Hematological Complications of Acute Pancreatitis: A Review

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Resid Staff Physician. Author manuscript; available in PMC 2021 Nov 10.

Published in final edited form as:

Resid Staff Physician. 2001 Sep; 47(10): 29–35.

PMCID: PMC8580406

NIHMSID: NIHMS1750067

PMID: 34764519

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Pancreatitis has been described as a complication in about 1. 7% to 2% of cases of thrombotic thrombocytopenic purpura (TTP) or hemolytic uremic syndrome (HUS), which has been generally attributed to the pancreatic vascular compromise. However, the reverse situation—the development of clinical features of TTP or HUS following the clinical and laboratory diagnosis of acute pancreatitis—is very rare. Other hematological abnormalities such as hypercoagulation, disseminated intravascular coagulopathy, changes in hematocrit, leukocytes, and thrombocytopenia also have been observed and correlated to the outcome of acute pancreatitis. The authors review the medical literature, describe different hematological abnormalities encountered in patients with pancreatitis, and discuss its pathogenesis.

Acute pancreatitis is a common disease attributed to a long list of etiologies. Pancreatitis has been reported as a complication of thrombotic thrombocytopenic purpura (TTP) or hemolytic uremic syndrome (HUS) in only about 2% of cases. Based on necropsy findings, pancreatitis in patients with thrombotic TTP or HUS may result from necrosis secondary to thrombi in the pancreatic arterioles. This hypothesis has been supported by animal studies in which thrombosis of the pancreatic veins resulted in pancreatitis in dogs.^1,2

The opposite finding—TTP or HUS occurring as a sequelae of acute pancreatitis—is an even more rare occurrence.^3,4 In the event of acute pancreatitis, not only local inflammation occurs, but also release of pancreatic enzymes and other inflammatory mediators that may result in systemic involvement.

Other hematological abnormalities in patients with acute pancreatitis include changes in hematocrit (HCT), hypercoagulability secondary to coagulation factors’ abnormalities, disseminated intravascular coagulopathy (DIC), TTP/HUS, leukocytosis, abnormal forms of red cells, increased reticulocyte count, acute hemolytic anemia, and thrombocytopenia.

Complications of acute pancreatitis include local pancreatic necrosis with the formation of a pseudocyst or an abscess, and renal, pulmonary, hepatic, and endocrine abnormalities (). Hematological abnormalities including coagulation upsets, TTP, and HUS also have been reported in patients with acute pancreatitis (). Vascular injury by local pancreatic enzymes, with thrombosis and impaired blood flow, has been implicated in the pathogenesis of pancreatic necrosis.^6-7 The pathogenesis of extra-pancreatic manifestations of acute pancreatitis is not well understood, but circulating factors originating in the inflamed pancreas may play a role.

Table 1

Extra-pancreatic manifestations of acute pancreatitis

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Table 2

Hematological abnormalities in patients with acute pancreatitis

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Changes in Hb/HCT

The fall in hemoglobin (Hb)/HCT during the first week of acute pancreatitis has been observed and may be attributable to multiple factors (). Similarly, an increase in HCT secondary to hemoconcentration at the time of presentation also can be seen.

Table 3

Causes for changes in hematocrit secondary to acute pancreatitis

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Alterations in Coagulation

Previous investigators have reported various alterations in coagulation during acute pancreatitis, including elevated fibrinogen level, elevated factor VIII levels, increased factor V levels, decreased factor V levels, initial decrease followed by increased prothrombin time, elevated plasminogen and antiplasmin levels, and elevated antithrombin levels (). Most of these studies cover a short time period or describe a relatively small number of patients.^6,8-13

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A hypothetical mechanism for coagulation abnormalities caused by acute pancreatitis

Similarly, abnormalities of blood coagulation factors consistent with DIC, such as elevated fibrin degradation products (FDPs) in conjunction with elevated plasma fibrinogen levels, shortened clotting time, and positive ethanol gelation test, also have been seen in patients with pancreatitis. Hematologists suggest that DIC with secondary fibrinolysis can cause increased FDPs and positive ethanol gelation tests.⁹ Although they could be interpreted as a non-specific reaction to injury (acute pancreatitis),⁹ elevated FDPs and decreased serum fibrinogen suggest a hypercoagulable state.¹⁰ Other explanations for increased FDPs may include obstructive jaundice, liver disease, pulmonary embolism, venous thrombosis, and local hemorrhage (). ^8-13

Table 4

Causes of increased FDPs in acute pancreatitis

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The infrequency of severe thrombocytopenia in such studies suggests that widespread intravascular coagulation is not present, but does not exclude local intravascular coagulation. Hence, this hypercoagulability may be associated with localized intravascular coagulation and, in rare instances, diffuse intravascular coagulation may occur. ^8,10

The pathogenesis of coagulation upsets secondary to acute pancreatitis has been attributed to the release of trypsin from the inflamed pancreas.¹³ Attempts to demonstrate circulating trypsin in the blood of patients with acute pancreatitis have conflicting reports, but it may result from the protein binding of trypsin. In a series of 35 patients, Ranson and colleagues found a relationship between early coagulation changes and initial amylase levels and postulated that the circulating pancreatic enzyme may play a role in the pathogenesis of the coagulopathies developed in patients with acute pancreatitis.¹⁴

An early leukocytosis has been recorded in patients with acute pancreatitis and is associated with a more severe form of the disease.^15,16 Ranson found that the initial white blood counts, which correlated with increased early fibrinogen levels, may reflect the degree of pancreatic inflammation.¹⁴

Abnormal Forms of Red Cells and Increased Reticulocyte Counts

Abnormal forms of red cells, including increased fragmentation and burr cell formation, and increased reticulocyte counts approaching 5%, have been seen in cases of acute pancreatitis. ¹⁶

Pancreatitis is a rare complication of TTP/HUS. Review of two series of patients with TTP/HUS showed that abdominal pain was present in 11% and 14% of cases and documented pancreatitis in 2% and 1.7% of cases, respectively.^1,2 The underlying mechanism may possibly involve thrombi in pancreatic arterioles.^3,4 Review of the literature shows that TTP/HUS also may occur in association with pancreatitis.⁵ Such patients with acute pancreatitis usually develop TTP/HUS within 2 to 3 days of the onset of pancreatitis, which resolves when the pancreatitis subsides.^3,4

Other circumstantial evidence supporting TTP/HUS as a complication of pancreatitis is the association between alcohol consumption and pancreatitis and the resolution of TTP/HUS following pancreatectomy in one case report.¹⁷

Pathogenesis underlying the occurrence of TTP/HUS as a complication of pancreatitis remains a theoretical question because the pathophysiologic mechanisms resulting in TTP/HUS have not been established. One possible mechanism is the endothelial damage alone that can precipitate TTP/HUS.^8,10,13 Evidence consistent with a direct endothelial injury comes from clinical observations in patients who develop HUS after an endothelial-damaging, verotoxin-producing Escherichia coli infection¹⁸; who develop TTP/HUS after ingesting quinine in the presence of quinine-dependent platelet reactive antibodies that cross-react with endothelium, possibly through cross-reactivity with GPIIIa receptors¹⁸; or who receive chemotherapeutic drugs that putatively damage endothelium.²⁰ This direct endothelial injury mechanism is further supported by the finding of pancreatic autoantibodies in 39 of 43 patients with both acute and chronic pancreatitis.¹⁹

Another possible mechanism is endothelium damage indirectly resulting from the action of monocyte-derived cytokines, such as in-terleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α).²¹ In vitro and in vivo studies showed that IL-1 and TNF-α may act in concert to initiate inflammatory or thrombophilic changes in both the granulocytes and the endothelium. ^21,22 IL-1 and TNF-α may modulate hemostatic mechanisms by increasing the secretion of plasminogen activator inhibitor and von Willebrand factor; increasing expression of activated tissue factor; increasing production of prostacyclin, nitric oxide, and platelet activation factor; decreasing expression of thrombomodulin; and decreasing the secretion of tissue plasminogen activator ().²²

Table 5

Mode of actions of IL-1 and TNF-α in the pathogenesis of hemostatic complications secondary to pancreatitis

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Consistent with indirect endothelial injury mechanism is the finding of elevated TNF-α in the urine of children with HUS,²³ resolution of TTP/HUS upon excision of damaged endothelium (pancreatectomy),¹⁷ and resolution of TTP/HUS upon treatment with antibiotics, presumably allowing healing of the damaged endothelium associated with pancreatitis and ulcerative colitis. ¹⁷ Whether the endothelial damage and resulting thrombophilic changes observed in TTP/HUS are primary or secondary remains an important question.^17-23

Acute hemolytic anemia in isolation has been seen in patients with acute pancreatitis, as evidenced by indirect findings of hemolysis, including elevated serum LDH, indirect hyperbilirubinemia, and reticulocytosis.^14,24 However, one report suggests that direct mechanical stress from a stenotic mitral valve caused fragmentation, which led to acute pancreatitis.²⁴ A peripheral smear should be examined to identify microangiopathic anemia either as a component of TTP or in isolation.

Thrombocytopenia, alone and/or as part of TTP/HUS, also has been reported in 27% of patients with acute pancreatitis, which does not imply a worse prognosis.²⁵

Management of hematological abnormalities in patients with acute pancreatitis includes general treatment for pancreatitis, along with therapy for the associated hematological abnormality. If clinical findings establish the diagnosis of TTP, plasmapheresis should be initiated as soon as possible.^26,27 Although plasmapheresis alone stands as the first-line treatment, steroids have been used with plasmapheresis in cases of TTP complicating acute pancreatitis.²⁶ It is possible that the benefit of plasmapheresis is related to the provision of new plasma rather than removal of the patient’s plasma, as previously suggested by some authors. However, the exact role of steroids is not clear.

Other possible therapies include antiplatelet agents, such as dipyridamole or aspirin, but they are associated with an increased risk of bleeding and should be used with caution.²⁶ A better understanding of the pathogenesis and the relationship between these two entities requires in vitro and in vivo studies that will also facilitate the development of preventive and treatment measures.

The review of the literature suggests that hematological abnormalities, including abnormalities of hemogram, and coagulation upsets are encountered in patients with acute pancreatitis. Changes in blood counts, particularly leukocytosis, have suggested a relationship with the outcome of pancreatitis since it was identified by Ranson. Such hemostatic abnormalities may be related to early intravascular consumption of coagulation factors, which may be secondary to circulating pancreatic enzymes, particularly trypsin, or secondary to vascular injury. Potentially fatal hematological complications like TTP or HUS also may occur rarely in patients with acute pancreatitis.

The recognition of these entities and their relationship to acute pancreatitis appear significant. Physicians caring for such patients should be aware of these complications.

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The simultaneous incidence of acute pancreatitis and autoimmune hemolytic anemia: a rare duo in a patient with SLE

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Ger Med Sci. 2014; 12: Doc12.

Published online 2014 Sep 25. doi: 10.3205/000197

Language: English | German

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A young female presented with acute abdominal pain of two days duration consistent with acute pancreatitis. During her stay in the hospital she had a sudden drop in hemoglobin to 6 g/dl without any overt blood loss. On evaluation, it was evident that she had acute pancreatitis, in addition to displaying features of autoimmune hemolytic anemia. She had been a known case of systemic lupus erythematosus (SLE) and had discontinued her treatment. She was managed with methylprednisolone pulse therapy. Her clinical condition improved, and she has been regularly attending our clinic for the last 2 years. According to a literature search in Medline, it would appear that this is the first report of a case in which SLE with autoimmune hemolytic anemia has been associated with acute pancreatitis in a single case.

Keywords: systemic lupus erythematosus (SLE), acute pancreatitis, autoimmune hemolytic anemia, massive hemolysis

Eine junge Frau stellte sich mit akuten Bauchschmerzen von zwei Tagen Dauer, die auf eine akute Pankreatitis hinwiesen, vor. Während ihres Aufenthaltes im Krankenhaus erlitt sie einen plötzlichen Abfall des Hämoglobins auf 6 mg/dl ohne offenen Blutverlust. Die Untersuchung ergab, dass sie eine akute Pankreatitis hatte und zusätzlich Symptome einer autoimmunhämolytischen Anämie zeigte. Die Patientin hatte eine bekannte Vorgeschichte von systemischem Lupus erythematodes (SLE) mit Behandlungsabbruch. Sie wurde mit Methylprednisolon-Pulstherapie behandelt. Ihre klinischer Zustand verbesserte sich, und sie wird seit den letzten 2 Jahren regelmäßig in unserer Klinik untersucht. Nach einer in Medline durchgeführten Literaturrecherche scheint es, dass dies der erste Bericht über einen Fall ist, in dem SLE mit autoimmunhämolytischer Anämie und akuter Pankreatitis zusammen auftritt.

Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease characterized by the presence of a plethora of autoantibodies and immune complex formation targeted to various organs of the body. SLE presents with mucocutaneous, musculoskeletal and/or renal involvement. Hematological disturbances are also common in SLE. Anemia in SLE is multi-factorial and can be part of the disease process or a complication of the treatment itself. Autoimmune hemolytic anemia (AIHA) is often associated with thrombocytopenia, lupus nephritis, and central nervous system activity. In comparison, common gastrointestinal (GI) manifestations of SLE are non-specific and reflect either lupus of the GI tract or the effects of medication. Serious gastrointestinal manifestations of SLE can include mesenteric vasculitis, acute pancreatitis and intestinal pseudo-obstruction. This report describes a rare combination of hematological and gastrointestinal complication found in a patient with SLE flare.

A 22-year-old woman came to the emergency department of the King Fahad Medical City in Riyadh, a tertiary care center in Saudi Arabia, presenting with history of acute abdominal pain of 2 days duration. She described the pain as severe (score of 6/10). The pain was in the epigastrium with reference to the back. There was no history of offending drug intake, jaundice or fever. She had also had two episodes of non-bilious vomiting She had been diagnosed as suffering from SLE (American College of Rheumatology ACR, criteria 5/11) 5 years prior to the current presentation, but had discontinued treatment of her own volition. On examination she showed stable vitals, with mild epigastric tenderness and no organomegaly. Her systemic examination was unremarkable. She had a hemoglobin of 9.8 g/dl, a leucocytic count of 11,500 and a platelet count of 110×10³. Her serum amylase was 380 IU (Ref. 110 IU) and the lipase levels were 850 IU. She was managed as a case of acute pancreatitis, was kept nil per mouth and was given normal saline intravenously. Her abdomen CT scan was consistent with grade B pancreatitis (Balthazar classification). She had a normal hepatobiliary system, and her serum lipids and serum calcium levels were also normal. On further evaluation, it appeared that she had an elevated ESR 66 mm/1^st hr. Her antinuclear antibody (ANA) levels were elevated 1:60 (reference 1:35 IU/ml), as were her double stranded DNA (DsDNA) levels (>19 AU/ml). During the hospital stay, her hemoglobin dropped further to 6 g/dl. She had no bleeding, and further evaluation was suggestive of acute hemolysis (positive direct Coombs test, indirect hyper-bilirubinemia 8. 6 g/dl, corrected retic count of 4%, elevated serum lactate dehydrogenase (LDH) 822 U/L). As a result of her past diagnosis of SLE, she was managed with pulse methylprednisolone 500 mg IV for 3 days. Her abdominal pain settled and her hemoglobin levels remained stable. She was later started on tab. prednisolone 40 mg once daily, which was tapered on follow-up. She has been asymptomatic for the past 2 years, and is regularly attending our clinic.

The diagnosis of acute pancreatitis is an important differential in the evaluation of abdominal pain in a patient with SLE. The patients usually present with pain of variable intensity. Several factors have been implicated in the pathogenesis of this condition, such as vasculitis, drugs and antiphospholipid antibodies. The role of corticosteroids as an etiologic factor remains controversial. Ben et al. described acute pancreatitis in six SLE patients, with favorable outcomes following steroid treatment [1]. Recently, data on 4,053 SLE patients from China showed the overall prevalence of pancreatitis to be 0. 67%, an annual incidence of 0.56% with a mortality rate of 37.04%. The authors of this study concluded that a combination of SLE activity and multiple organ system involvement were predictors both of severity and mortality due to acute pancreatitis in SLE patients. In this study, further glucocorticoid treatment was considered to lead to a better outcome in a majority of SLE patients [2].

The index case had been diagnosed with SLE 5 years prior to her current presentation and she had discontinued treatment of her own accord. It is quite possible that, in her case, stopping the maintenance dose of steroids was responsible for both the acute pancreatitis and the acute autoimmune hemolytic anemia (AIHA). The association of acute pancreatitis in a cohort study of 551 SLE patients included the withdrawal of a maintenance dose of steroids, the presence of seizures and of arthritis, and the authors of this study found no independent predictor of this complication [3]. In yet another study, hypertriglyceridemia appeared to be a strong associate of pancreatitis in SLE patients. Authors in this study further observed that SLE patients with psychosis and pleurisy were at increased risk for pancreatitis [4]. The index case had a normal lipid profile and no CNS or pleural involvement.

The combination of SLE and acute pancreatitis is a very serious complication, which could even be fatal, as reported by Cairoli et al. [5]. The spectrum of SLE is not solely restricted to acute pancreatitis as the association of SLE with chronic pancreatitis has been reported as well [6]. In addition to her acute pancreatitis, the index case also developed features of acute autoimmune hemolytic anemia during her hospital stay. Overt autoimmune hemolytic anemia has been noted up to 10% of SLE patients [7]. AIHA may manifest itself in SLE patients at the time of diagnosis, or within the first year following diagnosis. In this case, however, the index case presented with this complication 5 years after the diagnosis. AIHA is often associated with thrombocytopenia, lupus nephritis and CNS activity. To address the natural history and treatment response in AIHA among SLE patients, Gomrad et al. [8] studied 26 patients with severe isolated AIHA. The authors observed that AIHA is a serious complication of SLE, requiring urgent and appropriate management. In their study, patients responded to steroids in 96% of the cases and a recurrence rate of only 3 per 100 person-years was observed. Furthermore, in the same study, 7 patients (27%) experienced a relapse of AIHA and required immunosupressants. Based on their results, the authors recommended steroids as the first line of treatment, and advocated additional therapy with rituximab, danzol in refractory cases. Our index case responded well to the steroid treatment, with no relapse over the two years of follow-up.

Massive hemolysis due to any reason has been found to be another cause of acute pancreatitis. Drum et al. [9] retrospectively studied acute hemolysis due to different reasons in forty patients with drop of hematocrit greater than 12% over a period of 12 hours. Pancreatitis was observed to be a complication of massive hemolysis with a prevalence of above 20%. The authors were of the opinion that the back pain often found in acute hemolysis may originate from the pancreas rather than the kidneys. Experimental models have supported massive hemolysis as a cause of acute pancreatitis, and, in addition, histological changes following massive hemolysis have been observed in the pancreas in these experimental models [10].

Having said this, it is pertinent to mention here that the index case presented with acute pancreatitis and developed severe hemolysis during her stay in hospital, so there seems to be no temporal relation between the two (acute pancreatitis with hemolysis). However, it is possible that low grade hemolysis taking place a few days before the manifestation of the acute pancreatitis actually precipitated the attack, as she had no other established risk factor of acute pancreatitis. We cannot rule this out with any certainty. However, it is certain that due to massive hemolysis during her hospital stay, her pancreatitis could have worsened had she not been managed in time.

In conclusion, it may be said that the present case brings to the fore the multiple complications of SLE, a clinical scenario due to the generation of multiple autoantibodies directed towards the pancreas and the hemopoietic system. Acute vasculitis with its varied clinical presentation is often the commonest cause of abdominal pain in SLE, but acute pancreatitis and acute autoimmune hemolytic anemia, with its consequences, should be kept in mind in a given case of SLE. Further, this case emphasizes the need for close follow-up and proper health education in an SLE patient in order to circumvent any complication.

Competing interests

The author declares that he has no competing interests.

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Articles from GMS German Medical Science are provided here courtesy of German Medical Science

symptoms, treatment, causes, diagnosis, treatment, prevention and nutrition

Article content:

• Pancreatitis – what is it
• Types and forms of pancreatitis
• Pancreatitis in children
• Symptoms
• Causes of pancreatitis
• Diagnostics
• Treatment of pancreatitis
• Complications
• Prophylaxis
• Rehabilitation

What is pancreatitis?

Pancreatitis is a common disease of the digestive system associated with an acute inflammatory reaction of the pancreas. If not treated in a timely manner, pancreatitis can cause destruction of organ tissues and disruption of its vital functions. In addition, if there is a bacterial infection, inflammation can spread to nearby tissues and cause even more damage.

Severe pain in the left hypochondrium is the first sign of pancreatitis, but the chronic form can be hidden and without visible symptoms. The pancreas is an important organ of the digestive system responsible for secreting the enzymes needed to break down proteins, fats and carbohydrates in the intestines. It also plays an important role in the endocrine system, managing the storage and use of glucose in the body.

In the case of acute pancreatitis, digestive enzymes can become trapped inside the pancreas and begin to break down its tissues. Therefore, it is important to see a doctor in a timely manner if you experience pain in the left hypochondrium or other symptoms associated with digestion.

Check your pancreas health

Make an appointment with a gastroenterologist

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Types and forms of pancreatitis

Pancreatitis can have different forms, depending on the degree of development and the causes of the disease. Acute pancreatitis is a serious condition resulting from a destructive process in the tissues of the pancreas. The destruction of the tissues of the organ is the main source of acute pancreatitis, which requires immediate inpatient treatment in the surgical department.

Chronic pancreatitis is a diffuse inflammatory disease of the pancreas that progresses continuously and leads to irreversible structural changes in tissues and ducts. As a result, normally functioning tissue is replaced by denser and non-functioning connective tissue. This leads to dysfunction of the organ. Treatment of chronic pancreatitis can be outpatient or inpatient, depending on the severity of the disease and the patient’s condition.

There are different types of pancreatitis that differ in the nature of the course (alcoholic, biliary-dependent, infectious, medicinal, autoimmune, dysmetabolic, idiopathic pancreatitis). Each type of pancreatitis has its own characteristics, which affects the choice of treatment.

Pancreatitis in children

Pancreatitis in young children is usually caused by congenital malformations of the digestive system or enzyme deficiency. Also, pancreatitis can occur as a result of complications of mumps (mumps). In older children, pancreatitis may be associated with poor diet, overindulgence in sweets and carbonated drinks, or caused by intestinal parasites.

It is often difficult for a child to articulate complaints of pain. Therefore, when the first signs of the disease appear, such as complaints of abdominal pain, nausea, vomiting, unstable stools with impurities of undigested food, you should immediately consult a doctor. Infants with pancreatitis have hysterical crying, rapid weight loss, and bloating.

Prevention of pancreatic loss requires prompt diagnosis and treatment. It is important to know that children often do not express their feelings and pains clearly, so parents should be alert to changes in the behavior and condition of the child in order to quickly detect possible symptoms of pancreatitis and seek medical help.

Symptoms and signs of pancreatitis

Pancreatitis can present in different ways, depending on its form. Acute pancreatitis is characterized by the following symptoms:

• Intense pain that may be cutting or dull. Patients may feel pain in the left hypochondrium or in the upper abdomen.
• High body temperature, high or low blood pressure, pale or yellowish complexion.
• Nausea and vomiting that do not bring relief. Most often, patients experience dry mouth and a white coating on the tongue.
• Diarrhea, constipation or stools may be frothy, frequent, with a fetid odor.
• Bloating, stomach and intestines do not contract during an attack.
• Shortness of breath, which may be caused by loss of electrolytes through vomiting.

Chronic pancreatitis is characterized by the following features:

• Pain in the abdomen, which may be girdle or have a clear localization radiating to the back. Appears after eating.
• Intoxication of the body, which can be manifested by general weakness, loss of appetite, tachycardia, fever, lowering blood pressure.
• Endocrine disorders such as ketoacidosis, diabetes mellitus, tendency to hypoglycemia. Also, bright red spots may appear in the abdomen, back, chest, which do not disappear with pressure.
• With a long course of the disease, the patient gradually develops anemia, weight loss, dry skin, brittle hair and nails, vitamin deficiency and increased fatigue.

Seek medical attention at the first sign!

Causes of pancreatitis

• One of the main causes is prolonged and excessive alcohol consumption . Ethyl alcohol increases the saturation of pancreatic juices and can provoke a spasm of the sphincter, which regulates their flow into the duodenum. Currently, about 40% of patients suffering from pancreatitis associated with alcoholism, and about 70% of them periodically abuse alcohol.
• Gallstone disease can also be one of the causes of pancreatitis. A gallstone can cause blockage of the efferent ducts and become the result of inflammation of the glandular tissue. According to statistics, about 30% of patients suffering from pancreatitis have a history of gallstones.
• Lipid disorders associated with overeating and obesity can lead to increased production of enzymes and an increased risk of developing pancreatitis. According to statistics, about 20% of cases of pancreatitis are associated with overweight and lipid metabolism diseases.
• Viral infections such as hepatitis, tuberculosis, chicken pox, parotitis, measles, typhoid fever and others.
• Calcium metabolism problem , which can lead to sclerotization of gland tissues and spasm of ducts.
• Autoimmune diseases , some types of allergies, parasitic invasions, damage to the ducts during injuries and during operations, poisoning and intoxication of the body, endocrine diseases, pathologies of the structures of the digestive system, long-term use of certain drugs.
• Vascular pathologies such as arterial hypertension and atherosclerosis can lead to circulatory problems in the pancreas. Also, complications during pregnancy in women can develop pancreatitis.
• Hemolytic diseases – hemolytic-uremic syndrome, may also contribute to the development of pancreatitis. Hereditary pathologies, most often cystic fibrosis, associated with thickening of internal secretions, including pancreatic juices, can cause a violation of their outflow and cause the development of pancreatitis.

Thus, there are many factors that can trigger the development of pancreatitis. At the first symptoms, you should consult a doctor for diagnosis and appropriate treatment.

Diagnosis of pancreatitis

Laboratory methods

• Complete blood count, which reveals signs of inflammation – a high level of leukocytes and a low ESR.
• Biochemical blood test shows the level of pancreatic enzymes such as amylase, alkaline phosphatase and bilirubin pigment.
• Urinalysis allows to determine the residual content of amylase and diastase enzymes.
• Probeless diagnostic methods evaluate the activity of the digestive process by introducing substrates for pancreatic enzymes, followed by monitoring their absorption.
• Fecal parasite testing is done when needed.

Instrumental methods

• Ultrasound, which determines the shape and size of the organ, the presence of seals and fibrous areas.
• Gastroscopy assesses the degree of inflammation of the walls of the stomach and duodenum.
• X-rays and a variation, endoscopic retrograde cholangiopancreatography, help to detect accumulations of clots or stones in the ducts that cause blockage.
• Probe methods for determining the exocrine function of the gland, such as the secretin-pancreozymin test or the Lund test.
• CT or MRI can assess the extent of tissue necrosis in critically ill patients.
• Laparoscopy is used in difficult cases for visual assessment and tissue biopsy.

Thus, the diagnosis of pancreatitis is complex and includes a variety of methods to identify the disease at different stages of its development. Early diagnosis of pancreatitis allows timely treatment and reduces the risk of developing the disease.

Treatment of pancreatitis

Acute pancreatitis requires immediate intervention – hospitalization and bed rest. The main goals of treatment are to relieve pain, reduce the load on the pancreas and stimulate its self-healing.

There are several treatments for acute pancreatitis. Some of them include novocaine blockades and antispasmodics to relieve pain, hunger, ice on the gland projection area, pancreatic enzyme deactivators and antibiotic therapy to prevent infectious complications.

Surgery may be required for bile duct stones, fluid collections in or around the gland, areas of pancreatic necrosis, cysts, or abscesses. The operations performed in acute pancreatitis with the formation of cysts or abscesses include: endoscopic drainage, marsupialization of the cyst, cystogastrostomy, etc. When areas of necrosis are formed, depending on their size, necrectomy or resection of the pancreas is performed. The presence of stones is an indication for operations on the pancreatic duct.

Mild pancreatitis is usually easy to treat and improves within a week. However, severe pancreatitis can take much longer to heal. The postoperative period implies intensive measures for the prevention of purulent-septic complications and rehabilitation therapy.

Complications

Pancreatitis can lead to various complications that can be serious and dangerous to the health of the patient. The most common complications are:

1. bile outflow failure (cholestasis),
2. infectious diseases such as phlegmon and pancreatic abscess,
3. sepsis,
4. ruptured pseudocyst and pancreatic duct.

In addition, intra-abdominal bleeding, erosions and ulcers in the esophagus, stomach and duodenum, pancreatic adenocarcinoma, diabetes mellitus, disorders of carbohydrate metabolism and nutrient absorption are possible.

In addition, various cardiovascular, pulmonary, haematological and metabolic complications may occur. For example, pancreatitis can cause heart failure, arrhythmia, pulmonary embolism, anemia, thrombocytopenia, and thrombosis. In some cases, patients need to undergo resuscitation, including mechanical ventilation, blood replacement therapy, and fluid therapy to maintain vital body functions.

Prognosis and prevention of pancreatitis

Prevention of pancreatitis includes several key activities that help prevent its development. One of the key components of prevention is the rejection of alcohol, since this substance has a toxic effect on the tissues of the pancreas. In addition, it is necessary to follow a diet and avoid fatty, fried and spicy foods, as they can cause inflammation of the gland.

Another aspect of prevention is avoiding smoking and inappropriate use of medications, including hormones, diuretics, and corticosteroids. It is also recommended to treat diseases of the abdominal organs in a timely manner in order to prevent their complications and the associated risks for the pancreas. If you are experiencing symptoms associated with pancreatitis, you should seek immediate medical attention to prevent the disease from developing and its complications.

Diet No. 5 for pancreatitis

Table No. 5 for pancreatitis provides for limiting the intake of food that can cause increased secretion, and recommends split separate meals. The main foods that should be excluded from the diet include fatty, fried, smoked, salty, spices, chocolate, coffee, strong tea, meat, fish, mushroom broths, fresh fruits and vegetables with coarse fiber and alcoholic beverages.

In the first days after an exacerbation, it is recommended to adhere to a strict diet No. 5p, eat separately 8 times a day and not exceed the size of a single serving of 300 grams. The acceptable composition of food is products crushed into gruel, such as mashed potatoes, jelly, puddings, slimy porridges on water, croutons softened in tea. The food should include vegetables boiled in water or steamed (carrots, potatoes, zucchini, pumpkin), lean meat and fish, lean dairy products, chicken protein, vegetable broths, pasta, cereals, semi-sweet berries and fruits with an emphasis on protein foods low in fat and carbohydrates. Limiting salt intake should be no more than 10 grams per day, and instead of sugar, it is advisable to use a sweetener. The temperature of food should be warm, between 20 and 52 degrees, and hot or cold should not be consumed.

When remission is achieved, dietary requirements can be relaxed by reducing the number of meals to 5 times a day with increasing portions and allowing the use of whole foods, stews and baked dishes, milk porridges. You can also increase the amount of carbohydrates in your diet.

Rehabilitation

After undergoing treatment for pancreatitis, certain rules must be followed to restore the body. You should follow a diet that includes easily digestible foods. Gradually, the diet can be expanded, but it is still better to exclude fatty, fried and heavy dishes from the diet. Physical activity and thermal procedures should be limited, and medications should be taken only on the recommendation of a doctor. The duration of the recovery period may depend on the type of operation performed, as well as on the general condition of the patient.

Conclusion

Pancreatitis is a serious disease that develops due to improper digestion of food. It often occurs against the background of chronic diseases of the liver and gastrointestinal tract. Typical manifestations of pancreatitis are pain syndrome, health disorders, flatulence, jaundice. For an accurate diagnosis, diagnostic methods are used, such as ultrasound, computed tomography, magnetic resonance imaging, as well as laboratory methods, including hormone and cell tests. The therapeutic effect on the body includes the use of painkillers and anti-inflammatory drugs, as well as active hormones. At the initial stage, diet and fasting are often used. In the absence of positive dynamics, surgical removal of the affected tissues is prescribed. To get complete information, you need to contact a specialist – a gastroenterologist, therapist, surgeon, endocrinologist or oncologist. Remember that taking any medication on your own without a prescription from a specialist is dangerous to health. If you experience characteristic symptoms, be sure to consult a doctor and carry out the necessary diagnostic work.

You can sign up for a consultation with our doctors at the DNA Clinic medical center in Dubna, or ask any questions you are interested in by phone, in the feedback form or by mail. Be healthy!

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Author of the article:

Kucherenko Olga Alexandrovna
gastroenterologist

Pancreatitis: inflammation of the pancreas – symptoms, treatment, diet

Pancreatitis is an inflammation of the pancreas (the organ responsible for the production of digestive juices).

The pancreas in the human body performs a very important function: it produces enzymes that, getting into the small intestine, are activated and participate in the digestion of proteins, fats and carbohydrates. The body produces the hormone insulin, which regulates blood glucose levels.

Forms of pancreatitis

Acute – characterized by acute girdle pain in the upper abdomen. Often the pain appears after eating fatty foods or alcohol. Unpleasant sensations can be either barely noticeable or unbearable with irradiation to the shoulder blade or sternum. Nausea, vomiting, stool disturbance are observed. Due to the obstructed outflow of bile, the skin takes on a yellowish color.

Chronic – the main localization of pain is on the upper part of the abdominal wall with irradiation to the back, chest (left side), lower abdomen. Unpleasant sensations arise after taking heavy fatty foods, alcoholic beverages, constant stress.

The development of chronic pancreatitis is characterized by nausea, loss of appetite, bloating, impaired stool, and sometimes vomiting.

The chronic form of the pathology differs from the acute form by periods of remission and exacerbation. With the course of the disease, periods of exacerbation become more frequent, the development of intestinal disorders, disturbances in normal digestion, and weight loss are possible.

Chronic pancreatitis often gives complications (gastric bleeding, cancer, cysts and abscesses, liver damage, diabetes, enterocolitis). That is why the disease must be taken seriously and at the slightest suspicion of the development of inflammation, consult a doctor.

Causes of pancreatitis

The disease develops due to damage to the tissues of the pancreas. This happens for the following reasons:

• alcohol and tobacco abuse

• abdominal trauma, surgery

• uncontrolled and long-term medication: antibiotics, hormonal drugs, corticosteroids, some diuretics

• intoxication with food, chemicals

• genetic predisposition

• improper diet with a predominance of spicy and fatty foods and with long breaks between meals

Symptoms of pancreatitis

Manifestations of pathology differ depending on the form – acute or chronic pancreatitis. In acute pancreatitis, there are:

• The pain is intense, constant, the nature of pain sensations is described by patients as cutting, dull.

• High body temperature, high or low pressure – the patient’s health deteriorates rapidly due to the rapid development of the inflammatory process.

• Pale or yellowish complexion.

• Nausea and vomiting – dry mouth and white coating appear, bouts of vomiting do not bring relief. The most correct step at this moment is to starve, any meal can only worsen the situation.

• Diarrhea or constipation – the stool in acute pancreatitis is most often frothy, often with a fetid odor, with particles of undigested food. There are, and vice versa, constipation, bloating, hardening of the abdominal muscles, which may be the very first signal of an acute attack of pancreatitis.

• Bloating – the stomach and intestines do not contract during an attack.

• Shortness of breath – appears due to the loss of electrolytes during vomiting.

Chronic pancreatitis is characterized by the following symptoms:

• Abdominal pain – may be girdle or have a clear localization with irradiation to the back. Appears after eating.

• Intoxication of the body – there are general weakness, loss of appetite, tachycardia, fever, lowering blood pressure.

• Endocrine disorders – ketoacidosis, diabetes mellitus, a tendency to hypoglycemia. Also, bright red spots may appear in the abdomen, back, chest, which do not disappear with pressure.

With a long course of the disease, the patient gradually develops anemia, weight loss, dry skin, brittle hair and nails, symptoms of beriberi, increased fatigue.

First aid for an attack of pancreatitis

To reduce pain, you can use a heating pad filled with cold water. It must be applied to the abdomen, namely the epigastric region (the area under the xiphoid process, corresponding to the projection of the stomach on the anterior abdominal wall). This allows you to reduce the intensity of pain, slightly remove swelling and inflammation.

The patient must comply with the hospital regimen. This will reduce blood flow to the organ, which means it will reduce inflammation.

It is forbidden to eat. The process of digestion can cause more severe pain, nausea and vomiting. And the diet will reduce the production of enzymes that increase the inflammatory response and pain. You need to fast for 3 days. You can drink clean water without gases.

It is imperative to call a doctor for examination, even if the patient is not exactly sure that this is an attack of acute pancreatitis. As we already know, this pathology can subside, and then rapidly recur. At this time, you can drink an anesthetic drug to reduce discomfort.

Diagnostics of the disease at the private medical clinic “Medunion”

Diagnosing this disease is not difficult, as the first signs speak for themselves. However, in order to prescribe adequate treatment, it is necessary to determine the form of the disease. To do this, the doctor performs laparoscopy – a method that allows you to examine the abdominal cavity from the inside with a special tool.

If acute pancreatitis is suspected, laboratory tests are performed:

• General blood analysis

• Blood chemistry

• Analysis of urine

• Fecal analysis

• Ultrasound, MRI, or X-ray of the abdominal organs

• Computed tomography according to indications

In the chronic form, the same studies are carried out, but it is better to take tests during an exacerbation of the disease.

Treatment of acute pancreatitis

If acute pancreatitis is detected, the patient should be immediately hospitalized. Treatment should take place in a hospital, as this condition is very dangerous.

To relieve pain, antispasmodics are taken, in difficult cases, the contents of the stomach are pumped out to relieve the load on the gland.

With an exacerbation of pancreatitis, patients need to be hospitalized with daily monitoring of blood parameters, water balance, leukocyte count, and serum enzyme levels during the first week. In the first 1-3 days, fasting is recommended, taking alkaline solutions every 2 hours.

During an exacerbation of chronic pancreatitis, the patient is shown therapy similar to the acute process. The patient must follow a diet throughout his life and take drugs from the group of antispasmodics and drugs that normalize the secretory function of the organ.

The most important thing in the chronic form of the disease is to maintain a diet that involves the exclusion of fatty and fried foods from the diet. At the slightest violation of the regimen, the patient may experience discomfort and nausea. With intense pain, the doctor prescribes antispasmodics. Antisecretory therapy can be used for a short course.

Diet for pancreatitis

For any form of the disease, the patient is prescribed a strict diet “Table No. 5p”, according to which it is forbidden to eat spicy and fried foods. All dishes are steamed, boiled or baked. Alcohol and smoking are also prohibited.

It is also necessary to limit salt intake, eat small portions 6 times a day. Meals should always be served warm. It is necessary to exclude all products with a high content of extractives or essential oils (fish, meat broths, cocoa, coffee, etc.), fresh berries, vegetables, herbs, fruits, fruits, sour juices, carbonated drinks, marinades.

Where to get treatment for pancreatitis in Krasnoyarsk?

If you or your loved ones suffer from inflammation of the pancreas, seek help from the Mediunion Medical Center. We are engaged in the diagnosis and treatment of any diseases in Krasnoyarsk. Powerful equipment for CT, MRI and X-rays, experienced doctors who, if necessary, will conduct an initial examination at home, are waiting for you at Mediunion.