic treatment for collagenous and lymphocytic colitis look promising but cannot be suggested outside of such trials. Finally, case reports suggest that pentoxifylline, verapamil and subcutaneous octreotide might be treatment options, but their use cannot be recommended at this time. When medical therapy was unsuccessful and symptoms were very severe, surgical interventions such as a temporary or permanent loop ileostomy or even a proctocolectomy have been employed in smaller case series.

Recommended approach to treatment

Firstly, the diagnosis must be confirmed and other potential etiologies ruled out. Any complications related to chronic diarrhoea such as dehydration or electrolyte abnormalities must be identified and corrected. Potentially contributing medications such as PPIs or NSAIDs should be discontinued if possible. Depending on symptom severity, non-specific anti-diarrhoeal agents like loperamide, bile salt binding resins or bismuth should be tried. If this fails and the symptoms are sufficiently severe, the patient should be cared for or referred to someone with experience in dealing with this condition. Budesonide, 9 mg daily for at least 6 weeks, could then be used. Some clinical reports suggest a maintenance dose of budesonide 3–6 mg daily may be effective, but this approach has not been studied prospectively. If administration becomes long-term, patients have to be monitored for the development of the complications of chronic steroid therapy. If symptoms fail to improve, clinicians should consider alternative diagnoses. Prednisone, 5-ASA, immunosuppressive therapy or surgery could be cautiously considered for refractory cases.

Prognosis/Outcome

MC has a variable course, but overall, the long-term prognosis is good. Symptoms of diarrhoea and abdominal pain may precede the diagnosis by a number of months. These symptoms are generally mild. With most patients, symptoms resolve spontaneously or with symptomatic therapy. MC has not been associated with an increased risk of colorectal cancer — this information should be conveyed to the patients. There is only limited information about the long-term course and the prognosis of MC. One study followed 81 patients for an average of 37 months. Their initial symptoms were successfully treated with a number of different drugs. Approximately 30% of these patients relapsed with ∼70% remaining symptom free [59]. Prospective observational and clinical trials are warranted to specifically address the issue of prognosis and the durability of the response to initial therapy.

Conclusion

MC is a common cause of diarrhoea in older patients. After ruling our other causes of diarrhoea, flexible sigmoidoscopy (or colonoscopy) with appropriate biopsies allows for the diagnosis of either lymphocytic or collagenous colitis by histological analysis. Based on symptom severity, a stepwise approach to the treatment is suggested.

Key points

  • MC is common in older adults.

  • The incidence of MC is rising.

  • MC is diagnosed in biopsies taken during a colonoscopy.

  • MC is treated using a stepwise approach.

Conflicts of interest

None.

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© The Author 2010. Published by Oxford University Press on behalf of the British Geriatrics Society. All rights reserved. For Permissions, please email: [email protected]

Oxford University Press

Microscopic colitis — a common cause of diarrhoea in older adults | Age and Ageing

Abstract

Diarrhoeal diseases are common in older populations and often markedly affect their quality of life. Although there are numerous potential causes, microscopic colitis (MC) is increasingly recognised as a major diagnostic entity in older individuals. MC is comprised of two distinct histological forms — collagenous colitis and lymphocytic colitis, both of which frequently occur in older populations. Recent studies suggest that between 10 and 30% of older patients investigated for chronic diarrhoea with an endoscopically normal appearing colon will have MC. It is unclear why MC is more common in older populations, but it is associated with both autoimmune disorders and several drugs that are commonly used by seniors. A definitive diagnosis can only be made with colonic biopsies. Since MC was first described in 1976 and only recently recognised as a common cause of diarrhoea, many practising physicians may not be aware of this entity. In this review, we outline the epidemiology, risk factors associated with MC, its pathophysiology, the approach to diagnosis and the management of these individuals.

Introduction

At any one point in time, ∼9% of an older out-patient population will be experiencing diarrhoea [1]. While the prevalence of chronic diarrhoea in older patients is unknown, it is a significant cause of morbidity among them — especially in vulnerable populations like those residing in long-term care facilities. In older populations, chronic diarrhoea can arise from a variety of conditions like coeliac disease and inflammatory bowel disease (IBD) [2]. Microscopic colitis (MC) has emerged as a new and common cause of chronic diarrhoea in the general population.

MC is an umbrella term for a group of inflammatory diseases of the colon where the colonic lining appears endoscopically normal, but histologic examination on biopsy reveals increased intraepithelial lymphocytes (IEL) in the colonic mucosa. MC is subgrouped into two different forms that are characterised by histological means – lymphocytic and collagenous colitis. While both subgroups have increased numbers of IELs, a thickened collagen band on the basement membrane of the colonic epithelium is seen in the latter subtype.

MC is frequently associated with systemic disorders (such as hypothyroidism) and the use of certain medications. Not surprisingly, the disorder is being increasingly recognised as a common cause of diarrhoea in middle-aged and older patients. For many of these patients, especially women, the looser and/or more frequent movements may lead to rectal urgency and faecal incontinence or may result in a exacerbation of a previously controlled but latent insufficient anal sphincter [3].

Epidemiology

When first described over 30 years ago, MC was believed to be rare [4, 5]. However, studies have shown that it is a common cause of watery diarrhoea, particularly in older female patients [6]. MC is a disease that predominantly affects older patients, with incidence rates anywhere from 5 to 10 times higher in those over 65.

Some population-based studies have looked at the incidence of MC in European and North American populations [7–12]. The overall total population annual incidence of collagenous colitis has ranged from 1.1 to 5.2 cases per 100,000 (Table 1) while the annual incidence of lymphocytic colitis per 100,000 was reportedly 3.1–5.5 (Table 1). More recent studies suggest an even higher incidence for MC. This is likely because of an increased awareness of the entity with more colonic biopsies being performed. For example, American incidence rates of 7.1 and 12.6 per 100,000 person-years for collagenous and lymphocytic colitis, respectively, were recently reported with a point prevalence for MC of 103.0 (39.3 for collagenous and 63.7 for lymphocytic colitis per 100,000) [11]. Reports suggest that the incidence of MC approaches that of ulcerative colitis and Crohn’s disease [7].

Table 1

Epidemiology of microscopic colitis

Study
Patients (n)
Incidence CC per 105
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.8 N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.2 4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 
Study
Patients (n)
Incidence CC per 105
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.8 N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.2 4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 

Table 1

Epidemiology of microscopic colitis

Study
Patients (n)
Incidence CC per 105
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.8 N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.2 4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 
Study
Patients (n)
Incidence CC per 105
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.8 N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.2 4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 

Risk Factors and Disease Associations

Increasing age [7–9], female sex [7–9], autoimmune diseases such as thyroid disease [13] and coeliac disease [14, 15], past or current diagnosis of malignancy [12, 16] and solid organ transplant are identified as risk factors for MC [17].

The incidence of MC increases substantially with advancing age [7–9]. The mean age of diagnosis of the condition is in the fifth and sixth decades. In one Canadian study, patients greater than 65 years of age were more than five times as likely to have developed MC [12]. The reasons for this are unknown. While a genetic or environmental component seems possible since familial cases have also been reported [18–20], MC does appear to be an age-associated condition.

Female sex is also a major risk factor [7–9, 11, 21, 22]. This predisposition is more pronounced for the collagenous colitis subtype. Population-based studies report a female to male ratio of 4.4–7.9:1 for collagenous and 1.8–5.0:1 for lymphocytic colitis [7–12]. The reasons for the higher rate among women are also unknown but might be related to the higher likelihood of autoimmune diseases, hormonal alterations and/or an ascertainment bias as women may be more likely to seek help for intermittent watery diarrhoea.

Autoimmune diseases, particularly thyroid and/or coeliac disease, are associated with MC [8, 11, 13–15, 21–24]. Fifty-three percent of patients with collagenous and 43% of patients with lymphocytic colitis have at least one concomitant autoimmune disease. Thyroid disease is found in 8.6 to 21% of those with MC [7, 13, 14]. A recent epidemiological study of 164 patients with MC found that 18 (11.0%) had a prior diagnosis of hypothyroidism [12]. Several studies have documented an association between coeliac disease and MC. Later studies have supported that coeliac disease is found in 6–15% with lymphocytic [22, 24] and 3–23% in patients with collagenous colitis [14, 22]. In a recent study conducted by our group, 7% of patients with a new diagnosis of MC had a prior diagnosis of coeliac disease, which was nearly eight times higher than the expected rate for the general population [12].

The association of MC with neoplasia is less well studied. Several case reports have linked collagenous colitis with solid tumours [25, 26] and lymphoproliferative disorders [27]. Nearly 12% of patients with MC were found to have either a past or current diagnosis of malignancy [12]. After adjusting for age and sex, the risk was only higher in women over the age of 65. Other studies examining the risk of developing a malignancy after the diagnosis of MC have been unable to document an association [16, 28].

Only one study has looked at solid organ transplant recipients [17]. The authors reported a point prevalence of 8.8 cases of MC per 1,000 solid organ transplant patients and an annual incidence rate of 5.0 per 1,000 transplant person-years. This incidence rate is ∼50-fold higher than the rate found in the general population.

MC has been associated with the use of several medications including NSAIDs, SSRIs, beta-blockers, statins, biphosphonates, ticlopidine, flutamide and PPIs [23, 29–31]. A recent study showed that those with collagenous colitis more commonly consumed NSAIDs and SSRIs, than controls, while those with lymphocytic colitis more commonly consumed SSRIs, beta-blockers, statins and biphosphonates [30]. Other agents including PPIs [31], ticlopidine [30] and flutamide [29] have been linked in case studies. There have been a few reports of symptom improvement with cessation of NSAIDs [32].

Aetiology

Although MC is technically an IBD and shares a number of parallel etiological aspects with Crohn’s disease and ulcerative colitis (the ‘classical’ IBDs), it is thought to be unrelated to the latter two disorders. The aetiology of MC is likely multi-factorial with a specific mucosal response to various noxious luminal agents occurring in predisposed hosts.

Genetics

Data suggesting a strong genetic contribution are lacking, but as noted familial clusters of MC have been described [20]. In addition, up to 12% of patients with MC have a family history of inflammatory bowel or coeliac disease [24]. Koskela et al. recently reported an association between HLA-DQ2 and MC and also found that MC patients more commonly had an uncommon polymorphism in the tumour necrosis factor alpha (TNFα) gene that results in increased TNFα production [33].

Autoimmunity

There is some evidence of an autoimmune basis to the development of MC. There is a female preponderance and an association of MC with autoimmune-based disorders such as coeliac and thyroid disease. One study found that 40% of patients with Hashimotos’ thyroiditis had histological findings compatible with lymphocytic colitis [13]. Although perinuclear antineutrophil cytoplasmic and antinuclear antibodies are increased in some patients with MC, to date specific autoantibodies for MC have not been defined [34].

Exogenous factors

An increased number of T cells in the epithelium raise the suspicion that MC is the result of a dysfunctional immunological response to a yet undetermined luminal toxin. This theory is supported by the observation that in some patients an elemental diet results in symptom resolution [35]. Further support stems from the observation that diverting the faecal stream with an ileostomy can result in normalisation of histopathological changes in collagenous colitis [36]. After closure, both symptoms and histopathology changes recurred [36]. Proposed luminal/environmental toxins include medications, GI infectious agents and bile salts.

Beaugerie and Pardi [37] have reported that multiple drugs have a high or intermediate probability of causality (Table 2). The mechanism(s) underlying these associations is (are) unknown, but the strong relationship with the use of NSAIDs suggests that prostaglandins may play a role. With the remarkable ORs reported for a variety of medications and the occurrence of MC, which were detailed in the risk factors section, a possible role of these medications has to be considered and the therapeutic approach to MC should include medication withdrawal, if one of the risky medications is to be identified.

Table 2

Drugs associated with microscopic colitis

Strong association
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  
Strong association
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  

Table 2

Drugs associated with microscopic colitis

Strong association
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  
Strong association
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  

Some patients report a preceding gastrointestinal infection, and others with MC exhibit significant improvement with antibiotics [29]. Antibodies to Yesinia are more common in patients with collagenous colitis than in healthy controls [38], and there are case reports linking MC to Clostridium difficile [39] and Campylobacter [40].

Bile acids

Bile acid malabsorption has been documented in 9–60% of patients with lymphocytic and 27–44% of patients with collagenous colitis [41]. Interestingly, bile acid-binding therapy can result in improvement in both those with and those without documented bile acid malabsorption.

Pathophysiology

The precise mechanism of diarrhoea in these patients is not well understood. Factors that may play a role include bile salt induced injury, active chloride excretion, decrease in net sodium absorption, creation of a diffusion barrier by collagen band and increased local inflammatory mediators such as nitric oxide and prostaglandins. It remains unclear which of these results in the symptoms reported by patients.

Two studies have looked at inflammatory cytokines in MC. Patients with MC seem to have a predominantly Th2 type cytokine profile with significant increases in interferon gamma, TNFα and interleukin 15 as well as an increased inducible nitric oxide synthase. Others have found increased levels of TGF-β in patients with collagenous colitis [42].

Clinical Features

The clinical features of collagenous and lymphocytic colitis are similar. The two entities can only be differentiated on histopathological grounds. Both cause chronic (either recurrent or intermittent) watery, non-bloody diarrhoea. Although the clinical course is classically one of the chronic relapsing symptoms, a minority of patients present with an acute onset. Although the diarrhoea may be severe in some patients, complications such as dehydration are rare. Associated symptoms include nocturnal bowel motions, mild abdominal pain, fatigue, slight weight loss, arthralgias and faecal incontinence. Symptoms are often attributed to an irritable bowel syndrome.

The natural history of MC is variable. Many cases are self-limiting, with symptoms lasting a few weeks or months. Others may be symptomatic for years in a relapsing or continuous pattern. Although a small number of case reports have suggested that MC may lead to development of ulcerative colitis, a small case series of patients with MC showed that none developed ulcerative colitis or Crohn’s disease after a follow-up of at least 6 years [28]. Similarly, MC does not appear to affect colorectal cancer risk [16].

Diagnosis/Histopathology

The diagnosis of MC is dependent on (i) a convincing clinical history with other etiologies ruled out, (ii) normal or near normal endoscopic and/or radiographic findings and (iii) endoscopic biopsies with histopathologic findings consistent with MC (Table 3).

Table 3

Histopathological features of collagenous colitis and lymphocytic colitis

Lymphocytic colitis
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 
Lymphocytic colitis
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 

Table 3

Histopathological features of collagenous colitis and lymphocytic colitis

Lymphocytic colitis
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 
Lymphocytic colitis
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 

The first step in the diagnostic process is a thorough history with particular attention paid to risk factors and the disease associated with MC. A complete history helps one to rule out other etiologies that may cause a similar clinical picture such as IBD, coeliac disease, diarrhoea-predominant irritable bowel syndrome or infectious colitis.

Laboratory and radiographic investigations can be employed to help rule out other entities on the differential diagnosis list, but they are typically unremarkable.

Endoscopy with biopsy is necessary to confirm the diagnosis. Colonoscopy generally reveals macroscopically normal mucosa. However, non-specific changes such as erythema, edema, abnormal vascular markings or even tears associated with perforation have been described.

Microscopic evaluation of the colonic mucosa reveals significant inflammatory changes as outlined in Table 3. Both collagenous and lymphocytic colitis demonstrate lymphocytic infiltration of the lamina propria and epithelium. Collagenous is differentiated from lymphocytic colitis by the presence of marked thickening of the subepithelial collagen layer (Table 3). Histological assessment by a pathologist familiar with MC is required.

Since the macroscopic appearance is generally normal and the microscopic lesions can be skipped, random colonic biopsies are recommended. There is currently no consensus whether flexible sigmoidoscopy or colonoscopy is the best initial approach [43]. Flexible sigmoidoscopy is an attractive option due to efficiency (takes less time), cost savings, easier bowel preparation and no requirement for sedation. However, some studies suggest that biopsies of the rectosigmoid colon alone may be insufficient to rule out a diagnosis [44, 45] as up to 40% of cases are missed. Offner et al. reported that the diagnostic yield was highest from biopsies of the transverse colon (83%) and right colon (70%) and lowest from the rectosigmoid (66%) [45]. Other studies have reported lower false-negative rates with left-sided biopsies alone. Tanaka et al. reported that only 10% of patients with MC had isolated right-sided disease [44], and a larger study by Fine et al. reported that all 80 patients evaluated for chronic diarrhoea who were diagnosed with MC had histological evidence of MC in the left colon, whereas biopsies taken from other regions of the colon could be false negative [46].

The practical benefits of flexible sigmoidoscopy must be weighed against the potentially increased diagnostic yield of colonoscopy. The choice of which procedure to perform will depend on the clinical scenario, local expertise and resource constraints. If initial biopsies obtained on flexible sigmoidoscopy do not lead to a diagnosis and the suspicion of MC is high, we recommend a colonoscopy.

Treatment

Treatment recommendations for MC are largely based on case reports and uncontrolled studies, and Table 4 gives a suggested algorithm. Specific agents evaluated include 5-aminosalicylic acid (5-ASA), prednisone, immunomodulators, bismuth, probiotics and Boswellia extract. Small randomised controlled trials have shown that agents such as budesonide offer promise as an effective form of symptomatic therapy for both collagenous and lymphocytic colitis.

Table 4

Suggested treatment algorithm

Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e.g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 
Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e.g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 

Table 4

Suggested treatment algorithm

Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e.g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 
Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e.g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 

As a first step in managing MC, an in depth medication history should be taken with potentially precipitating medications stopped where possible. Associated conditions such as coeliac disease should be appropriately managed. In patients with mild symptoms, dietary restrictions like avoiding caffeine and lactose might be helpful.

Anti-diarrhoeal therapies

Non-specific anti-diarrhoeal therapies such as loperamide are commonly used in the management of MC. Retrospective studies have suggested benefit with doses ranging from 2 to 16 mg per day [29, 47]. Due to the safety of this agent and the possibility of spontaneous remission, we suggest loperamide for first-line therapy for MC. In our experience, however, those with moderate to severe diarrhoea or associated complaints of significant abdominal pain often fail to respond to anti-diarrhoeal therapy alone.

Aminosalicylates

Uncontrolled retrospective series have suggested symptomatic improvement in up to 50% of patients with MC treated with mesalamine (5-ASA) [24, 29, 48]. A recent randomised trial of 64 MC patients compared mesalamine (800 mg tid) to mesalamine (800 mg tid) and cholestyramine (4 g/day) [49]. Treatment resulted in resolution of diarrhoea in 84% overall after 2 weeks. If treatment was continued over 6 months, clinical and histological remission was achieved in 85% of those with lymphocytic and 91% of those with collagenous colitis. The number of relapsing patients after 6 months of treatment was low, and symptomatic relapses could be successfully retreated. Overall, the combination of mesalamine with cholestyramine was slightly superior [48].

Budesonide

Budesonide is currently the most promising treatment for collagenous colitis. Three trials involving 94 patients have shown that budesonide therapy (9 mg daily for 6–8 weeks) compared to placebo resulted in statistically significant improvements in clinical symptoms [50–52] and quality of life [53]. A recent Cochrane database meta-analysis reported pooled odds ratio of 12.3 for clinical response with budesonide with a number needed to treat of two [54]. Although effective in the short-term, all trials showed a high rate (61–80%) of relapse within ∼2 weeks of budesonide cessation. Age <60 was a significant risk factor for relapse. Although, there are no studies to support a tapering course of budesonide, many clinicians employ this in an effort to minimise the likelihood of relapse.

One randomised controlled trial of budesonide for the treatment of lymphocytic colitis has been conducted. When compared to the placebo arm, the patients randomised to budesonide (9 mg daily × 6 weeks) had a statistically significantly higher rate of remission (<3 bowel movements/day) at 3 and 6 weeks [55].

Prednisolone

A double-blind, placebo-controlled randomised trial of oral prednisolone 50 mg daily for 2 weeks for collagenous colitis was inconclusive because of the low number of patients enrolled [56]. Studies examining the effect of prednisone in the treatment of lymphocytic colitis have not been performed.

Immunosuppressive therapy

Immunosuppressive therapy with azathioprine or methotrexate has been utilised in patients either refractory to corticosteroid therapy or corticosteroid dependent, but there are no randomised controlled trials to guide therapy with these medications [57, 58].

Other therapies

Small clinical trials studying bismuth subsalicylate, Boswellia serrata extract, probiotics and empirical antibiotic treatment for collagenous and lymphocytic colitis look promising but cannot be suggested outside of such trials. Finally, case reports suggest that pentoxifylline, verapamil and subcutaneous octreotide might be treatment options, but their use cannot be recommended at this time. When medical therapy was unsuccessful and symptoms were very severe, surgical interventions such as a temporary or permanent loop ileostomy or even a proctocolectomy have been employed in smaller case series.

Recommended approach to treatment

Firstly, the diagnosis must be confirmed and other potential etiologies ruled out. Any complications related to chronic diarrhoea such as dehydration or electrolyte abnormalities must be identified and corrected. Potentially contributing medications such as PPIs or NSAIDs should be discontinued if possible. Depending on symptom severity, non-specific anti-diarrhoeal agents like loperamide, bile salt binding resins or bismuth should be tried. If this fails and the symptoms are sufficiently severe, the patient should be cared for or referred to someone with experience in dealing with this condition. Budesonide, 9 mg daily for at least 6 weeks, could then be used. Some clinical reports suggest a maintenance dose of budesonide 3–6 mg daily may be effective, but this approach has not been studied prospectively. If administration becomes long-term, patients have to be monitored for the development of the complications of chronic steroid therapy. If symptoms fail to improve, clinicians should consider alternative diagnoses. Prednisone, 5-ASA, immunosuppressive therapy or surgery could be cautiously considered for refractory cases.

Prognosis/Outcome

MC has a variable course, but overall, the long-term prognosis is good. Symptoms of diarrhoea and abdominal pain may precede the diagnosis by a number of months. These symptoms are generally mild. With most patients, symptoms resolve spontaneously or with symptomatic therapy. MC has not been associated with an increased risk of colorectal cancer — this information should be conveyed to the patients. There is only limited information about the long-term course and the prognosis of MC. One study followed 81 patients for an average of 37 months. Their initial symptoms were successfully treated with a number of different drugs. Approximately 30% of these patients relapsed with ∼70% remaining symptom free [59]. Prospective observational and clinical trials are warranted to specifically address the issue of prognosis and the durability of the response to initial therapy.

Conclusion

MC is a common cause of diarrhoea in older patients. After ruling our other causes of diarrhoea, flexible sigmoidoscopy (or colonoscopy) with appropriate biopsies allows for the diagnosis of either lymphocytic or collagenous colitis by histological analysis. Based on symptom severity, a stepwise approach to the treatment is suggested.

Key points

  • MC is common in older adults.

  • The incidence of MC is rising.

  • MC is diagnosed in biopsies taken during a colonoscopy.

  • MC is treated using a stepwise approach.

Conflicts of interest

None.

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© The Author 2010. Published by Oxford University Press on behalf of the British Geriatrics Society. All rights reserved. For Permissions, please email: [email protected]

Oxford University Press

Microscopic colitis — a common cause of diarrhoea in older adults | Age and Ageing

Abstract

Diarrhoeal diseases are common in older populations and often markedly affect their quality of life. Although there are numerous potential causes, microscopic colitis (MC) is increasingly recognised as a major diagnostic entity in older individuals. MC is comprised of two distinct histological forms — collagenous colitis and lymphocytic colitis, both of which frequently occur in older populations. Recent studies suggest that between 10 and 30% of older patients investigated for chronic diarrhoea with an endoscopically normal appearing colon will have MC. It is unclear why MC is more common in older populations, but it is associated with both autoimmune disorders and several drugs that are commonly used by seniors. A definitive diagnosis can only be made with colonic biopsies. Since MC was first described in 1976 and only recently recognised as a common cause of diarrhoea, many practising physicians may not be aware of this entity. In this review, we outline the epidemiology, risk factors associated with MC, its pathophysiology, the approach to diagnosis and the management of these individuals.

Introduction

At any one point in time, ∼9% of an older out-patient population will be experiencing diarrhoea [1]. While the prevalence of chronic diarrhoea in older patients is unknown, it is a significant cause of morbidity among them — especially in vulnerable populations like those residing in long-term care facilities. In older populations, chronic diarrhoea can arise from a variety of conditions like coeliac disease and inflammatory bowel disease (IBD) [2]. Microscopic colitis (MC) has emerged as a new and common cause of chronic diarrhoea in the general population.

MC is an umbrella term for a group of inflammatory diseases of the colon where the colonic lining appears endoscopically normal, but histologic examination on biopsy reveals increased intraepithelial lymphocytes (IEL) in the colonic mucosa. MC is subgrouped into two different forms that are characterised by histological means – lymphocytic and collagenous colitis. While both subgroups have increased numbers of IELs, a thickened collagen band on the basement membrane of the colonic epithelium is seen in the latter subtype.

MC is frequently associated with systemic disorders (such as hypothyroidism) and the use of certain medications. Not surprisingly, the disorder is being increasingly recognised as a common cause of diarrhoea in middle-aged and older patients. For many of these patients, especially women, the looser and/or more frequent movements may lead to rectal urgency and faecal incontinence or may result in a exacerbation of a previously controlled but latent insufficient anal sphincter [3].

Epidemiology

When first described over 30 years ago, MC was believed to be rare [4, 5]. However, studies have shown that it is a common cause of watery diarrhoea, particularly in older female patients [6]. MC is a disease that predominantly affects older patients, with incidence rates anywhere from 5 to 10 times higher in those over 65.

Some population-based studies have looked at the incidence of MC in European and North American populations [7–12]. The overall total population annual incidence of collagenous colitis has ranged from 1.1 to 5.2 cases per 100,000 (Table 1) while the annual incidence of lymphocytic colitis per 100,000 was reportedly 3.1–5.5 (Table 1). More recent studies suggest an even higher incidence for MC. This is likely because of an increased awareness of the entity with more colonic biopsies being performed. For example, American incidence rates of 7.1 and 12.6 per 100,000 person-years for collagenous and lymphocytic colitis, respectively, were recently reported with a point prevalence for MC of 103.0 (39.3 for collagenous and 63.7 for lymphocytic colitis per 100,000) [11]. Reports suggest that the incidence of MC approaches that of ulcerative colitis and Crohn’s disease [7].

Table 1

Epidemiology of microscopic colitis

Study
Patients (n)
Incidence CC per 105
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.8 N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.2 4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 
Study
Patients (n)
Incidence CC per 105
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.8 N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.2 4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 

Table 1

Epidemiology of microscopic colitis

Study
Patients (n)
Incidence CC per 105
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.8 N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.2 4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 
Study
Patients (n)
Incidence CC per 105
Incidence LC per 105
Sweden (1984–1993) [9] 30 1.8 N/A 
Spain (1993–1997) [10] 60 1.1 3.1 
Sweden (1993–1998) [7] 97 4.9 4.4 
Iceland (1995–1999) [8] 125 5.2 4.0 
USA (1985–2001) [11] 130 3.1 5.5 
Sweden (1984–2004) [60] 115 5.2 5.5 
Canada (2002–2004) [12] 164 4.6 5.4 

Risk Factors and Disease Associations

Increasing age [7–9], female sex [7–9], autoimmune diseases such as thyroid disease [13] and coeliac disease [14, 15], past or current diagnosis of malignancy [12, 16] and solid organ transplant are identified as risk factors for MC [17].

The incidence of MC increases substantially with advancing age [7–9]. The mean age of diagnosis of the condition is in the fifth and sixth decades. In one Canadian study, patients greater than 65 years of age were more than five times as likely to have developed MC [12]. The reasons for this are unknown. While a genetic or environmental component seems possible since familial cases have also been reported [18–20], MC does appear to be an age-associated condition.

Female sex is also a major risk factor [7–9, 11, 21, 22]. This predisposition is more pronounced for the collagenous colitis subtype. Population-based studies report a female to male ratio of 4.4–7.9:1 for collagenous and 1.8–5.0:1 for lymphocytic colitis [7–12]. The reasons for the higher rate among women are also unknown but might be related to the higher likelihood of autoimmune diseases, hormonal alterations and/or an ascertainment bias as women may be more likely to seek help for intermittent watery diarrhoea.

Autoimmune diseases, particularly thyroid and/or coeliac disease, are associated with MC [8, 11, 13–15, 21–24]. Fifty-three percent of patients with collagenous and 43% of patients with lymphocytic colitis have at least one concomitant autoimmune disease. Thyroid disease is found in 8.6 to 21% of those with MC [7, 13, 14]. A recent epidemiological study of 164 patients with MC found that 18 (11.0%) had a prior diagnosis of hypothyroidism [12]. Several studies have documented an association between coeliac disease and MC. Later studies have supported that coeliac disease is found in 6–15% with lymphocytic [22, 24] and 3–23% in patients with collagenous colitis [14, 22]. In a recent study conducted by our group, 7% of patients with a new diagnosis of MC had a prior diagnosis of coeliac disease, which was nearly eight times higher than the expected rate for the general population [12].

The association of MC with neoplasia is less well studied. Several case reports have linked collagenous colitis with solid tumours [25, 26] and lymphoproliferative disorders [27]. Nearly 12% of patients with MC were found to have either a past or current diagnosis of malignancy [12]. After adjusting for age and sex, the risk was only higher in women over the age of 65. Other studies examining the risk of developing a malignancy after the diagnosis of MC have been unable to document an association [16, 28].

Only one study has looked at solid organ transplant recipients [17]. The authors reported a point prevalence of 8.8 cases of MC per 1,000 solid organ transplant patients and an annual incidence rate of 5.0 per 1,000 transplant person-years. This incidence rate is ∼50-fold higher than the rate found in the general population.

MC has been associated with the use of several medications including NSAIDs, SSRIs, beta-blockers, statins, biphosphonates, ticlopidine, flutamide and PPIs [23, 29–31]. A recent study showed that those with collagenous colitis more commonly consumed NSAIDs and SSRIs, than controls, while those with lymphocytic colitis more commonly consumed SSRIs, beta-blockers, statins and biphosphonates [30]. Other agents including PPIs [31], ticlopidine [30] and flutamide [29] have been linked in case studies. There have been a few reports of symptom improvement with cessation of NSAIDs [32].

Aetiology

Although MC is technically an IBD and shares a number of parallel etiological aspects with Crohn’s disease and ulcerative colitis (the ‘classical’ IBDs), it is thought to be unrelated to the latter two disorders. The aetiology of MC is likely multi-factorial with a specific mucosal response to various noxious luminal agents occurring in predisposed hosts.

Genetics

Data suggesting a strong genetic contribution are lacking, but as noted familial clusters of MC have been described [20]. In addition, up to 12% of patients with MC have a family history of inflammatory bowel or coeliac disease [24]. Koskela et al. recently reported an association between HLA-DQ2 and MC and also found that MC patients more commonly had an uncommon polymorphism in the tumour necrosis factor alpha (TNFα) gene that results in increased TNFα production [33].

Autoimmunity

There is some evidence of an autoimmune basis to the development of MC. There is a female preponderance and an association of MC with autoimmune-based disorders such as coeliac and thyroid disease. One study found that 40% of patients with Hashimotos’ thyroiditis had histological findings compatible with lymphocytic colitis [13]. Although perinuclear antineutrophil cytoplasmic and antinuclear antibodies are increased in some patients with MC, to date specific autoantibodies for MC have not been defined [34].

Exogenous factors

An increased number of T cells in the epithelium raise the suspicion that MC is the result of a dysfunctional immunological response to a yet undetermined luminal toxin. This theory is supported by the observation that in some patients an elemental diet results in symptom resolution [35]. Further support stems from the observation that diverting the faecal stream with an ileostomy can result in normalisation of histopathological changes in collagenous colitis [36]. After closure, both symptoms and histopathology changes recurred [36]. Proposed luminal/environmental toxins include medications, GI infectious agents and bile salts.

Beaugerie and Pardi [37] have reported that multiple drugs have a high or intermediate probability of causality (Table 2). The mechanism(s) underlying these associations is (are) unknown, but the strong relationship with the use of NSAIDs suggests that prostaglandins may play a role. With the remarkable ORs reported for a variety of medications and the occurrence of MC, which were detailed in the risk factors section, a possible role of these medications has to be considered and the therapeutic approach to MC should include medication withdrawal, if one of the risky medications is to be identified.

Table 2

Drugs associated with microscopic colitis

Strong association
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  
Strong association
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  

Table 2

Drugs associated with microscopic colitis

Strong association
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  
Strong association
Possible association
NSAIDs Carbamazepine 
Lansoprazole Flutamide 
Aspirin Lisinopril 
Flutamide Modopar (levodopa and benserazide) 
Sertraline Oxetorone 
Ticlopidine Paroxetine 
Ranitidine Tardyferon 
Acarbose Vinburnine 
Simvastatin  

Some patients report a preceding gastrointestinal infection, and others with MC exhibit significant improvement with antibiotics [29]. Antibodies to Yesinia are more common in patients with collagenous colitis than in healthy controls [38], and there are case reports linking MC to Clostridium difficile [39] and Campylobacter [40].

Bile acids

Bile acid malabsorption has been documented in 9–60% of patients with lymphocytic and 27–44% of patients with collagenous colitis [41]. Interestingly, bile acid-binding therapy can result in improvement in both those with and those without documented bile acid malabsorption.

Pathophysiology

The precise mechanism of diarrhoea in these patients is not well understood. Factors that may play a role include bile salt induced injury, active chloride excretion, decrease in net sodium absorption, creation of a diffusion barrier by collagen band and increased local inflammatory mediators such as nitric oxide and prostaglandins. It remains unclear which of these results in the symptoms reported by patients.

Two studies have looked at inflammatory cytokines in MC. Patients with MC seem to have a predominantly Th2 type cytokine profile with significant increases in interferon gamma, TNFα and interleukin 15 as well as an increased inducible nitric oxide synthase. Others have found increased levels of TGF-β in patients with collagenous colitis [42].

Clinical Features

The clinical features of collagenous and lymphocytic colitis are similar. The two entities can only be differentiated on histopathological grounds. Both cause chronic (either recurrent or intermittent) watery, non-bloody diarrhoea. Although the clinical course is classically one of the chronic relapsing symptoms, a minority of patients present with an acute onset. Although the diarrhoea may be severe in some patients, complications such as dehydration are rare. Associated symptoms include nocturnal bowel motions, mild abdominal pain, fatigue, slight weight loss, arthralgias and faecal incontinence. Symptoms are often attributed to an irritable bowel syndrome.

The natural history of MC is variable. Many cases are self-limiting, with symptoms lasting a few weeks or months. Others may be symptomatic for years in a relapsing or continuous pattern. Although a small number of case reports have suggested that MC may lead to development of ulcerative colitis, a small case series of patients with MC showed that none developed ulcerative colitis or Crohn’s disease after a follow-up of at least 6 years [28]. Similarly, MC does not appear to affect colorectal cancer risk [16].

Diagnosis/Histopathology

The diagnosis of MC is dependent on (i) a convincing clinical history with other etiologies ruled out, (ii) normal or near normal endoscopic and/or radiographic findings and (iii) endoscopic biopsies with histopathologic findings consistent with MC (Table 3).

Table 3

Histopathological features of collagenous colitis and lymphocytic colitis

Lymphocytic colitis
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 
Lymphocytic colitis
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 

Table 3

Histopathological features of collagenous colitis and lymphocytic colitis

Lymphocytic colitis
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 
Lymphocytic colitis
Collagenous colitis
• Intraepithelial lymphocytosis (≥20 IEL per 100 surface epithelial cells) • Thickening of a subepithelial collagen layer of more than 10 μm 
• Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells • Inflammation in the lamina propria consisting of mainly lymphocytes and plasma cells; and 
• Epithelial damage, such as flattening and detachment and • Epithelial damage, such as flattening and detachment. Intraepithelial lymphocytosis (IEL) could be present but is not necessary for the diagnosis of CC. 
• Subepithelial collagen layer not present or < 10 μm 

The first step in the diagnostic process is a thorough history with particular attention paid to risk factors and the disease associated with MC. A complete history helps one to rule out other etiologies that may cause a similar clinical picture such as IBD, coeliac disease, diarrhoea-predominant irritable bowel syndrome or infectious colitis.

Laboratory and radiographic investigations can be employed to help rule out other entities on the differential diagnosis list, but they are typically unremarkable.

Endoscopy with biopsy is necessary to confirm the diagnosis. Colonoscopy generally reveals macroscopically normal mucosa. However, non-specific changes such as erythema, edema, abnormal vascular markings or even tears associated with perforation have been described.

Microscopic evaluation of the colonic mucosa reveals significant inflammatory changes as outlined in Table 3. Both collagenous and lymphocytic colitis demonstrate lymphocytic infiltration of the lamina propria and epithelium. Collagenous is differentiated from lymphocytic colitis by the presence of marked thickening of the subepithelial collagen layer (Table 3). Histological assessment by a pathologist familiar with MC is required.

Since the macroscopic appearance is generally normal and the microscopic lesions can be skipped, random colonic biopsies are recommended. There is currently no consensus whether flexible sigmoidoscopy or colonoscopy is the best initial approach [43]. Flexible sigmoidoscopy is an attractive option due to efficiency (takes less time), cost savings, easier bowel preparation and no requirement for sedation. However, some studies suggest that biopsies of the rectosigmoid colon alone may be insufficient to rule out a diagnosis [44, 45] as up to 40% of cases are missed. Offner et al. reported that the diagnostic yield was highest from biopsies of the transverse colon (83%) and right colon (70%) and lowest from the rectosigmoid (66%) [45]. Other studies have reported lower false-negative rates with left-sided biopsies alone. Tanaka et al. reported that only 10% of patients with MC had isolated right-sided disease [44], and a larger study by Fine et al. reported that all 80 patients evaluated for chronic diarrhoea who were diagnosed with MC had histological evidence of MC in the left colon, whereas biopsies taken from other regions of the colon could be false negative [46].

The practical benefits of flexible sigmoidoscopy must be weighed against the potentially increased diagnostic yield of colonoscopy. The choice of which procedure to perform will depend on the clinical scenario, local expertise and resource constraints. If initial biopsies obtained on flexible sigmoidoscopy do not lead to a diagnosis and the suspicion of MC is high, we recommend a colonoscopy.

Treatment

Treatment recommendations for MC are largely based on case reports and uncontrolled studies, and Table 4 gives a suggested algorithm. Specific agents evaluated include 5-aminosalicylic acid (5-ASA), prednisone, immunomodulators, bismuth, probiotics and Boswellia extract. Small randomised controlled trials have shown that agents such as budesonide offer promise as an effective form of symptomatic therapy for both collagenous and lymphocytic colitis.

Table 4

Suggested treatment algorithm

Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e.g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 
Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e.g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 

Table 4

Suggested treatment algorithm

Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e.g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 
Confirm diagnosis/rule out other disorders 
Withdrawal of medications associated with MC (Table 2) 
Dietary changes (avoid caffeine, lactose) 
Trial of anti-diarrhoeals 
Trial of budesonide 
If no improvement, confirm diagnosis and rule out other disorders (e.g. coeliac disease) 
Consider prednisone/azathioprine/mercaptopurine/methotrexate under supervision of an experienced gastroenterologist or other clinician with experience in the management of severe MC 
Surgical consideration 

As a first step in managing MC, an in depth medication history should be taken with potentially precipitating medications stopped where possible. Associated conditions such as coeliac disease should be appropriately managed. In patients with mild symptoms, dietary restrictions like avoiding caffeine and lactose might be helpful.

Anti-diarrhoeal therapies

Non-specific anti-diarrhoeal therapies such as loperamide are commonly used in the management of MC. Retrospective studies have suggested benefit with doses ranging from 2 to 16 mg per day [29, 47]. Due to the safety of this agent and the possibility of spontaneous remission, we suggest loperamide for first-line therapy for MC. In our experience, however, those with moderate to severe diarrhoea or associated complaints of significant abdominal pain often fail to respond to anti-diarrhoeal therapy alone.

Aminosalicylates

Uncontrolled retrospective series have suggested symptomatic improvement in up to 50% of patients with MC treated with mesalamine (5-ASA) [24, 29, 48]. A recent randomised trial of 64 MC patients compared mesalamine (800 mg tid) to mesalamine (800 mg tid) and cholestyramine (4 g/day) [49]. Treatment resulted in resolution of diarrhoea in 84% overall after 2 weeks. If treatment was continued over 6 months, clinical and histological remission was achieved in 85% of those with lymphocytic and 91% of those with collagenous colitis. The number of relapsing patients after 6 months of treatment was low, and symptomatic relapses could be successfully retreated. Overall, the combination of mesalamine with cholestyramine was slightly superior [48].

Budesonide

Budesonide is currently the most promising treatment for collagenous colitis. Three trials involving 94 patients have shown that budesonide therapy (9 mg daily for 6–8 weeks) compared to placebo resulted in statistically significant improvements in clinical symptoms [50–52] and quality of life [53]. A recent Cochrane database meta-analysis reported pooled odds ratio of 12.3 for clinical response with budesonide with a number needed to treat of two [54]. Although effective in the short-term, all trials showed a high rate (61–80%) of relapse within ∼2 weeks of budesonide cessation. Age <60 was a significant risk factor for relapse. Although, there are no studies to support a tapering course of budesonide, many clinicians employ this in an effort to minimise the likelihood of relapse.

One randomised controlled trial of budesonide for the treatment of lymphocytic colitis has been conducted. When compared to the placebo arm, the patients randomised to budesonide (9 mg daily × 6 weeks) had a statistically significantly higher rate of remission (<3 bowel movements/day) at 3 and 6 weeks [55].

Prednisolone

A double-blind, placebo-controlled randomised trial of oral prednisolone 50 mg daily for 2 weeks for collagenous colitis was inconclusive because of the low number of patients enrolled [56]. Studies examining the effect of prednisone in the treatment of lymphocytic colitis have not been performed.

Immunosuppressive therapy

Immunosuppressive therapy with azathioprine or methotrexate has been utilised in patients either refractory to corticosteroid therapy or corticosteroid dependent, but there are no randomised controlled trials to guide therapy with these medications [57, 58].

Other therapies

Small clinical trials studying bismuth subsalicylate, Boswellia serrata extract, probiotics and empirical antibiotic treatment for collagenous and lymphocytic colitis look promising but cannot be suggested outside of such trials. Finally, case reports suggest that pentoxifylline, verapamil and subcutaneous octreotide might be treatment options, but their use cannot be recommended at this time. When medical therapy was unsuccessful and symptoms were very severe, surgical interventions such as a temporary or permanent loop ileostomy or even a proctocolectomy have been employed in smaller case series.

Recommended approach to treatment

Firstly, the diagnosis must be confirmed and other potential etiologies ruled out. Any complications related to chronic diarrhoea such as dehydration or electrolyte abnormalities must be identified and corrected. Potentially contributing medications such as PPIs or NSAIDs should be discontinued if possible. Depending on symptom severity, non-specific anti-diarrhoeal agents like loperamide, bile salt binding resins or bismuth should be tried. If this fails and the symptoms are sufficiently severe, the patient should be cared for or referred to someone with experience in dealing with this condition. Budesonide, 9 mg daily for at least 6 weeks, could then be used. Some clinical reports suggest a maintenance dose of budesonide 3–6 mg daily may be effective, but this approach has not been studied prospectively. If administration becomes long-term, patients have to be monitored for the development of the complications of chronic steroid therapy. If symptoms fail to improve, clinicians should consider alternative diagnoses. Prednisone, 5-ASA, immunosuppressive therapy or surgery could be cautiously considered for refractory cases.

Prognosis/Outcome

MC has a variable course, but overall, the long-term prognosis is good. Symptoms of diarrhoea and abdominal pain may precede the diagnosis by a number of months. These symptoms are generally mild. With most patients, symptoms resolve spontaneously or with symptomatic therapy. MC has not been associated with an increased risk of colorectal cancer — this information should be conveyed to the patients. There is only limited information about the long-term course and the prognosis of MC. One study followed 81 patients for an average of 37 months. Their initial symptoms were successfully treated with a number of different drugs. Approximately 30% of these patients relapsed with ∼70% remaining symptom free [59]. Prospective observational and clinical trials are warranted to specifically address the issue of prognosis and the durability of the response to initial therapy.

Conclusion

MC is a common cause of diarrhoea in older patients. After ruling our other causes of diarrhoea, flexible sigmoidoscopy (or colonoscopy) with appropriate biopsies allows for the diagnosis of either lymphocytic or collagenous colitis by histological analysis. Based on symptom severity, a stepwise approach to the treatment is suggested.

Key points

  • MC is common in older adults.

  • The incidence of MC is rising.

  • MC is diagnosed in biopsies taken during a colonoscopy.

  • MC is treated using a stepwise approach.

Conflicts of interest

None.

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Chronic diarrhea: Causes and treatments

Diarrhea occurs when a person has loose or watery stools. Many different conditions have diarrhea as a symptom.

Most people experience this common illness at some point in their lives, with short-term cases of diarrhea being the second most commonly reported illness in the United States.

A person with chronic diarrhea will typically experience runny stools for longer than 4 weeks, according to the American College of Gastroenterology.

Acute diarrhea should not be a cause for medical concern. However, chronic diarrhea may cause other problems if a person does not receive treatment for it.

In this article, we discuss chronic diarrhea, its causes, and the available treatment options.

There are many potential causes of chronic diarrhea. Some of the most common include:

Excessive alcohol or caffeine intake

Drinking large amounts of alcohol or beverages that contain caffeine, such as coffee or cola, can cause loose and watery stools.

When a person stops consuming these substances or starts to consume them in more moderate amounts, the symptoms should resolve.

Sugar and dairy

Certain sugars and artificial sweeteners may cause diarrhea. Consuming these sweet substances every day can even lead to chronic diarrhea.

Examples of such sugars and artificial sweeteners include:

  • Sorbitol: Manufacturers use this calorie-free sugar substitute in candies, chewing gums, and sugar-free items.
  • Mannitol: This sweetener can have a laxative effect similar to that of sorbitol.
  • Fructose: This naturally occurring sugar is present in fruit and honey. Eating large amounts of fruit can cause diarrhea due to its high fructose content. Food producers may also add fructose to candies and sodas.
  • Lactose: This is a natural sugar in dairy that can cause chronic diarrhea in people whose bodies cannot digest it. Around 65% of people around the world have problems digesting lactose.

Herbs and herbal remedies

Herbal remedies and herbal teas, such as senna, may contain natural laxatives.

If a person is using several herbal products at once, it may be a good idea to stop using them all, then reintroduce them one at a time. This may help the person work out which product is the cause of the chronic diarrhea.

Medication

Chronic diarrhea can be an adverse effect of several prescription and over-the-counter (OTC) medications.

Some common medications that can cause diarrhea include:

  • most antibiotics, including cefpodoxime, amoxicillin, and ampicillin
  • some antidepressants, such as selective serotonin reuptake inhibitors and serotonin-noradrenaline reuptake inhibitors
  • antacids that contain magnesium hydroxide
  • laxatives and stool softeners
  • proton pump inhibitors, including omeprazole and lansoprazole
  • chemotherapy drugs to treat cancer

Also, diarrhea may signal toxicity from some medications, such as lithium and digoxin.

Infection

In some cases, an intestinal parasite can give rise to chronic diarrhea. This is less common in the U.S. than in countries with less developed food and water sanitation.

A stool test is usually necessary to diagnose a parasitic infection. A doctor may also carry out a biopsy.

Inflammatory bowel disease

Inflammatory bowel disease (IBD) is an umbrella term for several chronic conditions involving inflammation of the gut. Two of the most common are Crohn’s disease and ulcerative colitis.

Some symptoms of IBD include:

There is currently no cure for IBD. However, people can usually manage it using medications and by making lifestyle changes.

Other causes

These can include:

  • Irritable bowel syndrome (IBS): This is a functional disorder that can cause diarrhea, constipation, or both.
  • Gallbladder removal: Following this procedure, more bile may build up in the colon. This may lead to diarrhea.
  • Hormonal disorders: Some examples of hormonal disorders include overactive thyroid and diabetes.
  • Surgery: Diarrhea can be a complication of some types of abdominal or intestinal surgery.
  • Allergies: In rare cases, food allergies can lead to loose and watery stools.
  • Rare tumors: For example, carcinoid tumors produce hormones that cause diarrhea.

A doctor will carry out a physical examination to diagnose chronic diarrhea. Follow-up tests can help determine the underlying cause.

During the examination, the doctor will ask about any symptoms the person has experienced, as well as their family medical history. They will primarily focus on any history of digestive problems.

It can also be helpful for the person to disclose what they tend to eat and drink, any medications they are taking, whether or not they drink alcohol or take illicit drugs, and their recent travel history.

The doctor may then request:

  • blood tests
  • a stool sample to test for inflammation, bacteria, or parasites
  • an ultrasound or CT scan

If blood tests and stool samples do not reveal any reason for the chronic diarrhea, the doctor may order imaging tests to check for problems in the digestive system.

If the cause remains unknown despite these tests, the doctor may diagnose IBS. People with this condition have digestive systems that appear normal but do not function as they should.

Treating chronic diarrhea depends on its underlying cause. Some potential treatment options include:

Managing any related conditions

Diarrhea that occurs due to a medical condition, such as IBD, might resolve with treatment of the underlying condition.

It is important to work with a doctor to develop a treatment plan that addresses the diarrhea as well as any underlying illness.

Taking or switching medications

Antidiarrheal medications are a short-term remedy. Although they tend to relieve symptoms, people should not use them on an ongoing basis.

Other medications that may help include:

  • antibiotics, for bacterial infections that cause diarrhea
  • codeine-containing medications, which can reduce watery and loose stools
  • OTC medications to slow down the passage of stool through the digestive tract, including bismuth (Pepto-Bismol) and loperamide (Imodium)

People taking medications that can cause chronic diarrhea should talk to their doctor about alternative drugs that do not have this side effect.

Hydrating

Diarrhea can cause extreme dehydration, especially when it continues over an extended period of time.

As a result, it is important to drink plenty of clear fluids throughout the day. Options include water, noncaffeinated teas, and low sodium broths. This can help people with chronic diarrhea stay hydrated.

Making dietary changes

If a specific dietary item is the cause of the chronic diarrhea, a person can try removing this food or beverage from the diet to see whether or not symptoms improve.

Once the diarrhea symptoms clear up, it may be possible to gradually start eating these foods again on an infrequent basis, or in moderate amounts.

Keeping a food diary can also help people spot trigger foods.

Other dietary changes that may help include:

  • achieving better portion control
  • limiting or avoiding caffeine
  • limiting or avoiding alcohol

Trying natural remedies

Some natural products may help relieve chronic diarrhea. Probiotics, for example, can restore a healthy balance of bacteria in the gut.

Some fiber supplements, such as psyllium, can also relieve chronic diarrhea. They may be especially helpful for those with IBS or other digestive conditions that cause loose stools.

However, people should avoid using psyllium products that also contain laxatives.

Not all cases of chronic diarrhea are preventable. However, it is possible to reduce the risk of chronic diarrhea by:

  • keeping a food diary and seeing how cutting particular foods from the diet affect the diarrhea
  • discussing the side effects of any current medications with a doctor
  • requesting a change in medications if necessary
  • taking probiotic supplements regularly
  • drinking only clean or filtered water
  • washing the hands both before and after food preparation
  • cleaning and thoroughly cooking meat before eating it
  • washing fresh produce before eating it
  • cleaning kitchen surfaces regularly
  • washing the hands regularly, especially after using the bathroom or coming into contact with a person who is ill

A person should see a doctor if they have diarrhea that lasts longer than a few days or if other symptoms accompany it, such as fever or fatigue.

If a person notices any symptoms of dehydration, they should consult a doctor immediately.

The underlying cause of the chronic diarrhea will determine its treatment options and outlook.

People with food intolerances or those experiencing substance-related diarrhea will usually find relief if they avoid or limit their intake of the substance in question.

For other people, changing medications under the supervision of their doctor will be enough to resolve the symptom.

Antibiotics are usually successful in treating bacterial infections that cause chronic diarrhea.

If a digestive condition or other medical concern causes loose or watery stools, symptoms should gradually resolve once the person has received treatment for it.

The most important step for recovery is to consult a doctor.

Chronic diarrhea: Causes and treatments

Diarrhea occurs when a person has loose or watery stools. Many different conditions have diarrhea as a symptom.

Most people experience this common illness at some point in their lives, with short-term cases of diarrhea being the second most commonly reported illness in the United States.

A person with chronic diarrhea will typically experience runny stools for longer than 4 weeks, according to the American College of Gastroenterology.

Acute diarrhea should not be a cause for medical concern. However, chronic diarrhea may cause other problems if a person does not receive treatment for it.

In this article, we discuss chronic diarrhea, its causes, and the available treatment options.

There are many potential causes of chronic diarrhea. Some of the most common include:

Excessive alcohol or caffeine intake

Drinking large amounts of alcohol or beverages that contain caffeine, such as coffee or cola, can cause loose and watery stools.

When a person stops consuming these substances or starts to consume them in more moderate amounts, the symptoms should resolve.

Sugar and dairy

Certain sugars and artificial sweeteners may cause diarrhea. Consuming these sweet substances every day can even lead to chronic diarrhea.

Examples of such sugars and artificial sweeteners include:

  • Sorbitol: Manufacturers use this calorie-free sugar substitute in candies, chewing gums, and sugar-free items.
  • Mannitol: This sweetener can have a laxative effect similar to that of sorbitol.
  • Fructose: This naturally occurring sugar is present in fruit and honey. Eating large amounts of fruit can cause diarrhea due to its high fructose content. Food producers may also add fructose to candies and sodas.
  • Lactose: This is a natural sugar in dairy that can cause chronic diarrhea in people whose bodies cannot digest it. Around 65% of people around the world have problems digesting lactose.

Herbs and herbal remedies

Herbal remedies and herbal teas, such as senna, may contain natural laxatives.

If a person is using several herbal products at once, it may be a good idea to stop using them all, then reintroduce them one at a time. This may help the person work out which product is the cause of the chronic diarrhea.

Medication

Chronic diarrhea can be an adverse effect of several prescription and over-the-counter (OTC) medications.

Some common medications that can cause diarrhea include:

  • most antibiotics, including cefpodoxime, amoxicillin, and ampicillin
  • some antidepressants, such as selective serotonin reuptake inhibitors and serotonin-noradrenaline reuptake inhibitors
  • antacids that contain magnesium hydroxide
  • laxatives and stool softeners
  • proton pump inhibitors, including omeprazole and lansoprazole
  • chemotherapy drugs to treat cancer

Also, diarrhea may signal toxicity from some medications, such as lithium and digoxin.

Infection

In some cases, an intestinal parasite can give rise to chronic diarrhea. This is less common in the U.S. than in countries with less developed food and water sanitation.

A stool test is usually necessary to diagnose a parasitic infection. A doctor may also carry out a biopsy.

Inflammatory bowel disease

Inflammatory bowel disease (IBD) is an umbrella term for several chronic conditions involving inflammation of the gut. Two of the most common are Crohn’s disease and ulcerative colitis.

Some symptoms of IBD include:

There is currently no cure for IBD. However, people can usually manage it using medications and by making lifestyle changes.

Other causes

These can include:

  • Irritable bowel syndrome (IBS): This is a functional disorder that can cause diarrhea, constipation, or both.
  • Gallbladder removal: Following this procedure, more bile may build up in the colon. This may lead to diarrhea.
  • Hormonal disorders: Some examples of hormonal disorders include overactive thyroid and diabetes.
  • Surgery: Diarrhea can be a complication of some types of abdominal or intestinal surgery.
  • Allergies: In rare cases, food allergies can lead to loose and watery stools.
  • Rare tumors: For example, carcinoid tumors produce hormones that cause diarrhea.

A doctor will carry out a physical examination to diagnose chronic diarrhea. Follow-up tests can help determine the underlying cause.

During the examination, the doctor will ask about any symptoms the person has experienced, as well as their family medical history. They will primarily focus on any history of digestive problems.

It can also be helpful for the person to disclose what they tend to eat and drink, any medications they are taking, whether or not they drink alcohol or take illicit drugs, and their recent travel history.

The doctor may then request:

  • blood tests
  • a stool sample to test for inflammation, bacteria, or parasites
  • an ultrasound or CT scan

If blood tests and stool samples do not reveal any reason for the chronic diarrhea, the doctor may order imaging tests to check for problems in the digestive system.

If the cause remains unknown despite these tests, the doctor may diagnose IBS. People with this condition have digestive systems that appear normal but do not function as they should.

Treating chronic diarrhea depends on its underlying cause. Some potential treatment options include:

Managing any related conditions

Diarrhea that occurs due to a medical condition, such as IBD, might resolve with treatment of the underlying condition.

It is important to work with a doctor to develop a treatment plan that addresses the diarrhea as well as any underlying illness.

Taking or switching medications

Antidiarrheal medications are a short-term remedy. Although they tend to relieve symptoms, people should not use them on an ongoing basis.

Other medications that may help include:

  • antibiotics, for bacterial infections that cause diarrhea
  • codeine-containing medications, which can reduce watery and loose stools
  • OTC medications to slow down the passage of stool through the digestive tract, including bismuth (Pepto-Bismol) and loperamide (Imodium)

People taking medications that can cause chronic diarrhea should talk to their doctor about alternative drugs that do not have this side effect.

Hydrating

Diarrhea can cause extreme dehydration, especially when it continues over an extended period of time.

As a result, it is important to drink plenty of clear fluids throughout the day. Options include water, noncaffeinated teas, and low sodium broths. This can help people with chronic diarrhea stay hydrated.

Making dietary changes

If a specific dietary item is the cause of the chronic diarrhea, a person can try removing this food or beverage from the diet to see whether or not symptoms improve.

Once the diarrhea symptoms clear up, it may be possible to gradually start eating these foods again on an infrequent basis, or in moderate amounts.

Keeping a food diary can also help people spot trigger foods.

Other dietary changes that may help include:

  • achieving better portion control
  • limiting or avoiding caffeine
  • limiting or avoiding alcohol

Trying natural remedies

Some natural products may help relieve chronic diarrhea. Probiotics, for example, can restore a healthy balance of bacteria in the gut.

Some fiber supplements, such as psyllium, can also relieve chronic diarrhea. They may be especially helpful for those with IBS or other digestive conditions that cause loose stools.

However, people should avoid using psyllium products that also contain laxatives.

Not all cases of chronic diarrhea are preventable. However, it is possible to reduce the risk of chronic diarrhea by:

  • keeping a food diary and seeing how cutting particular foods from the diet affect the diarrhea
  • discussing the side effects of any current medications with a doctor
  • requesting a change in medications if necessary
  • taking probiotic supplements regularly
  • drinking only clean or filtered water
  • washing the hands both before and after food preparation
  • cleaning and thoroughly cooking meat before eating it
  • washing fresh produce before eating it
  • cleaning kitchen surfaces regularly
  • washing the hands regularly, especially after using the bathroom or coming into contact with a person who is ill

A person should see a doctor if they have diarrhea that lasts longer than a few days or if other symptoms accompany it, such as fever or fatigue.

If a person notices any symptoms of dehydration, they should consult a doctor immediately.

The underlying cause of the chronic diarrhea will determine its treatment options and outlook.

People with food intolerances or those experiencing substance-related diarrhea will usually find relief if they avoid or limit their intake of the substance in question.

For other people, changing medications under the supervision of their doctor will be enough to resolve the symptom.

Antibiotics are usually successful in treating bacterial infections that cause chronic diarrhea.

If a digestive condition or other medical concern causes loose or watery stools, symptoms should gradually resolve once the person has received treatment for it.

The most important step for recovery is to consult a doctor.

90,000 how dangerous it is and how it is treated

Abramova Irina Ivanovna

Therapist,

In elderly and senile people, disorders of the gastrointestinal tract are often diagnosed – constipation or diarrhea .Both of these conditions can be a consequence of malnutrition, age-related changes in the body, recently experienced excitement and stress, and symptoms of the development of diseases of the gastrointestinal tract, endocrine or nervous systems. Ignoring the problem leads to an aggravation of the condition: toxic poisoning with constipation and severe dehydration with diarrhea. Death is possible without emergency assistance.

Causes of diarrhea in the elderly

The recurrent occurrence of loose stools should not cause much concern, and does not require any measures other than dietary adjustments for 1-2 days.However, prolonged diarrhea lasting from several days to weeks requires a complete examination of the patient, identifying the causes of the disorder and prescribing an effective drug regimen. There can be several factors provoking diarrhea:

  • Weakness of the chewing muscles and dental problems interfere with the process of chewing and chopping food;
  • An insufficient amount of saliva secreted makes it difficult to swallow a food lump and move it along the esophagus;
  • A decrease in the number of taste buds in the oral cavity forces an elderly person to use more seasonings, salt, sugar, which can provoke attacks of gastritis, colic, and loosening of the stool;
  • chronic diseases of the stomach, pancreas, gallbladder disrupt the process of digestion, as a result, contents with large pieces, insufficiently treated with hydrochloric acid, are evacuated from the stomach; further, when moving through the intestines, the lack of enzymes and bile acids leads to impaired digestion and absorption of nutrients.As a result – pain in the intestines and stool disorders;
  • A decrease in the number of absorbing villi in the intestine leads to liquefaction of feces, together with a large amount of undigested and not absorbed fats, this provokes diarrhea;
  • chronic dysbiosis observed in old age;
  • eating low-quality food, overeating;
  • stress and nervous shock;
  • Regular intake of certain medicines.

Symptoms of diarrhea, its possible complications

The main symptom is loose stools, forcing an elderly person to go to the toilet 3 or more times a day.Concomitant symptoms: dry mouth, thirst, pain in the stomach and / or intestines, pallor of the skin, lack of appetite, sudden surges in blood pressure, apathy, weakness, drowsiness.

The main hazards of persistent diarrhea are dehydration and dysbiosis . Dehydration in the elderly occurs very quickly, on the second day after the onset of diarrhea. This leads to a violation of the water-salt balance, changes in blood pressure, muscle pain, cramps.The combination of diarrhea and indomitable vomiting increases dehydration and requires immediate medical attention.

Dysbacteriosis is dangerous with the subsequent development of candidiasis, a sharp decrease in immunity and a vicious circle of stool disorders, tk. when the balance of bacteria is disturbed, the number of lacto- and bifidobacteria decreases, chronic diarrhea occurs.

Diagnosis and treatment of diarrhea

Diagnosis of the disease is simple and includes a patient survey, fecal analysis, and general blood count.In some cases, a colonoscopy, abdominal ultrasound may be required. Diarrhea caused by stress, overeating is treated with a lean diet. Associated bacterial infection, as well as poisoning by low-quality products, requires the use of antibacterial agents. Saline solutions (Rehydron or Humana electrolyte, others) fight dehydration. It is also helpful to take sorbents and probiotics.

90,000 Diarrhea in the elderly: causes, symptoms, treatment

Age-related changes in the digestive system

The occurrence of regular diarrhea in the elderly is directly related to the aging process.The following changes take place:

• The amount of saliva, which is necessary for the digestion of food and good absorption of nutrients, is reduced. Lack of saliva provokes dry mouth, the chewing muscles also weaken, the esophagus becomes longer. Because of this, poorly chewed food gets into the stomach, which can lead to diarrhea and constipation. • The muscles in the stomach weaken and lose their elasticity. The stomach itself also changes in size. Gastric juice is produced more slowly. Food is poorly broken down, often fermenting in the stomach.Poorly digested, it passes into the intestines, thereby irritating it. The entire process of digestion results in loose stools. • The gallbladder enlarges, producing more and less bile. • Problems in the work of the pancreas are caused by a lack of digestive enzymes. Food is poorly digested, and the body quickly gets rid of it. Due to problems with the pancreas, a person is nauseous, he has a heaviness in the abdomen and loose stools. • Lack of lactase leads to poor absorption and lactose intolerance.For this reason, eating dairy products can cause flatulence, abdominal pain and diarrhea. • The work of the small intestine slows down, due to which there is no high-quality digestion of food. • Fecal stones are common in the elderly. Stones are caused by deposits on the walls of the large intestine. They interfere with the normal movement of food, due to which food is excreted partially digested. The stones provoke the development of harmful bacteria that create pathogenic microflora in the intestines.All this leads to severe diarrhea. • Reducing the size and strength of the liver. It begins to work worse, due to which the metabolism of proteins and carbohydrates is disrupted. This weakens the bowel function.

Treatment of diarrhea, diarrhea in the elderly, how to treat diarrhea at age?

Treatment of diarrhea in an elderly person should be preceded by a general medical examination. With its help, it becomes possible to detect a disease that entails such an unpleasant symptom as an intestinal disorder.Both examination and treatment are individual and depend on many factors. In this case, one thing remains common to any patient – ensuring a sufficient level of fluid in the body, since loose stools lead to strong and rapid dehydration.

Maintaining water-salt balance is especially important in old age. One of the best means for replenishing fluid in the body is Rehydron. Even taking into account all the advantages of Rehydron, before using it, you must definitely read the instructions in order to check for contraindications and avoid side effects.How to treat diarrhea in older people? In addition to the prescribed drugs, the attending physician may recommend that the patient apply activated charcoal and follow a diet for several days. Rice water is considered a non-drug remedy to get rid of profuse diarrhea. To cook it, you need to boil 1.5 tsp for 40 minutes. rice in 0.5 l. boiled water. After that, the broth is cooled, filtered through a sieve and taken during the day for a quarter of a glass every 2-3 hours.

It is noteworthy that most of the diseases manifested by diarrhea begin the same way in people of any age.Symptoms of discomfort are usually abdominal pain and loose stools. At the same time, a number of diseases provoke diarrhea at rather late stages, as a result of which a diagnosis based only on such a symptom as diarrhea leads to the loss of precious time. Some diseases require a complete examination and a careful approach to the selection of tests and other studies. Therefore, it is very important to pay attention to any deterioration in the well-being of an elderly person. You should not postpone a visit to a doctor for a long time if severe diarrhea appears.Timely diagnosis and initiation of treatment can help eliminate the disease even at the stage of its inception.

Causes of diarrhea

Against the background of age-related changes, various causes of diarrhea occur in the elderly. A specialist can diagnose and accurately determine the root cause of loose stools.

The reasons may be as follows:

• Diseases of the gastrointestinal tract: colitis, pancreatitis, inflammation, Crohn’s disease, intestinal tumors.Disorders of the gastrointestinal tract provoke chronic diarrhea; • Infection. Age-related changes make the human body vulnerable to various bacteria, viruses and helminths. Once inside, they cause intestinal upset; • Hormonal disruptions. Hormone imbalances and endocrine problems cause diarrhea in old age. To get rid of it, you need to cure the root cause; • Improper diet is a common cause of stool disorder in old age. Diarrhea is typical for those who often consume salty, sweet, spicy foods.The nature of nutrition in youth also affects the state of the gastrointestinal tract in old age. If for many years a person often drank alcohol, ate unhealthy food, negative changes in the digestive system begin earlier; • Prolonged stress, excessive stress on the body and mind. Strong emotions (fear, anxiety) increase intestinal peristalsis, which can cause diarrhea; • Operation in the gastrointestinal tract can disrupt intestinal motility. This can provoke constipation and diarrhea; • Long-term use of medications that have loose stools among the side effects; • Poisoning is the cause of one-time diarrhea.

Causes of diarrhea in older people, why does diarrhea occur in older people?

With age, a person experiences a natural weakening of the body and a decrease in the productivity of all basic processes. Therefore, maintaining the work of vital systems, reducing the load on them, can be done by following a diet.

Complications that are reflected in the work of the digestive system are expressed through a decrease in the level of enzymes and disruptions in the hydrolysis of nutrients, which directly affects the frequency of occurrence of loose stools.One of the reasons for this situation, when severe diarrhea appears, is a deterioration in the health of teeth and their loss, leading to careless chewing of food, which enters the stomach in large pieces and complicates the activity of the digestive organs in the process of digesting and assimilating the food eaten.

Also an important factor influencing the state and functioning of the digestive system and the appearance of diarrhea in the elderly is the age-related decrease in the number of taste buds. Because of this, a person, not feeling the fullness of the taste of the food taken, eats too much salty, sweet, spicy or sour food, overly irritating the walls of the esophagus, stomach and intestines.

Another age-related change in the digestion of an elderly person, which can also affect the appearance of diarrhea, is a decrease in the secretion of the salivary glands, as a result of which the oral cavity often dries up, which entails a weakening of the chewing muscles and instability of the swallowing process. These changes in themselves may not be noticeable, but their result – the loss of control over the amount eaten, has a serious impact on the body’s work. Therefore, for the elderly, it becomes necessary to follow a diet.

What other causes of diarrhea in the elderly, causes of diarrhea, frequent loose stools in elderly people can be. Transformations occur in the pancreas, in particular, by lowering the secretory function. The liver loses its former size, significantly shrinking. Along with this, the volume of bile secreted becomes scarce.

Due to the thinning of the intestinal mucosa, a disturbed fermentation process is triggered. This change can be felt by consuming dairy products and fats.They are absorbed worse than before, which causes diarrhea. Its onset can also be triggered by the consumption of sweets in large quantities. The elderly organism assimilates carbohydrates worse, therefore, in the case of eating a large amount of sweets, a violation of the digestive processes occurs, leading to diarrhea, the appearance of diarrhea.

It is important to know that antibiotics can cause diarrhea. In case of prolonged diarrhea in an elderly person, you should get rid of the stool plug and check for pseudomembranous colitis.If you ignore them, you can allow the development of serious complications – the formation of ulcerative colitis or Crohn’s disease. With these diseases, the patient begins to rapidly lose weight during loose stools.

Diarrhea, which does not stop for a long time, also causes diseases of the endocrine system. If the cause is one or more of them, diarrhea treatment will take a lot of effort and time. Diarrhea is associated with disorders such as diabetes mellitus and Addison’s disease, requiring the mandatory use of a special diet.

Observation is very important for diarrhea in the elderly. It is necessary to monitor not only the patient’s sensations, but also the color, consistency and composition of the stool. In particular, if they contain blood impurities, there is a high probability of developing infectious colitis or the presence of a malignant neoplasm. If blood appears in liquid feces, you should immediately contact a medical institution for an examination.

Nature of the disease in the elderly

The elderly are characterized by various gastric problems, which often leads to diarrhea.Diarrhea is a symptom of internal disorders in the body that must be diagnosed. This problem cannot be ignored: diarrhea leads to dehydration, which is dangerous in old age. Against the background of age-related changes and chronic diseases, this dehydration leads to negative consequences.

Many people under 60 years of age are characterized by ailments that are accompanied by recurrent diarrhea. These problems can be caused by food poisoning, stomach bacteria or infections, and certain medications.

Age-related changes in the body’s work, which cause disruptions in metabolism, play an important role. This problem is typical for older people. Diarrhea can occur as a reaction to the experience of fear or shock. In such a state, there is no high-quality digestion of food, from the stomach it passes into the intestine and is excreted from it.

Regular diarrhea in old age may indicate Addison’s disease or diabetes mellitus. You need to pay attention to diarrhea in a lying person.Constipation is characteristic of the bedridden. The appearance of diarrhea can indicate hormonal problems and gastrointestinal diseases.

Treatment of diarrhea in the elderly with folk remedies at home

As a rule, it is customary to treat diarrhea with medication. However, due to age characteristics, it is not always allowed to use it for the elderly. Knowledge of traditional medicine comes to the rescue, however, the use of its means must be coordinated with the attending physician. The best remedy for the treatment of diarrhea, including in the presence of blood inclusions in the feces, is the dried and powdered membranes of chicken stomachs.For medicinal purposes, take 1 tsp. powder 2-3 times a day. The use of a decoction of rice and an infusion of medicinal chamomile flowers is also considered effective. All these funds can only be used with the approval of the attending physician and adherence to a diet.

Diagnostics

For competent treatment, an accurate diagnosis of the root cause of diarrhea is needed. Various methods are used for diagnosis:

• Clinical blood test. It can be used to determine the inflammation that provokes diarrhea; • Coprogram.Examines feces to obtain information about the enzymatic and digestive functions of the gastrointestinal tract; • ultrasound of the abdominal cavity. Allows you to determine the state of organs, detect pathological processes; • Sigmoidoscopy – examination of the rectum and sigmoid colon; • Colonoscopy – examination of the colon; • Esophagogastroduodenoscopy (EGDS) – the study of mucous membranes in the esophagus, stomach and duodenum; • Culture on microflora to identify sensitivity to antibiotics.

Tests alone are not enough to make a diagnosis.Detailed comprehensive diagnostics allows you to accurately determine the pathological processes that lead to the appearance of loose stools. Based on the results of the examinations, the specialist will diagnose and prescribe treatment. Therapist, gastroenterologist, proctologist are engaged in diagnostics.

Symptoms

Diarrhea may be accompanied by additional symptoms. Frequent symptoms:

• Drawing, aching or cutting pain in the lower abdomen, cramping; • Bubbling and strong flatulence in the abdomen; • Feeling of nausea, vomiting; • Intense thirst, dry mouth; • The color of the urine becomes darker; • Heat; • Decreased appetite; • Disorders of attention and perception of the surrounding space; • Fast fatigue and lethargy.

Symptoms can occur in different combinations. If you find them, you need to contact a specialist. It should be remembered that an elderly person has a weak body, so when he gives alarming signals, they should be immediately paid attention to. If diarrhea is accompanied by fever, fainting, blood appears in the stool, the pain becomes very severe, you need to call an ambulance.

Why is it important to treat diarrhea in the beginning?

Diarrhea disrupts the normal functioning of the entire digestive tract of an elderly person, which is difficult to restore.

If you do not pay attention to the problem in time, diarrhea will lead to complications. The main complication is dehydration due to impaired intestinal absorption and rapid fluid loss. Dehydration, together with lowered immunity and chronic problems, leads to dysfunction of the entire body. In old age, it is especially dangerous.

If you do not start treatment, dehydration will increase even with plenty of drinking. Lack of moisture affects all systems and organs of the body, which causes weakness, lethargy, blood pressure decreases, and the pulse rises.

It is important to maintain a healthy water balance. Pay attention to the lack of moisture in the body. This may be indicated by dry mouth, decreased urine and urge to go to the toilet, and a drop in blood pressure. If an elderly person has such manifestations of a lack of moisture, it must be replenished.

In addition to liquid, a person loses useful minerals that are necessary for a healthy metabolism. This leads to worsening dehydration disturbances. Malnutrition develops, due to which a person does not receive the energy he needs.All this provokes a decrease in immunity and intestinal problems.

Loss of intestinal protection: in case of infectious diarrhea, beneficial intestinal bacteria that protect its microflora cannot cope with a large influx of pathogenic microorganisms. The beneficial microflora decreases, the infection spreads. Toxins are released, due to which diarrhea develops.

With improper nutrition, frequent loose stools lead to irritation of the intestines and anus, cracks appear on the skin.Such complications are typical for bedridden patients. To prevent skin problems, you need to carefully observe intimate hygiene. You can use antiseptics, medicated ointments, and moisturizers to restore your skin.

Great damage is caused to the weakened intestinal microflora of the elderly. To cope with the problem, you need competent professional treatment and subsequent long-term recovery. The recovery period can be accompanied by gastrointestinal problems for a long time in the form of unstable stools and uncomfortable sensations.

Old people often do not attach importance to their loose stools. They get used to it like other digestive disorders typical of old age. Pensioners ignore diarrhea, not understanding the importance of the situation, and thus miss the onset of a serious illness.

Relatives should closely monitor the condition of an elderly relative, inquire about his health. If symptoms of loose stools are found, treatment should be started as early as possible.

Treatment of diarrhea

Treatment of diarrhea in the elderly should be comprehensive.It includes: taking medication, healthy food with sufficient water intake, adherence to medical recommendations

Medicines

The doctor makes a treatment program taking into account the patient’s situation and the cause of diarrhea. The individual scheme takes into account the person’s age and well-being. Treatment should be such as to eliminate the cause of the diarrhea while avoiding dehydration. You can not take medications without a specialist appointment.

The following drugs are prescribed for drug therapy:

• Medicines for rehydration – to restore the water-salt balance; • Antimicrobial agents; • Adsorbents – to get rid of toxins; • Antibiotics – for bacterial diarrhea.The selection of funds occurs according to the type of microorganisms; • Probiotics – to restore healthy intestinal microflora.

Let’s take a closer look at how these drug groups work:

• Medicines for rehydration. During diarrhea, a lot of fluid is lost through feces and vomiting. It is not always possible to quickly restore a healthy water balance in the body with the help of plenty of drinking. To help the patient, compulsory rehydration agents are prescribed, which effectively cope with the problem of dehydration.• Means for reducing intestinal secretion and lowering intestinal motility. Nonsteroidal anti-inflammatory drugs are prescribed, which are good for bacterial diarrhea. Patients with Crohn’s disease are prescribed steroid medications. Octreotide is often prescribed to slow down the bowel movement. If the patient has pain, antispasmodics are included in therapy. It is impossible to slow down intestinal motility in the presence of infections in the gastrointestinal tract. • Preparations for the removal of toxins. It is prescribed for infectious bowel disorders.These funds must be used correctly so as not to cause intoxication of the body. If the patient’s intestinal absorption function is impaired, these medications should be taken strictly in consultation with a specialist. • Medicines to restore intestinal microflora. These drugs can be prescribed: Hilak-forte, Enterol, Atzilakt.

Nutrition

Nutrition for diarrhea in the elderly is the second important point in treatment. It is necessary to establish a healthy diet: follow the rules of the diet, include healthy foods, exclude harmful ones.

Basic recommendations for nutrition during diarrhea:

• On the first day, you need to restore a healthy water balance. To do this, you need to drink plenty of fluids (water, compotes, tea) and use medications for rehydration. Eating is not recommended. • On the second day, you can switch to light meals. Food must be healthy and free of gas. It can be cereals and vegetables without strong spices. After 2-3 days, you can include some dietary meat, such as chicken, in the diet.• In the future, vegetable soups and broths are added to the diet. The meat should not be fatty or allergic. Dairy products are also gradually introduced: cottage cheese, fermented baked milk, kefir and others. Dairy products must have a natural composition without chemical additives.

Nutrition after diarrhea in the elderly obeys the rule: introduce new foods and dishes gradually, after a day or two, thus expanding the menu. This is necessary for the digestive system to get used to a varied diet without problems.This approach will save her from irritation.

Any food that nourishes and is well absorbed, is rich in useful vitamins and microelements, does not cause irritation and strong gas formation can be included in a healthy diet. Foods with potassium, calcium and iron are especially useful. It is worth eating fractionally, the food should be well absorbed, be warm, half-mashed. A diet for diarrhea involves avoiding irritating and laxative foods.

Among healthy dishes and products: lean meat and fish, seafood, eggs, low-fat dairy and sour milk products, light broths and soups, whole grain cereals, vegetable oils, vegetable and fruit salads, fruit drinks and fruit drinks.Lean meat and fish, light cereals and dairy products are especially useful. It is useful to heat vegetables, fruits and berries.

Harmful foods that are best avoided: fatty meat, rice, egg yolk, confectionery, sweets, fatty dairy products, legumes, carbonated drinks, smoked meats, fried foods, sauces and spices.

Traditional medicine

Folk remedies play an auxiliary role, they cannot replace traditional medicines.When choosing a prescription, it is imperative to consult with your doctor: a folk remedy must correspond to the diagnosis.

Treatment of diarrhea with folk remedies in the elderly:

• Rice broth. 1 tsp Pour rice with 2 cups of boiling water, put on fire and cook for 15-20 minutes. Next, filter the broth. The tool is used in 2 tbsp. l., you can before or during meals; • Strawberries. It has a positive effect on the digestive system, improves immunity and fights infectious diarrhea.1 tbsp. l. Pour dry leaves with a glass of boiling water, leave for 20 minutes, then strain and cool. Take a decoction of 50 ml once an hour. The remedy is used until the symptoms of the disease disappear; • Infusion of oak bark. Dilute 1 tbsp. l. chopped oak bark in one glass of boiling water and leave for 2 hours in a warm dark place. Then strain and take 1 tsp. every 2-3 hours for three days, until the bowel function returns to normal; • Sage tincture. 1 tbsp. l. Mix sage with 300 ml of boiling water, leave for 2 hours in a thermos, strain through a sieve.Drink the medicine in small portions throughout the day. Sage helps the intestinal microflora to recover, removes loose stools.

A folk remedy should not cause allergies in humans. It gently solves the patient’s problem, taking into account the state of his digestion. Traditional medicines are aimed at normalizing bowel function. They help restore its microflora, establish a healthy digestion process, and remove inflammation.

Proper nutrition for the elderly with diarrhea

Healthy diet for diarrhea in the elderly will not only help get rid of this ailment, but also prevent its occurrence, as well as the appearance of many other diseases.Older people need to carefully monitor what they eat. You can not get carried away with junk food, but it is best to adhere to a certain diet. And this is not at all in order to lose weight, but in order for the digestive system to be healthy.

Proper nutrition for diarrhea in the elderly involves a diet of easily digestible foods that do not cause flatulence, rich in nutrients. The most important thing for a person of age is to eat food that replenishes the lack of calcium, iron and potassium in the body.It is also necessary to reduce the calorie content of meals, since energy consumption by the body is no longer as large as in youth.

So, what is the diet for diarrhea in older people?

You can and should use:

  • Oil from corn, soybeans, sunflower seeds.
  • Lean meat such as poultry.
  • Egg white.
  • Low fat milk and sour milk.
  • Soups based on fish, poultry or vegetable broths.
  • Lean fish.
  • Seafood.
  • Cereals excluding rice.
  • Vegetable and fruit salads.
  • Liver (excluding pork).
  • Whole grain baked goods.
  • Berry fruit drinks and fruit compotes.
  • Herbal, green and black teas.
  • Chicory drink as an alternative to coffee.

Do not use in case of diarrhea in the elderly or need to reduce consumption:

  • Pork and other meat with high fat content.
  • Egg yolks.
  • Fat milk and sour milk.
  • Flour.
  • Rice groats.
  • Sweet.
  • Effervescent drinks.
  • Legumes.
  • Fried and smoked meats.
  • Salts and spices.
  • Spicy food.
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Prevention of diarrhea

• To avoid the development of diarrhea in old age, it is necessary to establish healthy nutrition.It is better to accustom yourself to a healthy diet and diet from a young age and stick to it all your life. • Maintain a healthy water balance in the body by including clean water, fruit drinks, healthy herbal teas and infusions in the diet. • With the permission of the doctor, you can take enzymes and probiotics. • If there are any problems with the digestive system, you need to solve them. It is necessary to cure all diseases of the gastrointestinal tract in time. • Observe intimate hygiene. • It is helpful to visit the dentist periodically. • Avoid prolonged stressful situations.

Diarrhea in old age is most often not a one-time symptom of poisoning, but a consequence of age-related changes and internal health problems. Long-term diarrhea is dangerous for an elderly person: be aware of dehydration and its consequences.

To prevent loose stools, preventive measures and a healthy diet should be followed. If symptoms are found, you should go to the doctor without delay in order to avoid dangerous consequences. Do not self-prescribe drugs and self-medicate.Undergo high-quality diagnostics and follow medical recommendations. Considering all these points, an elderly person will be able to correctly cure diarrhea.

Article Nutrition for diarrhea in the elderly

Diarrhea is a gastrointestinal disorder characterized by frequent bowel movements, loose stools, and intestinal spasms. Diarrhea is rare in young and middle-aged people (the exception is acquired gastrointestinal diseases and infectious diseases), but quite often in elderly and senile people.It is very important to properly organize a diet for diarrhea in order to avoid its negative effects on the body as much as possible.

Gastrointestinal tract of an elderly person

Over time, the entire human body undergoes certain age-related changes. The digestive tract is no exception:

  • In the oral cavity, noticeable deterioration occurs – the number of teeth decreases, the mucous membrane of the mouth becomes thinner, the masticatory muscles are partially weakened, and less saliva is produced.All this leads to the fact that food is poorly chopped and wetted during chewing.
  • There is a physiological lengthening of the esophagus, which increases the risk of hernias and perforations.
  • The vertical position of the stomach gradually turns into a horizontal one. The organ itself becomes much smaller. There is a decrease in the production of hydrochloric acid and secretions, and atrophy of the gastric mucosa develops. There is a danger of the formation of acute gastritis and ulcers of the mucous membrane, up to perforated.
  • The small intestine works much more slowly, it is inhabited by a small number of beneficial bacteria.
  • The peristalsis of the large intestine is significantly weakened, poorly processed food forms dense lumps, senile constipation and fecal obstructions are formed. The microflora deteriorates, the absorption of vitamins and nutrients practically does not occur.
  • The functional ability of the liver decreases. The synthesis of proteins, fats and carbohydrates is disrupted, the body cannot cope with fatty foods, and cannot neutralize a number of toxic substances, including drugs.
  • The gallbladder increases in size, bile does not enter the intestines well, and stones are likely to form.
  • The pancreas loses its secretory functions, the number of iron cells is rapidly decreasing.

In every elderly person, the gastrointestinal tract undergoes tremendous age-related changes. Food is poorly absorbed, irritates the mucous membranes, and the secretion of the stomach is not enough to break it down.This provokes the appearance of diarrhea. If such a problem arises, it is necessary to consult a doctor to draw up a competent diet and select drug therapy.

Main causes of diarrhea in old age

The entire human body functions differently with age. The gastrointestinal tract undergoes a large number of changes – the amount of hydrochloric acid decreases, intestinal motility decreases, and there are fewer enzymes.

The main reasons for the deterioration of digestion:

  • Partial or complete absence of teeth;
  • Crohn’s disease;
  • Colitis;
  • Ulcers of the stomach and duodenum;
  • Poor nutrition;
  • Unsanitary conditions for eating;
  • High stress levels;
  • A number of endocrine diseases.

What is the role of proper nutrition in recovery from diarrhea in elderly and senile people

It is very important to be able to independently adjust your diet, making it as simple and harmless as possible. A properly organized diet for diarrhea helps:

  • Reduce the load on the entire human gastrointestinal tract;
  • Relieve inflammation of the mucous membranes;
  • Eliminate fermentation processes leading to gas formation and swelling;
  • Normalize digestion processes.

The mainstay of treatment for diarrhea is a complete adjustment of the diet and strict adherence to the prescribed diet. The main problem with severe diarrhea is dehydration. Therefore, it is necessary to control the process of taking not only food, but also water.

The main rule for the formation of a diet for diarrhea is that food and drinks should not irritate the mucous membranes of the gastrointestinal tract and be easily absorbed so as not to aggravate the current process.

Organization of meals for diarrhea

There are 10 simple rules for older people with diarrhea:

  • Frequent fractional meals in small portions.Food is taken every 3-3.5 hours in small portions. Thus, it is easier for the stomach and intestines to process and absorb it.
  • Refusal from products that cause fermentation and gas formation.
  • Reduction of the average daily food intake by 20-30%.
  • Be sure to consume fresh dairy products every day.
  • Exclude from the menu foods that provoke increased bile production.
  • Change in the ratio of proteins, fats and carbohydrates.The volume of fats and carbohydrates decreases, the amount of protein increases.
  • Drinking a lot of fluids and foods containing it. Preference should be given to light soups with vegetable broth.
  • Do not eat vegetables and fruits that have not undergone heat treatment. Pure fiber irritates the intestinal mucous membranes and exacerbates the situation.
  • The temperature of the food consumed should be between 32 and 37 degrees. Do not eat hot or very cold food.
  • It is required to reduce the daily amount of salt.

It is necessary to include in the diet the following dishes and products:

  • Porridge boiled in water with a little salt and butter. They have an enveloping effect and are a source of slow carbohydrates;
  • Lean meats – chicken, turkey, beef, rabbit;
  • Low-fat varieties of fish;
  • Fresh fermented milk products without dyes and flavors;
  • Bread, while eating fresh bread is strongly discouraged – it provokes fermentation:
  • Heat-treated vegetables – potatoes, pumpkin, zucchini.The use of cabbage and beets should be discarded.

Rice for diarrhea is consumed daily. It should not be rinsed before cooking, and the consistency of the finished porridge should be jelly-like. Blueberry jelly, decoctions of pomegranate crusts have a strengthening effect. Milk whey reduces putrefaction in the gastrointestinal tract. Strong sweet tea with breadcrumbs will be a great snack for diarrhea.

Fatty, spicy, smoked dishes, deep-fried dishes, pickled and canned vegetables are excluded from the diet.Avoid:

  • Various semi-finished products;
  • Giblets;
  • Mustard;
  • Horseradish;
  • Adjiki;
  • Fatty meats;
  • Dairy products high in fat;
  • Fresh bread and pastries;
  • Sour fruits and berries;
  • Specific spices;
  • Nuts;
  • Lentils, beans, soybeans;
  • Alcoholic drinks;
  • Freshly squeezed juices;
  • Carbonated drinks;
  • Strong coffee.

A number of products can be consumed in limited quantities:

  • Soft-boiled eggs can be consumed once every two days;
  • Once every two days, it is permissible to use small pasta or “spider line” vermicelli;
  • Milk can be added to cereals if diluted with water;
  • Raspberries and strawberries can be eaten fresh in season, no more than ½ cup.

Menu option for an elderly person suffering from indigestion on day

Meals should be six meals a day, fractional, consist of small portions.

The first breakfast is boiled rice, a slice of yesterday’s dried bread, a rosehip drink or jelly.

Second breakfast – dried fruit compote.

Lunch – low-fat meat soup, meatballs with buckwheat, raisins and dried apricots compote.

Afternoon snack – cottage cheese with a fat content of no more than 3%.

Dinner – steamed lean meat roll, baked vegetables, compote.

The second supper is jelly.

You can eat boiled, baked and steamed food. The use of fried, spicy foods is strictly prohibited. In some cases, you need to thoroughly grind food to a puree state.

The porridge should be boiled in water or milk diluted in half with water. If the patient is lactose intolerant, then milk is completely excluded from his menu.

Only freshly prepared food can be consumed.It is better to exclude yesterday’s or the day before yesterday’s food from the diet.

You must consume at least two liters of clean water per day. At the same time, with severe diarrhea, one must remember about a violation of the water-salt balance. A glass of water should be drunk once an hour and after each bowel movement. If diarrhea is accompanied by vomiting, you must drink every 10-15 minutes in small portions.

Compliance with the diet is required throughout the acute period of the disease.In the first 3 days after the onset of diarrhea, a strict diet is followed with the inclusion of a minimum amount of food. Gradually, other products are introduced into the menu. At the same time, after the end of the diarrhea, a sparing diet is observed for another week in order to exclude a relapse.

To maintain the health of their gastrointestinal tract, elderly and senile people should adhere to several rules:

  • Avoid overeating;
  • Eat fresh dairy products regularly;
  • There are boiled and baked food;
  • Adhere to a diet;
  • Take food in small portions, but often;
  • Avoid solid foods;
  • Include cream soups in the diet;
  • Do not use canned and pickled dishes, as well as dishes with hot peppers.

If you follow all the rules and instructions of your doctor, all symptoms of diarrhea will completely disappear after two weeks.

Very often, the elderly and elderly people suffer from regular digestive disorders. Some of them have chronic comorbidities. In this case, temporary or permanent stay in a specialized boarding house is possible.

Recommended reading:

Chronic diarrhea

Our network of medical clinics provides services for the diagnosis and treatment of chronic diarrhea in adults using imported drugs and modern equipment.

We have been in the private and family medicine sector since 2002 and offer the best possible treatment for the causes of diarrhea at the most affordable prices.

Our network of clinics employs more than 300 certified specialists who have vast experience in their medical industries and are able to find the optimal approach to the most demanding and demanding clients. Our doctors are able to identify the causes of chronic diarrhea in the shortest possible time and select the necessary complex of treatment, based on the individual characteristics of the organism of a particular patient.In addition, we offer one-year comprehensive health care programs at better pricing terms.

Symptoms and causes of chronic diarrhea in adults

Chronic diarrhea in adults can have many causes and a wide variety of symptoms. This disease is expressed as a pathological condition, in which, over a long period, from 3 weeks, there are problems with frequent bowel movements, the frequency of which increases by 50-100% of the usual needs of a particular organism.The main signs of such a disease, in addition to frequent bowel movements, are liquid and loose stools, tenesmus, bloating, rumbling, heaviness and recurrent pain.

This disease is diagnosed by examination, colonoscopy, analysis of feces. The main treatment for frequent diarrhea in adults is diet and medication.

Key causes of prolonged diarrhea in adults

Depending on the mechanism of development of the disease, several causes of prolonged diarrhea in adults are distinguished:

  • Hypersecretory causes of prolonged diarrhea
  • Hyperosmotic causes of diarrhea
  • Hyperkinetic group of causes
  • Hyperexudative causes of persistent diarrhea

Causes of occurrence:

  • Intestinal infection.
  • Non-infectious bowel disease.
  • Diseases of the digestive tract with damage to its upper sections.
  • Chronic intoxication.
  • Psychoemotional pathologies.
  • Diseases of other (non-digestive) organs.

How to recognize a disease?

It is worth noting that the symptoms of chronic diarrhea in adults can be a sign of more serious diseases of the body, therefore, the treatment of this ailment should be trusted exclusively by qualified doctors who have the necessary experience and resources to diagnose and treat the disease.

As already noted, the main characteristic symptoms of diarrhea are: frequent bowel movements, liquid and loose stools, tenesmus, bloated abdomen, rumbling, heaviness and recurrent pain in the stomach.

With pathologies of the small intestine, the main symptom is abundant stool of a fatty or watery type. Also, often in the feces, you can find a small admixture of pus or blood.

In pathologies of the large intestine, the main symptom is scanty stool with private false urges, as well as pain in the abdomen, which are uncharacteristic of the causes of diarrhea, which are associated with diseases of the small intestine.

Other symptoms largely depend on the specific disease that provoked the diarrhea. For example, colorectal cancer is associated with weakness, fatigue, appetite disorders, and weight loss. Inflammatory diseases that provoked problems with stool have characteristic hyperthermia and various external manifestations of the extraintestinal type, including stomatitis or arthralgia.

Attention! If you find any of these symptoms in yourself, it is recommended to contact a gastroenterologist for a comprehensive diagnosis of the gastrointestinal tract.Do not try to self-medicate, it can aggravate your health condition.

Benefits of working with our network of clinics

The network of medical clinics “IMMA” is extremely high European standards of private medicine at affordable prices.

Among our main competitive advantages are:

  • Impeccable market reputation and reviews of satisfied customers;
  • Huge staff of experienced qualified doctors;
  • Progressive methods of treatment;
  • Availability of imported effective drugs and diagnostic equipment;
  • Free consultations on any questions before making an appointment;
  • Possibility of providing a one-time treatment or examination, or concluding a contract for ongoing medical care at a more affordable price;
  • Transparent pricing policy and affordable fixed prices for the entire range of services;
  • Availability of a unified information and analytical system;
  • Availability of 6 medical and outpatient institutions in various districts of the city;
  • Home assistance;

Help desk work in a 24/7 format.

ABC-medicine

Ulcerative colitis of the intestine is a chronic gastrointestinal disease with a recurrent nature. The development of this disease involves inflammation of the mucous membrane of the large intestine, where areas of necrosis and ulcers are formed. The clinical manifestations of ulcerative colitis are bloody diarrhea, arthritis, weight loss, general weakness, and abdominal pain. This disease has been proven to increase the risk of developing colorectal cancer.

Reasons

The etiology of the disease has not yet been clarified, scientists are actively looking for the causes of ulcerative colitis. However, at the moment, the main risk factors for this disease are known.

Genetic factors. If a patient has one of the relatives in the family suffering from ulcerative colitis, the risk of developing this disease increases.

Influence of infection. The intestine is a place where various microorganisms constantly live, which can lead to inflammatory processes in the mucous membrane.

Autoimmune factors. Inflammation is caused by mass death of cells with antigens.

Influence of factors of inflammation. This cause is released during the immune response when an antigen-antibody complex is formed.

Symptoms

Bloody diarrhea. One of the main diagnostic symptoms of ulcerative colitis of the intestine is diarrhea with mucus and blood, in rare cases – with pus. The frequency of bowel movements in patients can be different – from 2-3 times a day to 15-20 times in severe cases.Stool especially frequent at night and in the morning.

Pain in the projection of the abdomen. Pains have varying degrees of severity in most patients – from mild to acute, severe, accompanied by significant discomfort. Pain is often localized to the left side of the abdomen. The main symptom of the onset of complications is acute abdominal pain, which cannot be stopped by taking analgesics.

Other signs of intoxication of the body. Weight loss, weakness, poor appetite, frequent dizziness.Tenesmus is a false urge to defecate. Flatulence. Some patients have fecal incontinence. Sometimes patients have constipation instead of diarrhea, which indicates a pronounced inflammation of the colon mucosa.

Diagnostics

Laboratory diagnostics . CBC results indicate anemia (a decrease in the number of red blood cells and hemoglobin) and leukocytosis. A blood biochemistry test can detect an increase in the blood of C-reactive protein, which is an indicator of inflammatory processes in the human body.In the analysis of feces, pathogenic microflora is sown, and the presence of blood, pus and mucus is also noted.

Instrumental diagnostics. Endoscopy (rectosigmoidoscopy, colonoscopy) allows you to identify a complex of symptoms characteristic of the disease in a patient:

  • edema and hyperemia;
  • 90,018 pseudopolyps;

  • granular character of the mucous membrane;
  • contact bleeding;
  • the presence of blood, mucus and pus in the lumen of the intestine;
  • severe atrophy of the colon mucosa in remission.

Treatment

An etiological treatment capable of eliminating the cause of ulcerative colitis has not yet been developed. Treatment is symptomatic, aimed at eliminating inflammation, maintaining remission and preventing complications. In the event that drug therapy is ineffective, surgery is performed.

Diet therapy. During an exacerbation, the patient should refrain from eating. You can only drink water.When remission occurs, the patient is advised to consume a minimum amount of fat and increase the protein content in food (lean fish and meat, eggs, cottage cheese are suitable). As carbohydrates, you should use honey, cereals, jelly, jelly, fruit and berry compotes, decoctions.

Drug treatment. Prescribed to take NSAIDs and antibiotics. The patient can take pain relievers in accordance with the dosage individually selected by the doctor. During an exacerbation of the disease, antibiotics are recommended.

Surgical intervention . Surgical treatment of ulcerative colitis of the intestine is prescribed when conservative methods are ineffective. The methods of colectomy, proctocolectomy are used.

To enroll in the ABC-Medicine clinic for the diagnosis and treatment of ulcerative colitis of the intestine, call +7 (495) 223-38-83 .

Salmonella (non-typhoid)

Review

The burden of foodborne illness is significant, with nearly one in ten people falling ill each year, resulting in the loss of 33 million years of healthy life.Foodborne illness can be severe, especially in young children. Diarrheal diseases are the most common illnesses caused by unhealthy foods. They affect 550 million people annually, including 220 million children under 5 years of age. Salmonella is one of the four leading causes of diarrheal diseases worldwide.

Salmonella is a rod-shaped genus of gram-negative bacteria and belongs to the family of Enterobacteriaceae.To date, within two species – Salmonella bongori and Samonella enterica – more than 2500 different serotypes or “serovars” have been identified. Salmonella is a ubiquitous and resistant bacterium that can survive for several weeks in dry environments and several months in water.

Although all serotypes can cause disease in humans, some are host specific and can live in only one or a few species: for example, the Dublin serotype Salmonella enterica lives in cattle, and the Choleraesuis serotype Salmonella enterica – in pigs.When these specific serotypes cause disease in a person, the disease is often invasive and can be life-threatening.

However, most serotypes are present in a wide variety of carriers. These serotypes usually cause gastroenteritis, which is often uncomplicated and does not require treatment, but can be severe in children, the elderly, and immunocompromised patients. This group includes the Enteritidis serotype Salmonella enterica and the Typhimurium serotype Salmonella enterica , the two most important serotypes of Salmonella transmitted from animals to humans in most regions of the world.

Disease

Salmonellosis is a disease caused by the bacteria Salmonella . It is usually characterized by a sharp rise in temperature, abdominal pain, diarrhea, nausea, and sometimes vomiting.

Symptoms appear 6 to 72 hours (usually 12 to 36 hours) after is ingested by Salmonella , and the disease lasts 2 to 7 days.

Salmonellosis symptoms are relatively mild, and in most cases, patients recover without specific treatment.However, in some cases, especially in children and the elderly, disease-related dehydration can become severe and life-threatening.

Although large outbreaks of Salmonella usually attract media attention, 60 to 80% of all Salmonella cases are not reported in known outbreaks. Such cases are classified as sporadic or not diagnosed at all as such.

Sources and transmission of infection

  • Bacterium Salmonella is widespread in domestic and wild animals, mainly in food animals such as poultry, pigs and cattle; as well as among domestic animals, including cats, dogs, birds and reptiles such as turtles.
  • Salmonella can pass through the entire food chain – from animal feed, primary production to the home and catering establishments.
  • Humans contract salmonellosis, usually through the consumption of contaminated food of animal origin (mainly eggs, meat, poultry and milk), although other foods, including green vegetables contaminated with manure, may be implicated in transmission.
  • Human-to-human transmission by fecal-oral route may also occur.
  • Human cases also occur through contact with infected animals, including domestic animals. Infected animals often do not show signs of the disease.

Treatment

In severe cases, treatment consists of electrolyte replenishment (to ensure that electrolytes such as sodium, potassium and chlorine ions are excreted through vomiting and diarrhea) and rehydration.

For mild or moderate illness in healthy individuals, conventional antimicrobial therapy is not recommended.This is due to the fact that antimicrobial drugs may not completely kill the bacteria and contribute to the selection of resistant strains, which can subsequently lead to the fact that the drug becomes ineffective. …

However, risk groups such as infants, the elderly, and immunocompromised patients may need antimicrobial treatment. Antimicrobials are usually prescribed when the infection spreads from the intestines to other parts of the body.

With the global increase in antimicrobial resistance, treatment guidelines need to be regularly reviewed, taking into account the bacterial resistance model, taking into account the local surveillance system

Methods of prevention

Prevention requires control measures at all levels of the food chain – from agricultural production to food processing, production and preparation, both in commercial organizations and at home.

Preventive measures to protect against Salmonella at home are similar to those used to protect against other bacterial foodborne diseases (see Guidelines for Food Handlers below).

Contact between infants and young children and pets (cats, dogs, turtles, etc.) that may carry Salmonella should be closely monitored.

National and regional foodborne disease surveillance systems are important tools for studying and monitoring the situation of such diseases, as well as for detecting and responding to salmonellosis and other intestinal infections in an early stage, thus preventing further spread of such diseases.

Advice for the public and travelers

The following recommendations will help to ensure safety while traveling:

  • Ensure food is properly cooked and still hot when serving.
  • Avoid raw milk and raw milk products. Drink only pasteurized or boiled milk.
  • Avoid eating ice unless it has been made with safe water.
  • If there is any doubt about the safety of the water, boil it or, if this is not possible, disinfect it with a reliable, slow-acting disinfectant (usually available from pharmacies).
  • Wash hands thoroughly and use soap frequently, especially after contact with pets or farm animals, and after using the toilet.
  • Wash fruits and vegetables thoroughly, especially if consumed raw. If possible, peel vegetables and fruits.

Advice for Food Handlers

WHO has formulated the following guidelines for food processors:

  • Food handlers, both professionally and at home, should be vigilant when preparing food and observe good hygiene practices related to food preparation.
  • Food handlers who have a fever, diarrhea, vomiting, or visible infected skin lesions should immediately report this to their employer.
  • The WHO brochure The Five Essential Principles for Safe Nutrition serves as the foundation for educational programs to prepare food handlers and to educate consumers. These principles are especially important for preventing foodborne illness.These five principles are as follows:

Recommendations for producers of fruits, vegetables and fish

The WHO brochures The Five Critical Principles for Growing Safer Fruits and Vegetables: Promoting Health by Reducing Microbial Contamination and The Five Critical Principles for Improving Aquaculture Product Safety to Protect Public Health educate agricultural workers, including smallholder farmers who grow fresh fruits and vegetables. and fish for themselves, their families and for sale in local markets, with key practices for preventing microbial contamination.

The five essential principles for growing safer fruits and vegetables are as follows:

  • Maintain good personal hygiene.
  • Protect fields from contamination by animal faeces.
  • Use treated faeces.
  • Assess and manage the risks of irrigation water.
  • Keep harvested crops and storage equipment clean and dry.

“Five essential principles for improving the safety of aquaculture products in order to protect public health”

  • Maintain good personal hygiene.
  • Keep the pond clean.
  • Monitor your water quality.
  • Monitor the health of your fish.
  • Use clean fish collection equipment and containers.

WHO Activities

In collaboration with other stakeholders, WHO strongly advocates the important role of food safety as a key ingredient in ensuring access to a safe and nutritious diet. WHO develops policies and recommendations that span the entire food chain from production to consumption, drawing on a variety of expertise and experience in a wide variety of areas.

WHO is working to strengthen food safety systems in an increasingly globalized world. Setting international food safety standards, improving disease surveillance, educating consumers and educating food processors in the safe handling of food are among the most important ways to prevent foodborne disease.

WHO is strengthening the capacity of national and regional laboratories for the surveillance of foodborne pathogens such as Campylobacter and Salmonella .

In addition, WHO promotes integrated surveillance of antimicrobial resistance of pathogens in the food chain by collecting human, animal and food samples and analyzing data from different sectors.

WHO works with FAO to assist Member States by coordinating international efforts for the early detection and response of foodborne disease outbreaks through a network of national authorities in Member States.

In addition, WHO carries out scientific assessments that are used as the basis for the international standards, principles and guidelines for food for the prevention of foodborne diseases developed by the FAO / WHO Codex Alimentarius Commission.

Influenza, coronavirus infection and other acute respiratory viral infections (ARVI)

Influenza, coronavirus infection and other acute respiratory viral infections (ARVI)

Influenza, coronavirus infection and other acute respiratory viral infections (ARVI) are in first place in terms of the number of people who become ill each year.

Despite constant efforts to combat the causative agents of influenza, coronavirus infection and other acute respiratory viral infections, they still have not been defeated.

Thousands of people die from complications of influenza every year.

This is due to the fact that viruses, primarily influenza viruses and coronaviruses, have the ability to change their structure and a mutated virus is capable of infecting a person again. So, a person who has had the flu has a good immune barrier, but nevertheless a new modified virus is able to easily penetrate through it, since the body has not yet developed immunity against this type of virus.

For whom is the most dangerous encounter with the virus?

Children and the elderly are especially hard to tolerate the infection; complications that can develop during the illness are very dangerous for these age groups. Children get sick more seriously due to the fact that their immune systems have not yet met this virus, and for the elderly, as well as for people with chronic diseases, the virus is dangerous due to a weakened immune system.

Risk groups

Children

People over 60 years old

People with chronic lung diseases (bronchial asthma, chronic obstructive pulmonary disease)

People with chronic diseases of the cardiovascular system (congenital heart defects, coronary heart disease, heart failure)

· Pregnant women

· Medical workers

Workers of public transport, catering establishments

How does the infection occur?

The infection is transmitted from a sick person to a healthy person through the smallest droplets of saliva or mucus that are released during sneezing, coughing, talking.Contact transmission is also possible.

Symptoms

Depending on the specific type of pathogen, symptoms can vary significantly, both in severity and in combination.

· Temperature increase

Chills, general malaise, weakness headache, muscle pain

Decreased appetite, possible nausea and vomiting

Conjunctivitis (possibly)

Diarrhea (possibly)

On average, the illness lasts about 5 days.If the temperature lasts longer, complications may have arisen.

Complications

Pneumonia

Encephalitis, meningitis

Complications of pregnancy, development of fetal pathology

Exacerbation of chronic diseases

Treatment of the disease is carried out under the supervision of a physician, who, only after examining the patient, prescribes a treatment regimen and gives other recommendations.The sick person must comply with bed rest, eat well and drink more fluids.

Antibiotics

Taking antibiotics in the early days of the disease is a big mistake. Antibiotics are not able to cope with the virus, in addition, they adversely affect the normal microflora. Antibiotics are prescribed only by a doctor, only in case of complications caused by the addition of a bacterial infection. Taking antibacterial drugs as a preventive measure for the development of complications is dangerous and useless.

A sick person should stay at home and not pose a threat of infection to others.

Prevention

The most effective way to prevent influenza is to get vaccinated annually. The composition of the influenza vaccine changes annually. First of all, it is recommended to get vaccinated for those who are at risk. The optimal time for vaccination is October-November. Influenza vaccination is possible from 6 months of age onwards.

Vaccines against most pathogens of acute respiratory viral infections have not been developed.

Universal prevention measures

Wash your hands often and thoroughly

Avoid contact with people who are coughing

Follow a healthy lifestyle (sleep, healthy food, physical activity)

Drink plenty of fluids

Regularly ventilate and humidify the air in the room where you are

Be in public places less often

Use a mask when you are in transport or in crowded places

Avoid hugging, kissing and shaking hands when meeting

Do not touch your face, eyes, nose with unwashed hands

At the first sign of a viral infection, consult a doctor!


Influenza, coronavirus, other acute respiratory viral infections – a mask will help!

During the period of active circulation of pathogens of influenza, coronavirus infection, and other pathogens of acute respiratory viral infections, we recall the advisability of using a disposable medical mask as an effective measure to prevent infection and limit the spread of infection.

These viruses are transmitted from person to person mainly by airborne droplets, through microdroplets of respiratory secretions that are formed when infected people speak, sneeze or cough.

With air, these droplets can get onto the surface of the mucous membrane of the upper respiratory tract of healthy people who are next to an infected person.

Infection can also occur as a result of direct or indirect contact of a healthy person with the respiratory secretions of an infected person.

The use of a disposable medical mask prevents droplets of respiratory secretions, which may contain viruses, from entering the body of a healthy person through the nose and mouth.

· Wear a mask when caring for a family member with symptoms of a viral respiratory illness.

· If you are sick or have symptoms of a viral respiratory illness, wear a mask before approaching other people.

· If you have symptoms of a viral respiratory illness and need to see a doctor, wear a mask well in advance to protect those around you in the waiting area.

· Wear the mask indoors, in crowded places.

· The mask should fit snugly to the face and cover the mouth, nose and chin. If there is a sewn-in attachment in the area of ​​the nose, it must be pressed tightly against the back of the nose.

· Wear the mask indoors, in crowded places.

· Use the mask once; reuse of the mask is not allowed.

· Change the mask every 2-3 hours or more often.

· If the mask is wet, it should be replaced with a new one.

· After using the mask, discard it and wash your hands with soap and water.

· The mask cannot be reused.

· Wearing a mask in deserted open spaces is not advisable.

Disposable medical mask, when used correctly, is a reliable and effective method of reducing the risk of infection and preventing the spread of influenza, coronavirus and other pathogens of ARVI!

Only in conjunction with careful hand hygiene and quarantine measures will the mask be used as effectively as possible to prevent infection and spread of infection!


Hygiene for influenza, coronavirus infection and other acute respiratory viral infections

What should you do during the period of active circulation of pathogens of influenza, coronavirus infection and other pathogens of acute respiratory viral infections (ARVI) in order to prevent your own infection and protect those around you if you get sick?

The causative agents of all these diseases are highly contagious and are transmitted mainly by airborne droplets.

When sneezing and coughing in the air around a sick person, microdroplets of his saliva, sputum and respiratory secretions, which contain viruses, are spread. Larger droplets settle on surrounding objects and surfaces, small ones stay in the air for a long time and are transported to distances of up to several hundred meters, while viruses retain the ability to infect from several hours to several days. The main measures of hygienic prevention are aimed at preventing healthy people from coming into contact with particles of a sick person’s secretions containing viruses.

Compliance with the following hygienic rules will significantly reduce the risk of infection or further spread of influenza, coronavirus infection and other SARS.

How not to get infected

· Wash hands after visiting any public places, transport, touching doorknobs, money, public office equipment in the workplace, before eating and preparing food.Pay special attention to thoroughly soaping (at least 20 seconds), and then completely drying your hands.

· After returning home from the street – wash your hands and face with soap, rinse your nose with isotonic salt solution.

· Touch the face, eyes – only with recently washed hands. If water and soap are not available, use alcohol-based hand sanitizers to clean your hands. Or use a disposable napkin if you need to touch your eyes or nose

· Put on a disposable medical mask in crowded places and transport.It is necessary to change the mask to a new one every 2-3 hours; the mask cannot be reused.

· Give preference to sleek hairstyles when you are in crowded places, loose hair, often in contact with your face, increases the risk of infection.

· Avoid close contact and stay in the same room with people who have visible signs of SARS (coughing, sneezing, nasal discharge).

· Do not touch doorknobs, handrails, other objects or surfaces in public spaces with bare hands.

· Limit welcome handshakes, kisses, and hugs.

· Ventilate the premises more often.

· Do not use shared towels.

How not to infect others

· Minimize contact with healthy people (welcome handshakes, kisses).

· If you feel unwell, but have to communicate with other people or use public transport – use a disposable mask, be sure to change it to a new one every hour.

· When coughing or sneezing, be sure to cover your mouth, if possible – with a disposable handkerchief, if not – with your palms or elbows.

· Use only personal or disposable tableware.

· Isolate your personal hygiene items from household members: toothbrush, washcloth, towels.

· Carry out wet cleaning of the house every day, including the processing of door handles, switches, office equipment control panels.

Memo: Prevention of influenza and coronavirus infection


Influenza and coronavirus viruses cause respiratory diseases of varying severity in humans. Symptoms are similar to those of regular (seasonal) flu. The severity of the disease depends on a number of factors, including the general condition of the body and age.

Predisposed to the disease: the elderly, small children, pregnant women and people suffering from chronic diseases (asthma, diabetes, cardiovascular diseases), and with weakened immunity.


RULE 1. OFTEN WASH HANDS WITH SOAP


Clean and disinfect surfaces using household detergents.

Hand hygiene is an important measure to prevent the spread of influenza and coronavirus infection. Washing with soap removes viruses. If you cannot wash your hands with soap and water, use alcohol or disinfectant wipes.

Cleaning and regular disinfection of surfaces (tables, doorknobs, chairs, gadgets, etc.)) removes viruses.

RULE 2. OBSERVE DISTANCE AND LABEL

Viruses are transmitted from a sick person to a healthy person by airborne droplets (when sneezing, coughing), therefore, it is necessary to maintain a distance of at least 1 meter from patients.

Avoid touching your eyes, nose, or mouth with your hands. The flu virus and coronavirus are spread by these routes.

Wear a face mask or other available protective equipment to reduce your risk of illness.

When coughing, sneezing, cover your mouth and nose with disposable tissues, which should be discarded after use.

Avoiding unnecessary travel and visits to crowded places can reduce the risk of illness.

RULE 3. LEAD A HEALTHY LIFESTYLE

A healthy lifestyle increases the body’s resistance to infection. Maintain a healthy schedule, including adequate sleep, eating foods rich in protein, vitamins and minerals, and being physically active.

RULE 4. PROTECT RESPIRATORY ORGANS WITH A MEDICAL MASK

Among other means of prevention, wearing masks occupies a special place, thanks to which the spread of the virus is limited.

Medical Respiratory Masks Use:

– when visiting crowded places, traveling by public transport during a period of increasing incidence of acute respiratory viral infections;

– when caring for patients with acute respiratory viral infections;

– when communicating with persons with signs of an acute respiratory viral infection;

– with the risk of infection with other infections transmitted by airborne droplets.

HOW TO WEAR A MASK CORRECTLY?

Masks can be of different designs. They can be one-time use or they can be applied multiple times. There are masks that last 2, 4, 6 hours. The cost of these masks is different due to the different impregnation. But you can’t wear the same mask all the time, so you can infect yourself twice. Which side to wear a medical mask inside is not important.

To protect yourself from infection, it is extremely important to wear it correctly:
– the mask should be carefully fixed, tightly covering the mouth and nose, leaving no gaps;

– try not to touch the surfaces of the mask when removing it, if you touched it, wash your hands thoroughly with soap or alcohol;

– a wet or damp mask should be changed to a new, dry one;
– do not reuse a disposable mask;

– the used disposable mask should be discarded immediately.

When caring for a patient, after the end of contact with a sick person, the mask should be removed immediately. After removing the mask, wash your hands immediately and thoroughly.

A mask is appropriate if you are in a crowded area, on public transport, and when caring for the sick, but it is not advisable in the open air.

It is good to breathe fresh air while you are outdoors and you should not wear a mask.

At the same time, doctors remind that this single measure does not provide complete protection against the disease.In addition to wearing a mask, other preventive measures must be followed.

RULE 5. WHAT TO DO IN CASE OF INFLUENZA, CORONAVIRUS INFECTION?

Stay home and see your doctor urgently.
Follow your doctor’s orders, stay in bed and drink as much fluids as possible.

WHAT ARE THE SYMPTOMS OF FLU / CORONAVIRUS INFECTION

high body temperature, chills, headache, weakness, nasal congestion, cough, shortness of breath, muscle pain, conjunctivitis.

In some cases, there may be symptoms of gastrointestinal disorders: nausea, vomiting, diarrhea.

WHAT ARE THE COMPLICATIONS

Viral pneumonia is the leading complication. Deterioration in viral pneumonia is rapid, and many patients develop respiratory failure within 24 hours, requiring immediate respiratory support with mechanical ventilation.

Prompt treatment can help alleviate the severity of the disease.

WHAT TO DO IF SOMEONE HAS A FLU / CORONAVIRUS INFECTION IN THE FAMILY?

– Call a doctor.

– Give the patient a separate room in the house. If this is not possible, maintain a distance of at least 1 meter from the patient.

– Limit to a minimum contact between the sick and loved ones, especially children, the elderly and people with chronic diseases.

– Ventilate the room frequently.

– Keep clean, wash and disinfect surfaces with household detergents as often as possible.

– Wash your hands often with soap and water.

– When caring for a sick person, cover your mouth and nose with a mask or other protective equipment (handkerchief, scarf, etc.