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Autoimmune disorders that cause hives: Understanding Autoimmune Hives and Its Treatment

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Advanced Allergy and Asthma: Allergists

Hives are hard to ignore. These patches of itchy, swollen skin can range in size from a tiny pinpoint to a large, uncomfortable rash the size of a dinner plate. 

When you have acute hives, they usually last for less than 24 hours. But they can also come in waves, coming and going over days or several weeks. However, it’s also possible to get chronic hives that last for six weeks or even longer.

Unfortunately, you can develop hives for several reasons, which can make their cause challenging to diagnose. Our team at Advanced Allergy & Asthma shared these insights into the most common medical causes behind hives.

Allergies

Most people associate hives with allergies. That’s because hives develop when cells in your body release chemicals and histamines into your bloodstream because of a perceived threat. 

Common allergens that trigger hives to appear can include:

  • Foods, especially citrus fruits, fish, peanuts, eggs, and milk
  • Food additives and preservatives
  • Pet dander
  • Pollen
  • Insect bites

If you have a food allergy, you can usually expect hives to appear within 30 minutes of eating your trigger.

Infections

Believe it or not, infection tops the list as the most common cause of hives, and viral infections alone are to blame for more than 80% in children.  In these cases, you often experience hives a week or two after your illness begins as your immune system tries to clear the infection from your body.

Common bacterial and viral infections known to cause hives include:

  • Colds and flu
  • Strep throat
  • Urinary tract infections
  • Infectious mononucleosis
  • Hepatitis

You can even develop hives from the bacteria in your body associated with tooth decay.

Autoimmune disease

In addition to infections, you can also develop hives because of autoimmune diseases. These diseases make your immune system attack tissue in your own body because it perceives them as a threat. 

The most common autoimmune conditions seen with hives include thyroid disease, rheumatoid arthritis, and Type 1 diabetes. You can also experience hives if you have lupus, vasculitis, and liver diseases.  

If you have an autoimmune condition, you usually have other symptoms in addition to hives.

Medications

Trying to manage your health or other symptoms with medications can also lead to hives, especially taking:

  • Antibiotics, like penicillin
  • Nonsteroidal anti-inflammatory drugs (NSAIDs), like ibuprofen, aspirin, or naproxen
  • Painkillers, like coding and morphine
  • Muscle relaxants used in anesthesia
  • Intravenous contrast dye used in digital imaging procedures

If you develop hives in response to a medication, you should contact your doctor as soon as possible.

Whether you have acute or chronic hives lasting longer than six weeks, our team can help determine their cause. To find relief for your hives breakout, contact one of our offices in Ogden, Utah, by calling or sending a message through our online contact form today.

Frontiers | Autoimmune Theories of Chronic Spontaneous Urticaria

Introduction

Urticaria, more commonly known as “hives”, is a prevalent disorder that affects between 15 and 25% of the population at some point during their lifetimes (1). The condition tends to be more common in adults than in children and in woman than in men with peak occurrence in the third to fifth decades of life. This condition is marked by the onset of pruritic “wheals,” which represent well-circumscribed areas of non-pitting edema with blanched centers and raised borders that involve only the superficial portions of the dermis and are seen in conjunction with surrounding erythema of the skin (2). Lesions can be as small as a few millimeters in diameter but can coalesce to form wheals as large as several centimeters wide. They often remit within 24 h since time of onset. Urticaria may be accompanied by the presence of angioedema, which is a similar process that occurs at submucosal surfaces of the upper respiratory and gastrointestinal tracts and deeper layers of the skin including subcutaneous tissue (3). Urticaria is classified as either acute or chronic depending on whether the onset of episodes lasts for less or >6 weeks in duration, respectively. In this review, we will focus specifically on the pathophysiology of chronic urticaria. Formerly referred to as chronic idiopathic urticaria, chronic spontaneous urticaria (CSU) refers to recurrent urticaria lasting more than 6 weeks that occur in the absence of an identifiable trigger. Urticaria that are incited by a well-defined eliciting factor (e.g., pressure, temperature, vibration) are referred to as inducible urticaria and will not be further discussed in this review. Prevalence of chronic urticaria is estimated to be anywhere from 0.5 to 5% in the general population but is not truly known, though incidence is thought to fall around 1.4% annually (4). Recent guidelines now include isolated idiopathic angioedema within the definition of CSU provided that other causes of angioedema, particularly those that are bradykinin mediated, have been excluded (5). Multiple studies have suggested that CSU may be an autoimmune condition in a substantial proportion of cases, but it is important to identify potential triggers of disease and exclude other differential conditions prior to making the diagnosis as outlined in Figure 1. In this article, we will discuss the pathophysiology of chronic urticaria and review the evidence surrounding its autoimmune etiology.

Figure 1. Diagnostic workup of chronic urticaria.

Mast Cells and Basophils as Centralized Regulators of Chronic Spontaneous Urticaria

The pathophysiology of CSU is not well-understood, but it is clear that derangement of both mast cell and basophil activation and degranulation remains central to the process. Of these, mast cells are most widely accepted as the primary effectors of chronic urticaria. While other cell types including lymphocytes and polymononuclear cells (PMNs) have been observed within the inflammatory infiltrates of patients with CSU, it is well-established that histamine and other mast cell products are predominantly responsible for development of this condition [note that skin biopsies are seldom needed for the diagnosis but are occasionally useful to distinguish CSU from other inflammatory conditions such as urticarial vasculitis (5)]. The physical manifestation of urticaria can be attributed to the enhanced vascular permeability that results from the release of preformed mediators from mast cells (e.g., histamine, tryptase, leukotrienes) and their delayed generation of cytokines. Ongoing research continues to probe into the mechanisms by which mast cells are activated by blood-borne antigens, with recent data from murine in vivo studies suggesting that CD301b+ dermal dendritic cells (DCs) are actually first to sample antigen and then relay it to nearby mast cells through secreted microvesicles (6). However, the vast majority of cases of chronic urticaria are not triggered by any identifiable substance and are in fact idiopathic. In these cases, anaphylaxis does not occur though angioedema may be present.

Two major mechanisms have been put forward with regards to the pathogenesis of chronic urticaria. The first is not autoimmune in nature, but involves dysregulation of intracellular signaling pathways within mast cells and basophils that lead to defects in trafficking or function of these cells. The second involves the development of autoantibodies to FcεRIα or IgE on both mast cells and basophils and will be discussed in more detail in the following sections (7). Both of these mechanisms will be further explored here and are outlined in Figure 2.

Figure 2. Model of the mechanisms underlying chronic urticaria. Pathologic activation of mast cells and basophils in patients with chronic spontaneous urticaria is thought to occur via two major mechanisms: intracellular signaling defects and autoimmune mechanisms. In the former, inappropriate activation of molecules such a spleen tyrosine kinase (SYK) or inhibition of negative regulators including the Src homology 2 (Sh3)-containing inositol phosphatases (SHIP) promotes spontaneous degranulation of mast cells/basophils with subsequent release of histamine and other protein and lipid mediators. The more commonly accepted theory of pathogenesis in CSU includes antibody-mediated mast cell and basophil activation, which can occur via IgG- or IgE- mediated pathways. In the former, IgG molecules directed against the Fc portion of IgE or the FcεR1 promote spontaneous cellular degranulation. In patients with autoallergy, crosslinking of Fc epsilon R1 (FcεR1) via autoreactive IgE molecules directed against self-antigens such as thyroid peroxidase (TPO) promote mast cell/basophil degranulation.

Dysregulation of Intracellular Signaling Pathways can Predispose to Pathologic Activation of Mast Cells and Basophils

Activation of the high-affinity IgE receptor, FcεR1, is an important step in the development of allergic responses and in the development of urticaria. This receptor is composed of an α-, β-, and two γ subunits (8). Whereas the α-subunit binds to the Cε3 constant region of the IgE molecule, the β-, and γ- subunits contain cell immunoreceptor tyrosine-based activation motifs (ITAMs) which, when phosphorylated, promote activation of spleen tyrosine kinase (SYK) and downstream recruitment of a host of secondary molecules including those involved in the phosphoinositide-3 kinase (PI3K) pathway. This series of events is responsible for degranulation of mast cells and can predispose to pathologic mast cell activation when inappropriately upregulated. SYK is recruited to the FcεR1 upon antigen stimulation, and inhibition of this protein has been shown to inhibit mast cell degranulation and production of both lipid mediators and cytokine activity (9). When mast cells from CSU patients with active urticarial disease at the time of blood sample collection were compared to those from healthy human donors, they were unsurprisingly found to release significantly more histamine in vitro than their healthy counterparts (10). Yet when these CSU patients were further subdivided into responders vs. non-responders based on their ability to degranulate in response to anti-IgE (with responders showing >10% degranulation activity), SYK levels were shown to be higher in the responder group than in the non-responder group, suggesting that this protein is a major determinant of predilection toward spontaneous degranulation. SYK expression is highly variable among the general population and is thought to correlate with the degree of IgE-mediated degranulation. Intriguingly, the presence of autoantibodies to FcεRIα or IgE do not predispose to upregulation of basophil SYK expression (11).

Negative regulation of mast cell activation occurs through phosphoinositide lipid phosphatases which function as well-described negative regulators of hematopoietic cell activation and proliferation. Src homology 2 (Sh3)-containing inositol phosphatases SHIP-1 and SHIP-2 associate with the FcεR1 β subunit and are activated upon stimulation with IgE or antigen (12). It is likely that dysregulation of these pathways that leads to an imbalance of positive signaling plays a pathogenic role in the development of CSU. One study demonstrated that when basophils from highly allergic IgE-positive donors (distinguished as having the ability to mount a response to human-recombinant histamine release factor, a complete stimulus for histamine release) were compared to those from healthy human donors, they contained lower levels of SHIP protein. As such, they demonstrated hyperresponsiveness (i.e., degranulation) in response to stimuli that did not appear to affect IgE-negative basophils (13). Similar results have been shown in mast cells from CSU patients highly sensitive to degranulation, with responders showing significantly lower levels of SHIP protein than both non-responders and healthy human donors (10).

The Autoimmune Theory of Mast Cell Activation in Chronic Spontaneous Urticaria

While cellular signaling defects may account for some cases of CSU, the autoimmune theory is the more widely accepted hypothesis to explain the inappropriate activation of mast cells and basophils in patients with chronic spontaneous urticaria. Up to 45% of cases of CSU are thought to be autoimmune in etiology. In a sentinel study conducted by Grattan et al., 12 patients with chronic urticaria were subjected to intradermal autologous serum injection (14). Seven of the 12 subjects (of whom six were female) mounted a positive wheal-and-flare reaction to this test, and fewer of these patients described a history of disease exacerbation with application of pressure when compared to patients with a negative injection test. This suggested that these patients with a positive result were less likely to have an inducible urticarial syndrome. Additionally, only one patient described a personal history of atopy, suggesting an alternative etiology for urticaria in the majority of cases. When the same serum was re-injected into the same subjects 1 year later, most of the patients with an initial positive test demonstrated a second positive result, though the same was not necessarily true when fresh serum was injected. In the small number of serum-positive patients who did not mount a second reaction at 1 year, the authors noted that their urticaria had cleared. On the contrary, the two patients who continued to mount a reaction with both original and fresh serum at the 1 year interval were noted to have continued disease activity. Ultimately, the authors concluded that many patients with chronic urticaria contain a “circulating mediator” in their serum which is capable of inducing urticaria. Over the past 30 years, the search has been ongoing to identify the mysterious culprit; multiple theories have since been put forth. However, it was these initial findings that opened the floodgates to the autoimmune theory of chronic spontaneous urticaria.

Though theoretically performed by Grattan et al. (14), the autoimmune etiology of CSU was further supported by formal development of the autologous serum skin test (ASST), an in vivo assay of mast cell activation that is induced by intradermal injection of a patient’s serum into self. It has now been accepted that nearly 50% of patients with CSU will have a positive test in response to factors present within their own serum within 30 min of injection. Additional groups have suggested that such “factors” are indeed autoantibodies or histamine-releasing factors that are capable of inducing mast cell degranulation. Unfortunately, these data have been somewhat difficult to interpret, as positive ASSTs are not unique to patients with CSU and have been noted in a substantial proportion of patients with allergic or non-allergic rhinitis, multiple drug allergy syndrome, and even in healthy control subjects (15). Furthermore, the positivity of the test has been shown to persist even when CSU patients are in clinical remission, particularly in subjects with autoimmune thyroiditis (16). Interestingly, it has been shown that levels of autoantibodies in CSU do not vary with disease activity which may, in part, explain this finding (17).

Some individuals have suggested that the autologous plasma skin test may be more sensitive than ASST for the diagnosis of CSU (18), though this result has not been reliably demonstrated (19). Since plasma and serum have similar levels of autoantibodies, additional mechanisms beyond autoantibody production have been put forth to explain the pathophysiology of the disease. One such theory states that factors that are uniquely present in plasma may be involved in the development of urticaria, and indeed it was shown that levels of the prothrombin fragment 1+2 (a marker of thrombin generation) were significantly higher in CSU patients than in control subjects (18). This suggests involvement of the clotting cascade in the development of the urticarial reaction. While the role of the coagulation cascade in the pathogenesis of urticaria is beyond the scope of this review, thrombin has been shown to directly increase mast cell degranulation, activate protease-activated receptors on mast cells, and enhance vascular permeability through actions on endothelial cells (20). It should also be noted that autoantibodies against the low affinity IgE receptor FcεRII (CD23) have been demonstrated in a large percentage of CSU patients (21). Anti-CD23 autoantibodies can activate eosinophils to release major basic protein, which in turn can trigger histamine release from mast cells, and basophils. Curiously, in CSU patients eosinophils are also a major cellular source of tissue factor, a protein which promotes activation of the extracellular coagulation cascade and generation of thrombin (22).

It has also been speculated that activated lymphocytes may play a role in the pathogenic activation of mast cells. Indeed it has been demonstrated that mast cells release inflammatory mediators including TNF-α upon direct contact with activated T cells (23). This TNF-α release is responsible for upregulation of several mast cell genes, among which includes matrix metalloproteinase 9 (MMP9) and tissue inhibitor of metalloproteinase 1 (TIMP1). Intriguingly, MMP9 and TIMP-1 have both been found at higher levels in the plasma of patients with chronic urticaria, and levels of MMP-9 may correlate with disease severity (24).

Chronic Spontaneous Urticaria Is Associated With Development of Autoantibodies to IgE and the High Affinity IgE Receptor

Circulating mediators with the potential to induce wheal-and-flare reactions in nearly half of all patients with CSU have been demonstrated in response to ASST. The identify of those factors became apparent in the early 1990s. One landmark study demonstrated that antibodies present in the serum of patients with chronic spontaneous urticaria (but not in patients with dermatographism or pressure urticaria) were able to elicit histamine release from healthy donor peripheral blood leukocytes with similar kinetics as anti-IgE antibodies (25). Intriguingly, the authors noted that preincubation of basophils with either anti-IgE or chronic urticarial serum abolished subsequent histamine release upon incubation with urticarial serum or anti-IgE, suggesting that both anti-IgE and chronic urticarial serum stimulate degranulation via a similar mechanism. Removing surface-bound IgE from leukocytes prior to incubation with urticarial serum or anti-IgE reduced histamine release. These important results suggested for the first time that histamine-releasing autoantibodies present in the serum of patients with chronic urticaria act by cross-linking cell surface IgE receptors.

In addition to the aforementioned findings, the authors astutely noted that histamine release could be elucidated when chronic urticarial serum was incubated with basophils from donors with very low serum IgE concentrations but not with anti-IgE (25). These data implied that non-IgE-dependent histamine releasing factors are present in the serum of patients with CSU. Shortly after the publication of this initial study, the same group determined the presence of IgG antibodies against the α subunit of the high-affinity FcεR1 in a group of patients with CSU (26). In this subset of patients, IgG anti-FcεR1α pathologically induced histamine release irrespective of the degree of IgE sensitization of the basophils. As proof of concept, histamine release was effectively neutralized in a concentration-dependent manner by preincubating donor basophils with soluble fragment of FcεR1α prior to the addition of purified IgG from sera of patients with CSU.

The concept that circulating IgG antibodies against IgE and the high-affinity IgE receptor FcεR1 likely contribute to the pathogenesis of CSU has since become widely accepted. Approximately 40% of patients with CSU have circulating antibodies to one of these targets (27) with a higher frequency of positivity in CSU patients who are ASST positive (28). Anti-FcεRI antibodies are thought to be the more common of the two. FcεRI is found on the surface of both dermal mast cells and basophils, and autoantibodies to this receptor can provoke chronic stimulation and degranulation of these cells in an IgE-independent fashion (2). On the contrary, IgG-anti IgE antibodies may bind to and crosslink receptor-bound IgE on the surface of mast cells and basophils, thus leading to activation and degranulation of these cells. As is the case with many autoimmune conditions, the presence of autoantibodies does not necessarily result in a disease phenotype. The presence of FcεR1α autoantibodies have been noted in the sera of patients with other autoimmune skin conditions and even in healthy subjects, though these have not been shown to display pronounced histamine-releasing activity in individuals without CSU (29). The authors attribute this difference to the fact that anti-FcεR1α antibodies tend to be of the complement-fixing IgG1 and IgG3 subtypes in patients with chronic urticaria but of IgG2 and IgG4 subtypes in patients with other inflammatory skin conditions. Other groups have shown that in vitro basophil activation and subsequent histamine-releasing activity fails to correlate with the presence of autoantibodies to FcεR1α even among patients with chronic urticarial (27).

The presence of autoantibodies to IgE and to FcεR1α infers the presence of antigen-specific lymphocytes in individuals with chronic urticarial disease. FcεR1α-specific T lymphocytes are detectable in a large percentage of patients with CSU and these cells more typically adopt a Th2 cytokine profile with the largest percentage being INF-γ secretors (30). Intriguingly, the relationship between INF-γ and autoantibody responses to FcεR1α has been found to be inversely related, similar to that which has been observed for T cell and autoantibody reactivity to glutamic acid decarboxylase antigen in individuals at risk for type 1 diabetes mellitus (31). It remains unclear how T cell reactivity vs. antibody reactivity to FcεR1α affects pathogenesis of CSU. However, it has been demonstrated that markers of T cell activation are directly proportional to markers of mast cell degranulation in chronic urticaria patients, particularly in patients known to have positive antibodies against FcεR1 (32). Further evidence for the involvement of T lymphocytes in the pathogenesis of CSU stems from observed variations in protein tyrosine phosphatase 22 (PTPN22) in patients with CSU (33). PTPN22 is a strong susceptibility gene for a variety of autoimmune disorders and encodes lymphoid specific tyrosine phosphatase (Lyp), which normally serves as an inhibitor of T cell activation.

An increased frequency of the HLA-DR4 allele has been found in patients with CSU (34). Intriguingly, the HLA-DR4 has been found at an increased frequency in a variety of other autoimmune disorders including rheumatoid arthritis, type 1 diabetes mellitus, and multiple sclerosis. Patients with autoimmunological subtypes of CSU have been noted to have a particularly high likelihood of carrying this HLA class II allele (35). However, these data have not been replicable across a wide spectrum of populations, with other studies noting increased frequencies of HLA-DR9 (30) and HLADR12 (30, 36) among patients with CSU. Heterogeneity in allelic association with this disease likely indicates that FcεR1α contains a number of different epitopes which act as targets of autoreactive T lymphocytes.

The Overlap Between Chronic Spontaneous Urticaria and Other Autoimmune Diseases

The concept of “overlapping autoimmune diseases” suggests that disorders which are autoimmune in nature occur at increased frequency in patients with known autoimmune disease. Numerous autoimmune conditions including systemic lupus erythematosus, polymyositis, dermatomyositis, and rheumatoid arthritis have been associated with chronic urticaria (2).

One large population study of over 12,000 subjects derived from a large health maintenance organization in Israel determined that female patients with CSU demonstrate a significantly higher incidence of rheumatoid arthritis, Sjögren syndrome, celiac disease, type I diabetes, and systemic lupus erythematosus than patients without CSU (37). While men also demonstrated higher odds of having these autoimmune conditions when compared with control subjects, these numbers did not reach statistical significance. When further investigation into serologic markers of autoimmune disease was performed, it was determined that patients with CSU as compared to control subjects had significantly higher levels of anti-thyroid peroxidase (anti-TPO) antibodies, antinuclear antibodies (ANA), antithyroglobulin (i.e., antimicrosomal) antibodies, rheumatoid factor, anti-transglutaminase IgA antibodies, and anti-parietal cell antibodies with anti-dsDNA, and anti-cardiolipin antibodies trending toward significance. Moreover, the mean platelet volume (MPV) was noted to be abnormally high in 29% of CSU patients and only in 1% of control subjects. Elevations in MPV occur when the body produces platelets at a more rapid rate and tend to correlate with levels of systemic inflammation.

As this study was the first of its kind to examine the relationship between CSU and other autoimmune diseases, it has shed some light on some intriguing commonalities between these two conditions. As is the case with most autoimmune conditions, CSU tends to affect women more commonly than it does men, and women with CSU tend to have much higher odds of developing other autoimmune conditions vs. men. This sex difference is also mirrored by the observation that both CSU and autoimmune diseases on the whole tend to occur more commonly in young adulthood as opposed to in older, post-menopausal adults. Additionally, the high prevalence of the aforementioned autoimmune conditions in CSU patients at much higher frequencies than occurs in the general population adds more strength to the theory that the underlying pathology of CSU is autoimmune in nature. When overlapping autoimmune conditions did occur, they were frequently diagnosed within the first 10 years after onset of CSU and quite commonly within the first 6 months. A recently conducted systematic review of autoimmune comorbidities in individuals with CSU also noted that organ-specific autoimmune disorders are more common than systemic autoimmune disorders in patients with urticaria, with endocrine, hematologic and skin disorders being among the most common (38). The reasons for this discrepancy remain largely unclear.

The common pathogenic mechanism between these conditions is the presence of autoantibodies on a background of chronic inflammation. However, autoimmune disorders are incredibly heterogenous in nature and thus it is difficult to extrapolate whether the link between chronic urticaria and the aforementioned conditions truly stems from a common pathologic tie or is merely reflective of detection bias. If a true connection does exist, one would imagine that CSU would be found at a higher frequency in patients with established autoimmune disease, but this link has been difficult to definitively make. For example, the prevalence of CSU in patients with SLE ranges from 0 to 22% depending on the individual study (39).

Autoallergy in Chronic Spontaneous Urticaria

With regards to the idea of overlapping autoimmune diseases, the well-established link between chronic urticaria and autoimmune thyroid disease deserves particular mention. Even among euthyroid subjects, many patients with CSU have detectable levels of antibodies against thyroglobulin or microsomal-derived antigen (40). Furthermore, an increased prevalence of clinical hypothyroidism (i. e., Hashimoto’s thyroiditis) as well as hyperthyroidism has been found among patients with CSU, with one study estimating a 23 times and seven times greater odds for hypothyroidism in female and male patients with chronic urticaria compared to control subjects, respectively (37). In 80% of these cases, the diagnosis of thyroid disease was made within 10 years, of the diagnosis of urticaria. The occurrence of IgG anti-thyroid antibodies in patients with CSU documented in studies where more than 100 patients were enrolled was noted to be anywhere from 3.7 to 37.1% with two-thirds reporting increased anti-thyroid antibody levels in >10% of patients (41).

Patients with CSU also demonstrate higher levels of IgE anti-thyroid peroxidase (anti-TPO) antibodies relative to healthy controls, though this distribution was found to be bimodal with 39% of CSU patients exhibiting IgE anti-TPO levels similar to control subjects (IgE anti-TPOlow) (42). It is theorized that autoallergic mast cell activation may contribute to the pathophysiology in CSU patients with detectable levels of IgE anti-TPO. IgE has a well-established role in the defense against helminthic infections and in recognition of exogenous allergens, but it was not until very recently that its potential role in autoimmunity has emerged. The term “autoallergy” refers to a type I, IgE-mediated hypersensitivity reaction against self-antigens which can, in turn, promote degranulation of basophils and mast cells. It was first put forth by Rorsman et al. as an explanation for urticaria-induced basopenia (43). Rorsman theorized that unlike in physical causes of urticaria, antigen-antibody interactions in non-physical causes of urticaria are likely to occur in both the skin and within the circulation (44). Autoallergic mast cell activation has been shown to occur in a variety of skin disorders including atopic dermatitis (45, 46) and bullous pemphigoid (47). In such disorders, IgE directed against skin antigens may bind to these cognate antigens and activate mast cells residing within the skin. On the contrary, TPO can be released from the thyroid into circulation, where it is free to bind to the surface of FcεR1-expressing cells. This extracutaneous nature of TPO may be one reason why the manifestations of CSU are not simply limited to the skin as they are in many other autoimmune skin disorders. Indeed it has been shown that anti-IgE TPO antibodies have the ability to induce basophil degranulation in vitro in the presence of TPO antigen and likely play a role in the pathogenesis of CSU (48). Recent findings have demonstrated that IgE anti-TPO antibodies are present at higher frequency and amounts in patients with CSU and have greater potential to induce TPO-mediated skin reactions in these subjects vs. in healthy controls (49). These results were validated by increased upregulation of basophil activation markers in CSU subjects upon exposure to TPO and ability of anti-TPO IgE to induce positive skin reactions upon passive transfer of this antibody from a patient with CSU to the skin of a healthy subject. In addition to IgE anti-TPO antibodies, IgE anti-dsDNA antibodies have also been noted at higher frequency in patients with CSU (50). However, no significant difference in IgE anti-dsDNA levels were observed between ASST-positive vs. ASST-negative patients, which suggests that these antibodies may be correlated with but are not likely to be involved in the pathogenesis of CSU.

IgE-mediated autoimmunity is becoming increasingly recognized as a possible contributor to the pathogenesis of a variety of systemic conditions including systemic lupus erythematosus and rheumatoid arthritis (51). A multicenter study in patients with SLE showed over half of all subjects had detectable levels of IgE against at least one common nuclear autoantigen (dsDNA, SS-A, SS-B, Sm) (52). This frequency increased during active disease and was strongly associated with the presence of active nephritis. There is still much to learn about the fields of autoallergy and IgE-mediated autoimmunity, which currently remain in their infancy, but it is likely that this will reveal a host of novel, targetable autoantigens. Over 200 IgE autoantigens were recently demonstrated in CSU subjects that were not present in healthy controls, among which included IL-24, which were detected in all patients with CSU (53). Further in vitro analyses demonstrated that IL-24 contributes to histamine release from human mast cells sensitized with IgE from CSU but not control subjects and that IgE-anti-IL-24 levels have reasonable predictive value for disease activity. The questions of why and how IgE autoantibodies develop and to what degree they contribute to CSU pathogenesis when compared to IgG autoantibodies has yet to be determined and is likely to be the focus of many future studies in this field.

Treatment of Chronic Spontaneous Urticaria

The primary treatment for chronic urticaria is to address the underlying pathology whenever possible and prevent mast cell activation. In any patient with chronic urticaria, elimination of potential triggers including drugs which can cause non-allergic hypersensitivity reactions (most commonly NSAIDs) should first be undertaken (5) Multiple guidelines have been put forth for management of CSU, though the EAACI/GA2LEN/EDF/WAO remain the most popular among practicing clinicians (5). If cases where no triggers can be identified, antihistamines (particularly the modern 2nd-generation antihistamines) are recommended as the mainstay pharmacologic treatment modalities for this condition. In patients who are poorly responsive to antihistamine therapy, it is recommended that the dosage be increased up to four times the normal limit prior to initiating a new agent. In cases of severe urticaria not adequately controlled with antihistamines alone, the EAACI/GA2LEN/EDF/WAO guidelines have recommended the addition of anti-IgE therapy, with cyclosporine being reserved for the most refractory cases of CSU. While short courses of prednisone do have a role in acute exacerbations of CSU, there is a strong recommendation against the use of long-term oral steroids given risk for adverse effects.

Evaluating the Use of Omalizumab for the Treatment of Chronic Spontaneous Urticaria

Omalizumab is an IgG monoclonal antibody against the Fc portion of the IgE antibody and prevents free IgE from binding to high-affinity FcεR1 receptors on mast cells and basophils. The first multicenter, placebo-controlled study evaluating omalizumab use in CSU examined efficacy of this therapy in subjects with IgE autoantibodies and found that 70% of omalizumab-treated patients who were otherwise refractory to standard antihistamine therapy were completely protected against wheal development (vs. 4.5% of placebo-treated subjects) (54). Another phase three study demonstrated that omalizumab given in three subcutaneous doses of either 150 or 300 mg over a 12 week period significantly reduced symptoms in antihistamine-refractory CSU patients without rebound of symptoms following discontinuation of the medication (55). Lack of relapse after discontinuation and very good safety profile have made omalizumab suitable for long-term therapy in patients with CSU, though cost still limits its use in many circumstances.

The mechanism by which omalizumab benefits patients with CSU has yet to be fully elucidated but the aforementioned results strongly argue for the contribution of IgE autoantibodies in the pathogenesis of CSU with rapid neutralization of these antibodies being an effective component of therapy. While the exact mechanisms by which omalizumab treatment benefits patients with CSU remain unclear, clearance of IgE autoantibodies is certainly likely to be of relevance. It has been well-established that omalizumab rapidly reduces levels of free IgE, which promotes downregulation of FcεR1 on basophils within the span of weeks and on mast cells within the span of months (56). The reason for this is because FcεR1 is effectively degraded when it is not stabilized by IgE binding (56, 57). Additionally, omalizumab has been shown to improve the genetic signature of lesional skin in patients with CSU to reflect non-lesional skin signatures by downregulating expression of genes involved in mast cell and leukocyte infiltration (FCER1G, C3AR1, CD93, S100A8), oxidative stress, vascularization (CYR61), and skin repair (KRT6A, KRT16) (56). Notably, non-responders to omalizumab do not demonstrate these genetic alterations. Basophils are also thought to be recruited to the urticarial lesions of patients with active CSU (58). Post hoc analysis of randomized clinical trial data have demonstrated that omalizumab increases peripheral blood basophil counts by likely reducing recruitment of these cells to the skin (59) and may also help to regulate defective basophil IgE receptor pathways (57). Clinical trials are currently underway to better characterize the effects of omalizumab on basophil responses.

Treatment with omalizumab has been shown to decrease levels of both FcεR1- and IgE- positive skin cells in skin of patients with CSU (60). In theory, omalizumab may reduce the autoimmune effects of self-antigen by mediating this decrease in pathogenic IgE levels and/or IgE receptors on the mast cell surface. Recently, a great deal of attention has been placed on the utility of IgE levels for predicting responses to omalizumab. Patients who have lower IgE levels prior to receiving omalizumab and lower IgE levels 4 weeks after undergoing treatment tend to respond less well to this therapy than those with higher baseline and post-treatment IgE levels (61), suggesting that these laboratory tests may help to guide management of CSU patients being considered for second- and third-line treatment options (61, 62). Interestingly, total IgE levels have been shown to positively correlate with basophil FcεR1 expression, the latter of which tends to be higher in those who respond quickly to omalizumab therapy (62). Despite our poor knowledge of the precise role of basophils in CSU pathophysiology, it is becoming clear that the time to effect for omalizumab in CSU appears to correlate with the expected time for reduction of FcεR1 on basophils (54) as opposed to on mast cells. Similar results were noted in prior studies examining use of omalizumab for cat allergy, which demonstrated that reduction of nasal symptoms correlated directly with a reduction in basophil responsiveness as opposed to mast cell responsiveness (63).

The question of how omalizumab benefits patients whose disease is mediated by a type I hypersensitivity reaction (autoallergy) vs. a type II hypersensitivity reaction (autoimmunity) is still largely unclear, however, it does appear that patients with autoallergy experience faster response times when treated with omalizumab. In one study, subjects refractory to standard antihistamine therapy with IgE anti-TPO antibodies were randomized to receive omalizumab in 2 or 4 week intervals for a span of 24 weeks. Patients with anti-IgE TPO antibodies experienced early responses to omalizumab, suggesting that rapid neutralization of IgE is the major mechanism by which omalizumab benefits this particular cohort (54). On the contrary, subjects who display a slow response to omalizumab are thought to have IgG antibodies against FcεRI since downregulation of this receptor occurs only after free IgE is first complexed by the drug (64). The authors validated this hypothesis by demonstrating a high correlation between length of time to the onset of omalizumab efficacy and positive basophil histamine release activity, with the latter predicting slower response times to treatment (64). Basophil activation, which is more specific for the detection of histamine-releasing autoantibodies in CSU patients than the ASST, may thus be a useful test in assessing patient responsiveness to omalizumab (64). As such, patients with refractory CSU may benefit from longer, more “personalized” courses of omalizumab (65). Further investigation on the mechanisms by which omalizumab benefits patients with CSU is certainly in need as are biomarkers to predict the efficacy of responsiveness and likelihood of relapse among patients with various subtypes of CSU.

Conclusion

Chronic spontaneous urticaria is a common and complex disorder that occurs in the absence of any identifiable provoking factor. While there are many aspects regarding CSU that have yet to be understood, it is becoming increasingly clear that both autoimmunity (IgG-mediated disease) and autoallergy (IgE-mediated disease) can contribute to the pathogenesis of this disorder and predispose subjects to the development of additional autoimmune diseases. Subjects with IgE autoantibody-mediated CSU appear to have a faster onset of improvement in response to omalizumab than those with IgG-mediated disease due to the unique mechanisms by which this drug sequentially affects IgE levels and FcεR1 status. Further investigation is required to determine how the presence of unique autoantibodies can predict the disease course and comorbidities associated with various subtypes of CSU as well as overall responsiveness to therapy.

Author Contributions

SB and ASM conceptualized the topic of the review article and wrote the review. SA and ASM supervised the writing of this review.

Funding

ASM is supported by the Duke Department of Dermatology and receives research funding through the National Institutes of Health (1R01AI139207-01 to ASM). ASM acts a consultant for Silab that is on a different topic than the content of this review article.

Conflict of Interest Statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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  • PLCG2-associated antibody deficiency and immune dysregulation: MedlinePlus Genetics

    PLCG2-associated antibody deficiency and immune dysregulation (PLAID) is an immune system disorder characterized by an allergic reaction to cold temperatures. Other immune system problems can also occur. The hallmark feature of PLAID is the development of a red, itchy rash (hives) when the skin is exposed to cool temperatures, which is known as cold urticaria. In PLAID, the hives typically develop in response to evaporative cooling, such as when a cool breeze or air conditioning blows on damp or sweaty skin. Being in a cold swimming pool can also trigger hives. In contrast, people with PLAID do not have a reaction when they touch a cold object, like an ice cube. (The ice cube test is a common test for a cold allergy; it triggers a reaction in people with other forms of cold urticaria, which usually begin later in life than PLAID.) However, some people with PLAID do experience a burning sensation in their throats when they eat cold foods, like ice cream. In PLAID, the hives go away once the skin warms up. Prolonged exposure to cold can lead to loss of consciousness or a serious allergic reaction known as anaphylaxis.

    Other skin problems can also occur in PLAID. A small number of affected individuals develop a blistering rash on the tip of their nose, ears, and fingers shortly after birth. The rash usually heals on its own in infancy, although in rare cases, it worsens over time. After the initial rash goes away, a different rash sometimes develops on the torso and limbs later in life. This rash, called a granuloma, can affect small patches of skin or be widespread. In people with PLAID, the granulomas do not occur in warm regions of the body, such as the armpits and other skin folds.

    In many people with PLAID, immune system function is reduced, leading to recurrent infections such as frequent colds, ear infections, or bouts of pneumonia. The infections are likely related to lower-than-normal levels of special proteins called antibodies or immunoglobulins, particularly immunoglobulin M (IgM) or immunoglobulin G (IgG). Antibodies attach to specific foreign particles and germs, marking them for destruction. The number of immune system cells called natural killer (NK) cells may also be reduced.

    Autoimmune disorders, which occur when the immune system malfunctions and attacks the body’s own tissues and organs, can also occur. Autoimmune disorders associated with PLAID include autoimmune thyroiditis and vitiligo. Autoimmune thyroiditis results from damage to the butterfly-shaped, hormone-producing gland in the lower neck (the thyroid). Vitiligo is caused by attacks on the pigment cells in the skin, resulting in a patchy loss of skin coloration. Most people with PLAID have abnormal antibodies called autoantibodies in their blood. One such antibody common in people with PLAID is known as antinuclear antibody (ANA). Autoantibodies attach to normal proteins and can trigger an immune attack against the body’s own tissues. However, not everyone with these abnormal antibodies has an autoimmune disease.

    Causes, Symptoms, What Is It & Treatment

    Overview

    What are autoimmune diseases?

    Your immune system is made up of organs and cells meant to protect your body from bacteria, parasites, viruses and cancer cells. An autoimmune disease is the result of the immune system accidentally attacking your body instead of protecting it. It’s unclear why your immune system does this.

    There are over 100 known autoimmune diseases. Common ones include lupus, rheumatoid arthritis, Crohn’s disease and ulcerative colitis.

    Autoimmune diseases can affect many types of tissues and nearly any organ in your body. They may cause a variety of symptoms including pain, tiredness (fatigue), rashes, nausea, headaches, dizziness and more. Specific symptoms depend on the exact disease.

    How do autoimmune diseases work?

    Experts don’t know why your immune system turns on you. It’s like it can no longer tell the difference between what’s healthy and what’s not — between what’s you and what’s an invader. There are some theories about why this happens, but experts aren’t completely sure.

    What’s a list of autoimmune diseases?

    Some common autoimmune diseases include:

    Diseases of the joints and muscles:

    Diseases of the digestive tract:

    Diseases of the endocrine system:

    Diseases of the skin:

    Diseases of the nervous system:

    Other diseases:

    How common are autoimmune diseases?

    Many autoimmune diseases are more common in women than in men. The diseases are common — 1 in 15 people in the U.S. have an autoimmune disease. One million people in the U.S. have lupus and 1.4 million have Crohn’s disease or ulcerative colitis.

    Are autoimmune diseases genetic?

    Yes. Some autoimmune diseases run in families.

    Are autoimmune diseases contagious?

    No.

    Are autoimmune diseases fatal?

    Autoimmune diseases are one of the top 10 causes of death in women in all age groups (up to age 64).

    How do autoimmune diseases affect you if you’re trying to get pregnant?

    Some autoimmune diseases can affect your ability to get pregnant and some have adverse effects on pregnancy. You may need fertility treatments to get pregnant. You might also want to wait until your disease is in the remission stage to try to conceive.

    There is a higher risk for stillbirth or preterm birth if you have lupus. If you have myasthenia gravis, you may experience trouble breathing.

    Symptoms and Causes

    What causes autoimmune diseases?

    The precise cause of autoimmune diseases is unknown. However, there are risk factors that may increase your chances of getting an autoimmune disease. Risk factors include:

    • Some medications. Talk to your healthcare provider about the side effects of medications for blood pressure, statins and antibiotics.
    • Having relatives with autoimmune diseases. Some diseases are genetic — they run in families.
    • Smoking.
    • Already having one autoimmune disease. You’re at a higher risk of developing another.
    • Exposure to toxins.
    • Being female — 78% of people who have an autoimmune disease are women.
    • Obesity.
    • Infections.

    What are the autoimmune disease symptoms?

    Symptoms categorized by type of disease include:

    Diseases of the joints and muscles:

    • Muscle aches and pains.
    • Joint pain, stiffness and swelling.
    • Muscle weakness.
    • Inflammation.

    Diseases of the digestive tract:

    • Bloating.
    • Constipation.
    • Abdominal pain.
    • Acid reflux.
    • Nausea.
    • Food sensitivities.
    • Blood or mucus in stool (poop).

    Diseases of the skin:

    • Rashes.
    • Itching.
    • Dry eyes.
    • Dry mouth.
    • Inflammation.
    • Hair loss.
    • Dry skin.

    Diseases of the nervous system:

    • Dizziness.
    • Headaches.
    • Anxiety and depression.
    • Confusion and difficulty thinking.
    • Blurry vision.
    • Insomnia.
    • Memory issues.
    • Migraines.
    • Lightheadedness.
    • Numbness and tingling.

    Other diseases:

    • Fatigue.
    • Pain.
    • Fever.
    • Chest pain.
    • Swollen glands.
    • Weight gain or loss.
    • Rapid or irregular heartbeat.
    • Shortness of breath.
    • Temperature sensitivity.

    How long do autoimmune diseases last?

    It varies. Some are easily treated and some are not. Some autoimmune diseases can last a lifetime.

    Diagnosis and Tests

    How are autoimmune diseases diagnosed?

    Diagnosing an autoimmune disease usually takes healthcare providers longer than it does to diagnose other diseases. This is because many autoimmune diseases have similar symptoms with each other and with other diseases. You can help your healthcare provider with the diagnosing process by bringing the following to your appointment:

    • A detailed list of any symptoms and how long you’ve had them.
    • A record of your family’s health history. Note if anyone in your family has an autoimmune disease.

    In addition to interviewing you about your symptoms, your healthcare provider may do some blood tests to check for autoimmune diseases, including:

    • Antinuclear antibody test (ANA).
    • Complete blood count (CBC).
    • Erythrocyte sedimentation rate (ESR).

    Specific symptoms combined with specific blood markers may prove that you have an autoimmune disease.

    Which healthcare providers diagnose autoimmune diseases?

    If your primary healthcare provider can’t diagnose you, you may have to see a specialist like a gastroenterologist or a rheumatologist.

    What questions might a healthcare provider ask to help diagnose an autoimmune disease?

    When your healthcare provider interviews you, they might ask you one or more of the following questions:

    • What medications are you taking?
    • What are your symptoms?
    • How severe are your symptoms?
    • Have you had to go to the emergency department because of your symptoms?
    • How long have you had these symptoms?
    • In what ways are your symptoms affecting your quality of life?
    • Is there anything that “triggers” your symptoms? Anything that makes them worse?
    • Is there a history of autoimmune diseases in your family?
    • Which autoimmune diseases run in your family?
    • What over-the-counter or alternative medicines have you tried, if any?

    Management and Treatment

    How are autoimmune diseases treated?

    There are no cures for autoimmune diseases, but symptoms can be managed. Everyone’s immune system, genetics and environment are different. That means that your treatment must be unique.

    Some examples of medications used to treat autoimmune diseases include:

    • Painkillers.
    • Antiinflammatories.
    • Medications for depression and anxiety.
    • Insulin injections.
    • Sleeping medications.
    • Plasma exchanges.
    • Corticosteroids.
    • Rash creams and pills.
    • Intravenous immune globulin.
    • Drugs that suppress (subdue) your immune system.

    Some people try complementary (alternative) medicines and procedures. Examples include:

    What kind of healthcare provider treats autoimmune diseases?

    The specialist you need depends on the type of autoimmune disease you have. Your healthcare provider may refer you to a:

    • Rheumatologist.
    • Gastroenterologist.
    • Endocrinologist.
    • Dermatologist.

    Does diet play a role in the treatment of autoimmune diseases?

    Some experts say that what you eat affects autoimmune diseases. Talk to your primary healthcare provider or dietitian about an ideal nutrition plan.

    Does exercise help with autoimmune diseases?

    Yes, but talk to your healthcare provider about what type and amount of exercise is right for you.

    Prevention

    Can autoimmune diseases be prevented?

    It may not be possible to prevent autoimmune diseases. But, some experts recommend that you try:

    • Exercising consistently.
    • Staying away from cigarettes.
    • Avoiding toxins.
    • Eating a healthy diet.
    • Limiting processed foods from your diet.

    Outlook / Prognosis

    What’s the outlook for people with autoimmune diseases?

    Your autoimmune disease symptoms may change with time. They may go into remission, where you have minimal or no symptoms, or they could flare up, making the disease worse. Although they can’t be cured, some of the symptoms can be treated. Many people with autoimmune diseases can live a normal life.

    Can autoimmune diseases go away on their own?

    There have been instances where an autoimmune disease disappears. However, most are chronic (meaning that they last a long time, if not a lifetime).

    Living With

    Can I live a normal life with an autoimmune disease?

    Yes, but it may be more difficult if your symptoms are severe. Your healthcare provider can help you figure out how to manage your symptoms so that you can participate in your daily activities.

    How do I take care of myself?

    Learn how to manage your symptoms, reduce your stress, exercise and eat a healthy diet.

    What questions should I ask my healthcare provider about autoimmune diseases?

    It’s helpful to have some questions ready to ask before you see your provider. Examples to consider include:

    • Do I have an autoimmune disease?
    • What tests should I go through?
    • What type of autoimmune disease do I have?
    • Do I need to see a specialist?
    • What specialist should I see?
    • What’s the best treatment for me?
    • Should I let my family members know that I have an autoimmune disease?

    When should I go to the emergency department?

    Go to the emergency department if any of the following autoimmune disease symptoms get severe:

    • Trouble breathing/shortness of breath. Remember that some people with an autoimmune disease can experience this when they’re pregnant.
    • Severe chest pain/pressure to your chest.
    • A headache that starts suddenly and feels like the “worst headache you’ve ever had.”
    • Sudden weakness, especially if you can’t move.
    • Dizziness that doesn’t stop.
    • Pain so severe that you can’t stand it.

    A note from Cleveland Clinic

    Living with an autoimmune disease can be complicated. Diseases like lupus, rheumatoid arthritis and multiple sclerosis are complex and serious. Although there are no cures for these diseases, many of their symptoms can be treated, and sometimes they go into remission. Stay in touch with your healthcare provider about any advances in understanding and treating autoimmune diseases.

    If you think you may have an autoimmune disease, see your healthcare provider as soon as possible for diagnosis and treatment. Your symptoms will be easier to control if the condition is treated promptly.

    Autoimmune Skin Conditions Causes & Treatment

    The skin is the largest organ in your body, and it can tell you a lot about your health. Many different autoimmune diseases can affect your skin, and these skin changes may be the first — or only — symptoms you see. Here, we’ll review why autoimmune disorders affect the skin, what those skin changes look like, and how you can treat them.

    Why do some autoimmune disorders affect the skin?

    You may be surprised to know that your skin is an important part of your immune system. It has many different cells that identify and target foreign invaders (like certain bacteria) and it’s constantly communicating with other cells in your body. 

    So, it’s not a surprise that your skin can be affected by autoimmune diseases, which happen when your immune system mistakenly attacks normal parts of your body. Some autoimmune conditions only affect the skin. Others can affect the skin and other parts of the body. And because your skin is so visible, it may be the first sign of an autoimmune disease.

    What does an autoimmune rash look like?

    Different autoimmune diseases can cause different skin changes. Some symptoms are general while others are pretty specific for a specific condition. Some common skin changes are:

    • Pink or red rashes

    • Scaly patches

    • Itchy skin

    • Open sores

    • Blisters in the skin (with clear or milky fluid)

    Seeing a dermatologist or healthcare provider with skin expertise may be needed to get the right diagnosis. This may require a skin biopsy, a procedure done in your provider’s office that removes a small piece of tissue. Below, we’ll discuss common skin changes seen in certain autoimmune diseases.

    Rashes on the face

    Two autoimmune diseases — lupus and dermatomyositis — have rashes that can affect the face in different ways. 

    Lupus

    Lupus is a chronic autoimmune disease that most commonly affects women age 15 to 44. There are different types of lupus. Some forms mainly affect the skin, like cutaneous lupus. Others can affect many parts of your body in addition to your skin, like your: 

    • Kidneys

    • Joints

    • Heart

    • Blood vessels (systemic lupus)

    If you have lupus involving your skin, your provider may do more tests, like blood work, to see if other organs are involved.

    The first sign of systemic lupus may show up on your face as a butterfly rash. This pink-red rash gets its name from its butterfly shape across your cheeks and the bridge of your nose. In some people, it can itch or hurt, and it’s often mistaken for sunburn.

    In cutaneous lupus, the rash can have different patterns:

    • Red, scaly, round patches mainly on skin that’s exposed to the sun (called subacute cutaneous lupus)

    • Thick, discolored, scaly patches on the face, scalp, or ears that can be associated with hair loss (called discoid lupus)

    Dermatomyositis

    Dermatomyositis is a rare autoimmune disease that causes muscle weakness, skin changes, and sometimes difficulty breathing or a cough. It usually affects children between the ages of 5 and 15 and adults between the ages of 40 and 60.

    The first sign of dermatomyositis can also affect the face: a reddish-purple rash on the eyelids (called a heliotrope rash). Other skin changes include:

    • Red or purple bumps on the outer joints of the hand, knees, or elbows

    • Red or discolored skin on the shoulders, neck, and upper back

    There is no cure for lupus or dermatomyositis, but different medications that lower the immune response can help manage symptoms.

    Blisters in the skin

    There are many autoimmune diseases that can cause blisters in the skin. Blisters can look different depending on what part of the skin is involved. Some are large, firm, and filled with clear fluid. Others are small and form yellow crusts. Below, we’ll review some of the more common autoimmune conditions with blisters. 

    Dermatitis herpetiformis

    Dermatitis herpetiformis is a chronic autoimmune skin condition that happens as a reaction to eating gluten, which is a protein found in many foods like wheat and rye. Dermatitis herpetiformis is related to Celiac disease, an autoimmune disease that damages part of the intestine when gluten is in the diet. Between 10% and 15% of people with Celiac disease will have skin symptoms.

    Dermatitis herpetiformis usually starts in people between the ages of 30 and 40 as extremely itchy blisters and red bumps on the: 

    Many people will also experience: 

    • Stomach pain

    • Cramping

    • Diarrhea

    • Constipation

    In some people, the symptoms will come and go, which can make diagnosing it harder.

    Treatment includes removing all gluten from the diet. Some medications can also help (read on to learn about treatments).

    Pemphigoid

    Pemphigoid is a group of rare autoimmune diseases that form blisters in the skin. The most common one is called bullous pemphigoid, which usually affects people over the age of 70. Bullous pemphigoid causes itchy, firm blisters on any part of the skin, including the mouth or the genitals. Some people will just have a few spots while others can have large parts of their bodies covered. Neurologic diseases — like dementia and Parkinson’s disease — are more common in people with bullous pemphigoid.

    There are different medications that can help treat pemphigoid (more on treatments below). For many people, the rash will go away on its own after a few years.

    Pemphigus

    Pemphigus is another group of rare autoimmune diseases that form blisters in the skin, but it’s very different from pemphigoid. Pemphigus vulgaris is the most common one, and it usually affects adults who are middle-aged or older.

    Most people will get small blisters that don’t itch and break easily. This causes ulcers that can join together and be quite painful. It’s common for the blisters to start in the mouth and then spread to any part of the skin. Some people will have fewer blisters. Others will have large areas of skin involved. People with pemphigus may also get skin infections where the blisters are. In some people, pemphigus vulgaris can become life-threatening if it’s not treated.

    There is no cure for pemphigus, but there are good treatments that can control symptoms (see treatments section, below).

    Hardened or firm skin

    Scleroderma is an autoimmune disease that causes your body to make too much collagen, a protein found in your skin and other tissues. Anyone can get scleroderma, but it usually affects people between the ages of 30 and 50. There are two main types:

    • Localized scleroderma (called morphea) affects the skin and underlying tissue.

    • Systemic scleroderma (called systemic sclerosis) can affect the skin and other organs, like your heart, lungs, kidneys, and blood vessels. This is the more serious type.

    In both forms, scleroderma causes patches of hardened, thick skin that feel firm to the touch. The patches are usually darker than normal skin. They can be round and oval, or they form lines that run down your arm or leg, or appear on your forehead.

    There is no cure for scleroderma, but treatments can help manage the different symptoms. Some people with localized scleroderma may not need treatment since the skin changes may go away on their own. 

    Sores in the mouth or genitals

    Mouth ulcers, like canker sores, are common and usually go away on their own. If mouth ulcers keep coming back, or if you also have them on the genitals, it could be a sign of a rare autoimmune disorder called Behçet disease.

    Behçet disease can happen at any age, but it usually affects people in their 20s and 30s. We don’t know the exact cause, but many symptoms are caused by inflammation of blood vessels. The condition can be different in each person, and it’s common for symptoms to come and go. Some other symptoms include:

    • Skin rashes (acne-like spots, or painful, firm bumps)

    • Eye problems (like blurred vision, pain, or light-sensitivity)

    • Pain in the joints

    • Diarrhea

    • Headaches

    There is no cure for Behçet disease, but symptoms can usually be controlled with different medications. In some people, the symptoms will go away for a period (called a remission), and treatment may not be needed for a while.

    It’s important to note that other autoimmune diseases can also cause sores in the mouth or genitals, including lupus and pemphigus. It’s a good idea to be checked out by your provider to determine what the underlying cause is. 

    Thick skin with scale

    Psoriasis is a common autoimmune disease that affects about 3% of adults in the U.S. It’s a chronic condition that causes patches of skin to grow too quickly. There are different types of psoriasis, and the most common one is called plaque psoriasis. This causes red patches with thick white scales to form, usually on the: 

    • Elbows

    • Knees

    • Lower back

    • Scalp

    Psoriasis doesn’t just affect the skin. People with psoriasis are can also have other conditions, like:

    • Psoriatic arthritis, which causes painful, swollen joints

    • Heart disease

    • Diabetes

    • Depression

    Psoriasis is usually a life-long condition, and treatment depends on how severe the symptoms are. This usually includes medicated creams and pills or shots that can help lower the immune system. 

    Dermatomyositis – Symptoms and causes

    Overview

    Dermatomyositis (dur-muh-toe-my-uh-SY-tis) is an uncommon inflammatory disease marked by muscle weakness and a distinctive skin rash.

    The condition can affect adults and children. In adults, dermatomyositis usually occurs in the late 40s to early 60s. In children, it most often appears between 5 and 15 years of age. Dermatomyositis affects more females than males.

    There’s no cure for dermatomyositis, but periods of symptom improvement can occur. Treatment can help clear the skin rash and help you regain muscle strength and function.

    Symptoms

    The signs and symptoms of dermatomyositis can appear suddenly or develop gradually over time. The most common signs and symptoms include:

    • Skin changes. A violet-colored or dusky red rash develops, most commonly on your face and eyelids and on your knuckles, elbows, knees, chest and back. The rash, which can be itchy and painful, is often the first sign of dermatomyositis.
    • Muscle weakness. Progressive muscle weakness involves the muscles closest to the trunk, such as those in your hips, thighs, shoulders, upper arms and neck. The weakness affects both the left and right sides of your body, and tends to gradually worsen.

    When to see a doctor

    Seek medical attention if you develop muscle weakness or an unexplained rash.

    Causes

    The cause of dermatomyositis is unknown, but the disease has much in common with autoimmune disorders, in which your immune system mistakenly attacks your body tissues.

    Genetic and environmental factors also might play a role. Environmental factors could include viral infections, sun exposure, certain medications and smoking.

    Complications

    Possible complications of dermatomyositis include:

    • Difficulty swallowing. If the muscles in your esophagus are affected, you can have problems swallowing, which can cause weight loss and malnutrition.
    • Aspiration pneumonia. Difficulty swallowing can also cause you to breathe food or liquids, including saliva, into your lungs.
    • Breathing problems. If the condition affects your chest muscles, you might have breathing problems, such as shortness of breath.
    • Calcium deposits. These can occur in your muscles, skin and connective tissues as the disease progresses. These deposits are more common in children with dermatomyositis and develop earlier in the course of the disease.

    Associated conditions

    Dermatomyositis might cause other conditions or put you at higher risk of developing them, including:

    • Raynaud’s phenomenon. This condition causes your fingers, toes, cheeks, nose and ears to turn pale when exposed to cold temperatures.
    • Other connective tissue diseases. Other conditions — such as lupus, rheumatoid arthritis, scleroderma and Sjogren’s syndrome — can occur with dermatomyositis.
    • Cardiovascular disease. Dermatomyositis can cause heart muscle inflammation. In a small number of people who have dermatomyositis, congestive heart failure and heart rhythm problems develop.
    • Lung disease. Interstitial lung disease can occur with dermatomyositis. Interstitial lung disease refers to a group of disorders that cause scarring of lung tissue, making the lungs stiff and inelastic. Signs include a dry cough and shortness of breath.
    • Cancer. Dermatomyositis in adults has been linked to an increased likelihood of developing cancer, particularly ovarian cancer in women. Risk of cancer appears to level off three years or so after a diagnosis of dermatomyositis.


    July 01, 2020

    Show references

    1. Dermatomyositis. Myositis Association of America. https://www.myositis.org/about-myositis/types-of-myositis/dermatomyositis/. Accessed March 20, 2020.
    2. Dermatomyositis information page. National Institute of Neurological Disorders and Stroke. https://www.ninds.nih.gov/Disorders/All-Disorders/Dermatomyositis-Information-Page. Accessed March 20, 2020.
    3. Miller ML, et al. Clinical manifestations of dermatomyositis and polymyositis in adults. https://www.uptodate.com/contents/search. Accessed March 20, 2020.
    4. AskMayoExpert. Dermatomyositis. Mayo Clinic; 2019.
    5. DeWane ME, et al. Dermatomyositis: Clinical features and pathogenesis. Journal of the American Academy of Dermatology. 2020; doi:10.1016/j.jaad.2019.05.105.
    6. Dermatomyositis. Genetics and Rare Diseases Information Center. https://rarediseases.info.nih.gov/diseases/6263/dermatomyositis. Accessed March 20, 2020.
    7. Waldman R, et al. Dermatomyositis: Diagnosis and treatment. Journal of the American Academy of Dermatology. 2020; doi:10.1016/j.jaad.2019.06.1309.

    Chronic urticaria and autoimmune diseases

    Chronic urticaria (HC) – urticaria that occurs every day for more than 6 weeks. Chronic idiopathic urticaria, which has no apparent external cause, includes most cases of HC. It is believed that in more than half of all cases of chronic idiopathic urticaria, an autoimmune mechanism takes place due to antibodies to high affinity receptors (FcεRI) of immunoglobulin E. It is assumed that HC occurs due to the propensity of the patient’s immune system to develop reactions against its own body.A strong association has been found to support this hypothesis between HC and autoimmune diseases such as thyroid disease (autoimmune thyropathies), rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), Sjogren’s syndrome, celiac disease, and type 1 diabetes. Based on this, we consider the relationship between CC, autoimmune thyropathies and other autoimmune disorders, as well as the consequences of this situation, which may be important for therapeutic intervention in CC.

    Introduction.

    According to a rough estimate, during life, urticaria occurs in 25% of the population. HC – urticaria that occurs daily for more than 6 weeks. HC usually lasts 1 to 5 years, but can last more than 5 years in about 14% of patients. \ Individuals with HC noted emotional distress, a feeling of isolation and fatigue from this disease, similar findings are observed in patients with coronary heart disease. This emphasizes the importance of treating HC while minimizing both the physical and mental impact of the disease.HC can arise from drugs, physical stimuli, be part of an inflammatory or congenital disease, or it can be idiopathic. Acetylsalicylic acid (ASA) or non-steroidal anti-inflammatory drugs (NSAIDs) exacerbate CC, presumably by inhibiting the cyclooxygenase pathway by increasing the production of leukotrienes. Physical urticaria (classically divided into heat, cold, solar, vibrational, delayed pressure response, dermatographic, aquagenic, and cholinergic) occurs in response to external stimuli.Urticarial vasculitis is the appearance of urticarial eruptions lasting more than 24 hours with histopathological changes in the vessels. Congenital syndromes with CC include a spectrum of cryopyrinopathies such as familial cold autoinflammatory syndrome, Macle-Wales syndrome, and multisystem neonatal inflammatory disease / chronic neurological infantile articular cutaneous syndrome (NOMID / CINCA). Hives can be a symptom of many inflammatory diseases such as Schnitzler’s syndrome, Still’s disease, and Gleich’s syndrome.Chronic idiopathic urticaria, unlike physical urticaria and intolerance to ASA or NSAIDs, has no apparent external cause. Chronic idiopathic urticaria is the most common type of CC, including up to 90% of all cases of CC. Chronic idiopathic urticaria is believed to affect 0.6 to 5% of the population. More than half of chronic idiopathic urticaria cases are thought to have an autoimmune mechanism. This is supported by the observation that 60% of patients with chronic idiopathic urticaria develop blisters or an exacerbation reaction with intradermal administration of autologous serum when skin testing with autologous serum is performed.About 50% of patients with chronic idiopathic urticaria have specific IgG, high affinity IgE receptors (FcεRI). These autoantibodies activate skin mast cells, circulating basophils, and the complement system. Additional immunological abnormalities have been described that play a causal role in CC and include IgG directed against IgE and low affinity IgE receptors (FcεRII), antiendothelial antibodies, and C8 alpha-gamma deficiency in the complement system. Approximately 35% of patients with chronic idiopathic urticaria have episodes of angioedema, and 25% have positive dermatographism.Like many autoimmune diseases, chronic idiopathic urticaria is more common among women than among men, with a gender frequency of 2: 1 to 4: 1 reported by the authors. The many autoimmune conditions associated with chronic idiopathic urticaria include autoimmune thyropathy, celiac disease, and RA. The purpose of this review is to discuss the relationship of CC with autoimmune thyropathy and other autoimmune diseases, as well as the implications of this situation that may be important for therapeutic intervention in CC.

    Autoimmune thyropathy and HC.

    Autoimmune thyropathy is the most commonly reported autoimmune condition in patients with CC. In the literature, the incidence of autoimmune thyroid lesions in patients with CC varies from 6.5% to 57%. Patients with coexisting autoimmune disorders and CC have a longer duration of urticaria than those who do not. Patients with both CC and autoimmune pathology have an increased risk of developing angioedema. Leznoff and Sussmann reported that the triad of autoimmune thyropathy, HC, and angioedema occurs in 15% of those with HC.The risk of developing angioedema in patients with autoimmune thyropathy and CC is estimated 16.2 times higher than in CC without thyropathy. In the latest large study on 12778 patients with HC, Cofino-Cohen et al. it was found that 9.8% of patients had hypothyroidism, compared with 0.6% in the control group. Hypothyroidism was the most frequently diagnosed autoimmune thyropathy in patients with CC. Women were more likely to have a combination of hypothyroidism and HC than men. Patients with hyperthyroidism and HC accounted for 2.7% of the study population, compared with 0.09% in the control group.In the majority of patients, autoimmune thyropathy was detected in the next 10 years after the diagnosis of CC. This means that autoimmune thyropathy developed after the first manifestation of CC. In the same study, antithyroid antibodies were significantly more frequent in patients with CC than in controls. Among patients with CC, who clinically had no signs of thyroid lesion, antibodies to thyroid peroxidase were detected on average in 2.7%, antibodies to thyroglobulin – in 0.6%. Aamir et al.also noted the relationship between antithyroid antibodies and HC, since the level of antibodies to thyroglobulin and microsomes was significantly increased among patients with CC and hypothyroidism. The development of autoimmune thyropathy is often considered a marker of autoimmunity. Autoimmune thyropathy is associated with a variety of autoimmune diseases, including, in addition to CC, pernicious anemia, celiac disease, type 1 diabetes and SLE. the patient to the development of autoimmune reactions.It has been hypothesized that autoimmune thyropathy can worsen the course of urticaria and angioedema by activating the complement system. Blanchin et al. demonstrated that thyroid peroxidase contains a domain that binds to the C4 complement protein, activates it to C4a, and activates complement in a classical way. Kirpatrick noted that C4a levels are reduced with treated autoimmune thyropathy, resulting in CC remission. Based on this, a theory has been put forward that autoimmune thyropathy and CC can coexist due to the patient’s tendency to autoimmune reactions, that autoimmune thyropathy can further exacerbate the course of urticaria and angioedema through direct mechanisms of complement activation.

    Other autoimmune diseases and chronic urticaria.

    In addition to autoimmune thyropathy, many autoimmune diseases have been studied in relation to HC. Confino-Cohen et al. showed that 12.5% ​​of patients have another autoimmune disease, 2.1% – 2 diseases, 0.1% – 3 diseases, and single patients – 4 or 5 diseases. Among patients with HC and hypothyroidism, RA was the most common. The incidence of RA was 13.25 times higher among patients with CC than in the control group.Ryhal et al. showed that the main laboratory marker of RA, rheumatoid factor, was significantly increased in patients with CC. Patients with CC of both sexes are at increased risk of developing type 1 diabetes. Among women with HC, the development of Sjogren’s syndrome, celiac disease, or SLE was significantly higher than in controls. The majority of patients were diagnosed with an additional autoimmune disease within 10 years after the diagnosis of CC, which emphasizes that the diseases progressed sequentially and were not accidentally identified during the diagnosis of CC.The relationship between celiac disease and HC has been previously discussed in the pediatric population. Asero et al. HC and Raynaud’s phenomenon with positive anti-centromeric antibodies have been described. Other autoimmune diseases like vitiligo and pernicious anemia have also been associated with HC. HC has been shown to have a genetic link to the human leukocyte antigen, the HLA-DR4 and HLA-DQ8 alleles. HLA-DR4 is significantly associated with RA, HLA-DQ8 with celiac disease and type 1 diabetes. Complement deficiency is associated with autoimmune diseases such as Sjogren’s syndrome, RA, SLE, as evidenced by Park et al.about the development of CC, spondyloarthropathy and the presence of antinuclear antibodies in a 9-year-old boy with C8α-γ deficiency. HC has been described in a 10-year-old boy with a strong autoimmune phenotype. The complete list of diseases included alopecia totalis, vitiligo, psoriasis, Graves’ disease, HC, the autoimmune form of Lambert-Eaton myasthenic syndrome, and IgA deficiency. This patient had HLA genes that were found in the extended haplotype 8.1 (ancestral haplotype), which is associated with the development of many autoimmune conditions.These cases clearly show that HC can occur as a manifestation of a combination of autoimmune diseases.

    Treatment.

    The guidelines for the management of HC were based on the GRADE approach. The second generation of non-sedating type 1 histamine receptor blockers is the first line of treatment for patients with CC. If the effect is not achieved in 2 weeks, the 2nd line of therapy is used, which consists in a 4-fold increase in the dose of antihistamines from the standard dose.Patients should be advised that sedation symptoms and drug interactions may occur with increasing dosage. Cetirizine, desloratodine, fexofenadine and bilastine have been identified as the safest antihistamines when the dosage is increased. In 50% of the observed patients, symptoms persist with antihistamine monotherapy. The 3rd line of therapy includes the replacement of antihistamines or their joint use with leukotriene receptor antagonists.Leukotriene receptor antagonists are indicated for the improvement of the condition of patients with ASA or NSAID intolerance in CC, with a positive skin test with autologous serum, or with CC in case of hypersensitivity to food components, but not in chronic idiopathic urticaria. In conjunction with the 3rd line of therapy, a short 3-7 day course of systemic steroids can be used. If the 3rd line of therapy is unsuccessful, they switch to the 4th line of therapy, which includes the use of cyclosporin A, type 2 histamine receptor blockers, dapsone or omalizumab. treatment of severe forms of asthma.Mauer et al. published a randomized, double-blind study evaluating the efficacy of omalizumab in CC patients who were unresponsive to 1st line therapy and showed a significant reduction in CC symptoms. Omalizumab decreased free IgE and high affinity IgE levels for receptors on mast cells and basophils (cells thought to be responsible for blistering in CC). The literature reports an adjunctive treatment for patients not eligible for 4th line therapy, which includes mycophenolate mofetil, methotrexate, tacrolimus, sulfasalazine, and intravenous immunoglobulin.Treatment of concomitant autoimmune thyropathy has been reported to induce CC remission. Kirkpatrick conducted a study in HC patients with obvious clinical or serologic autoimmune thyropathy. In addition, 1st line antihistamine therapy was ineffective among these patients. It was demonstrated that levothyroxine induced remission of angioedema and urticaria in all 6 patients with autoimmune thyropathy and CC. Rumbryt reported clinical remission of CC in 7 out of 10 euthyroid patients with antithyroid antibodies by administration of thyroxine, but if CC recurred, therapy was canceled.These studies suggest that levothyroxine treatment may play a role in CC remission in patients with CC and clinically diagnosed autoimmune thyropathy. However, Magen et al. recently compared patients with CC and autoimmune thyropathy treated with levothyroxine and patients with CC and euthyroid status (controls). Patients treated with levothyroxine showed clinical improvement in urticaria, but no such improvement was observed in the control group. This led to the conclusion that the improvement of clinical symptoms in CC was spontaneous, regardless of treatment.Controversial data in the literature regarding the importance of treating autoimmune thyropathy in CC indicates the need for additional extensive studies to establish the role of levothyroxine in patients with CC. The use of NSAIDs demonstrated a deterioration in the course of CC on average in 20% of patients with a primary diagnosis of CC. NSAIDs are widely used to treat pain and inflammation associated with RA, inflammatory spondylopathies, and lupus arthritis. It has been shown that autoimmune inflammatory arthropathies, especially RA, are more common in patients with CC than in the general population.Therefore, exacerbation of CC symptoms due to the use of NSAIDs should be closely monitored in patients with CC and autoimmune arthropathies. Zembowitcz et al. demonstrated that selective COX-2 inhibitors do not cause urticaria in patients with CC, as is the case with NSAIDs. According to this, it is assumed that selective COX-2 inhibitors are preferable to NSAIDs from the point of view of preventing exacerbation of CC. Earlier it was assumed that Helicobacter pylori (H. pylori) may be the etiological factor of CC.This was confirmed by reports demonstrating a high incidence of H. pylori among patients with CC, and an improvement in clinical symptoms following eradication. But this assumption raised doubts, since a number of authors did not find differences in antibody production in patients with H. pylori and CC and in the control group. Additional evidence has also been demonstrated that eradication did not affect clinical recovery in CC. This divergence of opinion in the literature is due to differences in detection methods, resistance to therapy, and the possible return of H.pylori shortly after treatment. Even more confusing is the recent evidence that eradication may be a trigger for HC. Shakouri et al. performed a literature review of H. pylori and CC eradication using the GRADE system, and concluded that the evidence for treatment was weak and more research is needed to establish whether H. pylori eradication is beneficial for patients with CC.

    Conclusion.

    HC – urticaria with a daily rash lasting more than 6 weeks.It is currently believed that up to 50% of CC cases are caused by autoimmune mechanisms. The most commonly identified antibodies with high affinity for IgE receptors activate mast cells, basophils and the complement system, leading to blistering and increased rash. It is assumed that HC occurs when the patient is predisposed to autoimmune diseases. In accordance with this hypothesis, other autoimmune diseases are observed in patients with CC. Autoimmune thyropathy, hyperthyroidism in particular, is the most common concomitant autoimmune disease.Moreover, autoimmune thyropathy can directly exacerbate the severity of CC by activating the complement system. Other autoimmune diseases that most often occur in patients with CC are RA, SLE, vitiligo, pernicious anemia, celiac disease, Sjogren’s syndrome. In practice, HC may be part of a larger autoimmune phenotype. These connections are supported by the theory that patients who develop CC have an intrinsic predisposition to the development of autoimmune reactions. According to the literature, the treatment of autoimmune thyropathy has different effects on CC: induction of remission and no effect on the clinical course of CC.The treatment of autoimmune diseases, especially autoimmune thyropathy, in patients with CC is of great importance, but further research is needed to justify this treatment in CC.

    “Shock in half of the patients.” Doctor about an unusual reaction to winter frosts

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    “Shock in half of the patients.” Doctor about an unusual reaction to winter frosts

    “Shock in half of the patients.” A doctor about an unusual reaction to winter frosts – RIA Novosti, 20.09.2021

    “Shock in half of the patients.” Doctor about an unusual reaction to winter frosts

    In some people, severe frosts cause a real allergic reaction – nasal congestion and itchy blisters on the skin. Why this is happening is still not clear RIA Novosti, 09/20/2021

    2021-01-21T08: 00

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    Sechenov First Moscow State Medical University

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    MOSCOW, 21 Jan – RIA Novosti, Alfiya Enikeeva. In some people, extreme cold causes a real allergic reaction – nasal congestion and itchy blisters on the skin. Why this happens is still not clear, but it is treated like a rash that appears after contact with pollen or animal dandruff. RIA Novosti understands who has more chances of winter allergies and where they suffer from this ailment more often.Shock Shower At the end of last year, a 34-year-old American fainted as he came out of the shower, his heart rate increased, and his body was covered in a rash. Relatives called an ambulance. Doctors diagnosed anaphylactic shock and brought the patient to consciousness with epinephrine and the antihistamine diphenhydramine. Only now the patient did not suffer from allergies in the usual sense of the word. A severe systemic reaction was the body’s response to a sharp temperature drop. According to experts, the patient washed himself with very hot water, and then returned to a rather cool room.This provoked anaphylactic shock. Moreover, the standard test for winter allergies, carried out in the hospital, turned out to be positive: an ice cube was applied to the skin, and a red spot formed in this place – this is one of the rare cases of so-called cold urticaria. Those suffering from this disease, upon contact with low temperatures – frosty air, a glass of ice water or even ice cream – develop itchy blisters on their skin. Edema of internal organs and anaphylactic shock are possible.The disease occurs at the age of 30-40, and more often in women than in men. In countries with a cold climate, such as Russia, there are slightly more such patients. Incomprehensible reaction of the body “Increased sensitivity to cold occurs in less than 0.1 percent of the population. The mechanism of cold urticaria is not fully understood and differs from the classic reaction to allergens There are several hypotheses, the most common is that contact with cold changes the proteins in the skin.And it is on them that an allergic reaction is formed. According to the other, there is an autoimmune activation of mast cells, which begin to release histamine and other substances involved in inflammation. Histamine, in turn, acts on blood vessels, nerve endings, and itchy blisters form on the skin. More serious consequences are also possible – a drop in blood pressure, which we already interpret as anaphylactic shock, “Professor of the Department of Skin and Venereal Diseases named after V.A. Rakhmanova, Sechenov University, MD, allergist-immunologist Elena Borzova. According to the professor, anaphylactic shock occurs, according to some reports, in 52 percent of patients with cold urticaria. It occurs on contact with low temperatures of large areas of the body. Even swimming in a river or lake with cold water provokes a severe reaction. “This is a very alarming statistic. Cold urticaria must be diagnosed in time and measures must be taken to prevent it. After all, it does not always develop at absolutely low temperatures, this is a myth.Studies have shown that in some patients, itchy blisters on the skin appear at zero, plus four, and even plus 20 degrees Celsius. That is, the temperature threshold is an individual parameter. Often, patients note that the rash appeared after being in the cold, in a warm room. I must say that cold urticaria goes away quickly enough – usually within an hour. But there are also unusual cases, including potentially life-threatening ones. Therefore, if there are rashes after contact with a cold one, no doubt, you need to consult a specialist so that he can diagnose, assess the possible risks and select a therapy, “the doctor notes.Causes of Cold Allergy Cold urticaria can be associated with viral or bacterial infections. However, Elena Borzova specifies, there is still too little data to state this with full confidence. “We know very well that patients with cold urticaria often have infections, both viral and bacterial. Among the first, the Epstein-Barr virus (the causative agent herpes of the fourth type. – Ed.). Associations with viral hepatitis are not excluded. Among bacterial infections, Helicobacter pylori and mycoplasma are distinguished.Even parasitic infestations have been described in the context of cold allergy. At the same time, some researchers point to autoimmune diseases, others – to the use of antibiotics, oral contraceptives, drugs to lower blood pressure. But here it is very important to remember that clinical association does not always mean a causal relationship, “the professor emphasized. For a very small number of patients, the reasons for the unusual reaction of the body are still known – these are genetic mutations. As a rule, such people have from childhood on contact with frosty air blisters form on the skin, and there have already been cases of cold urticaria in the family.Be that as it may, at the first symptoms of an unusual allergy, it is worth contacting a specialist. It’s not just about treatment, but also about preventing potentially life-threatening situations. After all, a person is constantly faced with low temperatures. As noted by Professor Borzova, patients are usually offered individual precautions. In particular, in case of serious allergies, it is recommended to avoid cold rooms in shops, buildings with air conditioning, give up water sports, and sometimes even change profession.

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    Sechenov First Moscow State Medical University, health , allergy, biology, cells, genes

    MOSCOW, January 21 – RIA Novosti, Alfiya Enikeeva. In some people, severe frosts cause a real allergic reaction – nasal congestion and itchy skin blisters. Why this happens is still not clear, but it is treated like a rash that appears after contact with pollen or animal dandruff. RIA Novosti understands who has more chances of winter allergies and where they suffer from this ailment more often.

    Shock shower

    At the end of last year, a 34-year-old American fainted as he came out of the shower, his heart rate increased, and his body was covered with a rash.Relatives called an ambulance. Doctors diagnosed anaphylactic shock and brought the patient to consciousness with epinephrine and the antihistamine diphenhydramine. Only now the patient did not suffer from allergies in the usual sense of the word. A severe systemic reaction became the body’s response to a sharp temperature drop.

    As suggested by experts, the patient washed himself with very hot water, and then returned to a rather cool room. This provoked anaphylactic shock. Moreover, the standard test for winter allergies, carried out in the hospital, turned out to be positive: an ice cube was applied to the skin, and a red spot formed in this place.

    This is one of the rare cases of so-called cold urticaria. Those suffering from this disease, upon contact with low temperatures – frosty air, a glass of ice water or even ice cream – develop itchy blisters on their skin. Edema of internal organs and anaphylactic shock are possible.

    The disease occurs at the age of 30-40, and more often in women than in men. In countries with a cold climate, such as Russia, there are slightly more such patients. 30 October 2015, 12:33 often suffer from food and other forms of allergy.

    Incomprehensible reaction of the body

    “Increased sensitivity to cold occurs in less than 0.1 percent of the population. The mechanism of cold urticaria is not fully understood and differs from the classic reaction to protein allergens. There are several hypotheses. According to the most common, upon contact with the cold in the skin proteins change, and it is on them that an allergic reaction is formed.Histamine, in turn, acts on blood vessels, nerve endings, and itchy blisters form on the skin. More serious consequences are also possible – a drop in blood pressure, which we already interpret as anaphylactic shock “, – told RIA Novosti Professor of the Department of Skin and Venereal Diseases named after V.A. According to the professor, anaphylactic shock occurs, according to some reports, in 52 percent of patients with cold urticaria.It occurs on contact with low temperatures of large areas of the body. Even swimming in a river or lake with cold water will provoke a severe reaction.

    “This is a very alarming statistic. Cold urticaria must be diagnosed in time and measures must be taken to prevent it. After all, it does not always develop at absolutely low temperatures, this is a myth. Studies have shown that in some patients itchy blisters on the skin appear both at zero and at plus four, and even at plus 20 degrees Celsius.That is, the temperature threshold is an individual parameter. Often, patients note that the rash appeared after being in the cold, in a warm room. I must say that cold urticaria goes away quickly enough – usually within an hour. But there are also unusual cases, including potentially life-threatening ones. Therefore, if there are rashes after contact with a cold one, no doubt, you need to consult a specialist so that he can diagnose, assess the possible risks and select a therapy, “the doctor notes.

    Causes of cold allergy

    Cold urticaria can be associated with viral or bacterial infections. However, Elena Borzova clarifies, there is still too little data to state this with full confidence.

    “We are well aware that patients with cold urticaria often have infections, both viral and bacterial. Among the first, the Epstein-Barr virus is especially relevant (the causative agent of herpes simplex of the fourth type. – Ed.). Associations with viral hepatitis.Among bacterial infections, Helicobacter pylori and mycoplasma are distinguished. Even parasitic infestations have been described in the context of cold allergy. At the same time, some researchers point to autoimmune diseases, others – to the use of antibiotics, oral contraceptives, drugs to lower blood pressure. But here it is very important to remember that clinical association does not always mean a causal relationship, “the professor emphasized. Dermatologist Larisa Alekseeva answered this question in an interview with Radio Sputnik.

    For a very small number of patients, the reasons for the unusual reaction of the body are still known – these are genetic mutations. As a rule, such people have blisters on their skin from childhood on contact with frosty air, and there have already been cases of cold urticaria in the family.

    Be that as it may, at the first symptoms of an unusual allergy, it is worth contacting a specialist. It’s not just about treatment, but also about preventing potentially life-threatening situations. After all, a person is constantly faced with low temperatures.

    As noted by Professor Borzova, patients are usually offered individualized precautions. In particular, in case of serious allergies, it is recommended to avoid cold rooms in shops, buildings with air conditioning, give up water sports, and sometimes even change profession.

    October 22, 2020, 02:17 am Spread of coronavirus Allergy and coronavirus found the same symptoms 90,000 Urticaria from stress. Allergy from stress

    Daniil Davydov

    medical journalist

    Author’s profile

    Chronic stress increases the risk of developing many diseases, from cardiovascular diseases to stomach ulcers.

    But the disease will not develop if other factors do not act on a person, for example, the invasion of harmful microbes, smoking, overeating or heredity. Therefore, it is wrong to say that people suffer from allergies and dermatitis due to intense anxiety or overwork at work.

    What is stress

    Stress is a normal reaction of the body to abrupt changes in the surrounding world that cannot be ignored. Stress helps us mobilize and avoid danger – for example, dodging a person on an electric scooter whom we didn’t even see a moment ago.

    What is Stress – Medlineplus Medical Encyclopedia

    How the Brain Regulates Stress – Cleveland Clinic Bulletin

    The stress response is controlled by the command center in the brain. Nerves descend from the brain to each organ, united in a thick cable that we know as the spinal cord.

    Nerve fibers belonging to the sympathetic or parasympathetic nervous system run from the spinal cord to almost every blood vessel, sweat gland and muscle.

    If something unexpected suddenly happens around us, the sympathetic nervous system gives the order to our internal organs to mobilize. At her command, the pupils dilate, breathing and heart rate accelerate, and the liver releases glucose stores into the blood – the fuel that muscles urgently need to fight or flee. At the same time, digestion is suppressed, because the body is now not up to the assimilation of food. As a result, we come to a state of full combat readiness.

    Once the danger has passed, the parasympathetic system comes into play.It gives the whole body the command “At ease”: it narrows the pupils, slows down breathing and heartbeat, and allows the digestive system to continue working as usual. The liver stops releasing glucose into the bloodstream and focuses on the production of bile, which is needed for digestion. As a result, we calm down a little.

    The parasympathetic nervous system helps us to relax, and the sympathetic nervous system mobilizes us

    The parasympathetic nervous system helps us to relax, and the sympathetic nervous system mobilizes us

    Normal stress response saved us in ancient times, when humans were hunter-gatherers.In those days, stress was short-lived. If they succeeded in successfully catching up with the prey or avoiding a meeting with a flock of hyenas, people immediately calmed down, because nothing more threatened them.

    When humanity moved from deserts and forests to big cities, there were fewer reasons for short-term stress. But new sources of stress have emerged, such as unloved jobs or crowds on the subway, that have affected us for years. As a result, the stress became chronic. Unlike short-term stress, which saves a person’s life, chronic stress is not at all good for health.

    How stress increases the risk of developing disease

    Since stress is a complex response that involves the entire body, its effects increase the risk of both mental and physical illness.

    Mental illness. When stress reactions last not a few minutes or hours, but months and years, the sympathetic nervous system is constantly on the alert. As a result, a healthy person spends too much energy on the most common everyday tasks and gradually loses strength.The less strength a person has, the higher the risk that he will not cope with a difficult life ordeal like losing a job or divorce – and will get sick, for example, with depression.

    If the sympathetic nervous system is constantly activated, the risk of depression increases – Journal of Modern Neuropharmacology

    Chronic diseases. Stress is even more dangerous for people who have a predisposition or have already developed some kind of illness. For example, chronic stress increases heart rate and blood pressure.In a person with cardiovascular disease, additional stress on the heart and blood vessels can provoke a heart attack.

    By approximately the same principle – overstraining already damaged systems – stress can provoke the onset of the disease in people with a predisposition to type 2 diabetes, cancer and some other diseases.

    Infectious diseases. Chronic stress directly affects the immune system – it increases the level of suppressor T-lymphocytes.The task of these immune cells is to keep the inflammatory process under control and prevent the immune system from destroying the body itself along with microbes. But if suppressor T cells turn on for no reason, they begin to suppress the normal immune response. It is known for certain that this increases the risk of contracting a viral infection.

    Chronic stress disrupts the immune system – Journal of Stress Problems and Immunity in Space

    Wounds and trauma. Wound healing begins with inflammation of the damaged area of ​​the body.This allows you to kill germs and damaged cells. Then the cells in the damaged area begin to divide vigorously, and the wound heals. By suppressing inflammation, chronic stress prevents wounds from healing normally.

    Psychological stress interferes with wound healing – Journal of the Clinic of Immunology and Allergy of North America

    Chronic stress generally increases the risk of illness because it acts as a straw that breaks the back of an already overworked camel.But this does not mean at all that if people with a predisposition to chronic diseases did not stand in traffic jams, did not communicate with quarrelsome neighbors or with harmful bosses and were not nervous for other reasons, then they would not get sick.

    The role of the last straw can be played not only by chronic stress, but also by other factors – for example, a viral infection. Science knows cases when people with a predisposition to autoimmune diseases fell ill with them after they had a rotavirus infection or caught the herpes virus.

    Viruses and autoimmune diseases – the journal “Viruses”

    Is there a link between stress, urticaria and allergies

    Allergy is an error of the immune system that occurs when it mistakes a harmless protein from food, pollen or dust for a dangerous microbe and tries to destroy it. For most allergies, the immune system uses its favorite superweapon, a biologically active substance called histamine.

    What is allergy – UK NHS

    Genetic predisposition increases the risk of allergies – Nature

    Histamine provokes a spasm of blood vessels, due to which edema occurs, and triggers inflammation.As a result, a person’s snot flows, his eyes turn red, and an itchy rash appears on the skin. Skin manifestations of allergies are called atopic dermatitis, or urticaria.

    Most allergists today believe that chronic stress cannot cause an initially well-functioning immune system to make mistakes. Although the causes of allergies are not yet fully understood, it is believed that many people are already born with a genetic predisposition to allergies. Stress, even chronic stress, cannot reshape the genome.

    Stress and Allergic Disease – Journal of the Clinic of Immunology and Allergy of North America

    But stress is quite capable of provoking an extraordinary attack in a person who is already prone to allergies. It can also make an allergy attack more severe.

    It works like this. When a person with hives gets upset, their sympathetic nervous system dilates their blood vessels. This causes the immune cells to release more histamine – and as a result, the rash becomes even more itchy.

    How to reduce chronic stress levels

    A modern city dweller has no way to completely avoid the effects of factors that cause chronic stress. But you can try to regulate the intensity of the impact of sources of chronic stress on our lives.

    How to Deal with Chronic Stress – Bulletin of the American Psychological Association, APA

    Here’s what the American Psychological Association advises.

    Limit stressor intervention. Try listing all projects and commitments that make you nervous or overwhelmed. Leave on the list of daily tasks only those items that you cannot do without – for example, exams or trips on the subway.

    If work tasks are causing a lot of stress, it makes sense to discuss this with your manager. It may be possible to distribute the load. It may turn out that a task that causes you great discomfort could be done without any problems by one of your colleagues, and you could take on some of his tasks in return.

    Complain to a loved one. Some people experience chronic stress from not being told that times are tough. This does not mean that you should turn into a whiner. But many people feel better simply from the fact that they tell loved ones about their problems.

    There is nothing wrong with asking a friend or relative for support sometimes. Perhaps they too have faced similar problems and know how to solve them.For example, they will advise on a convenient way to organize work tasks or provide contact with a trusted psychologist or psychotherapist.

    Reduce the amount of coffee. Caffeine invigorates, but too much caffeine can trigger nervousness. Try limiting yourself to one cup of morning coffee. If you’ve been drinking this drink a lot during your workday before, it might feel better.

    Add daily walks to your schedule. Physical activity increases the concentration of endorphins, chemical compounds that improve mood and reduce stress.Not every job allows you to visit the gym, but you can almost always find time for a half-hour walk around your home or office, or at least to the subway.

    Get enough sleep. A healthy 7-8 hour sleep reduces the harmful effects of stress. But the catch is that chronic stress itself disrupts sleep, and it’s a vicious circle.

    In addition to the usual advice to eat less at night, give up glowing gadgets and sleep in the dark, you can try to get into the habit of writing down all disturbing thoughts in a notebook.This works in much the same way as complaining to a loved one, that is, it reduces stress. Once you’ve written everything down, the chances of falling asleep increase.

    If all else fails, seek help. Some people find it easier to deal with chronic stress when they work with a psychologist or therapist. True, sometimes it takes some time to find a specialist who is right for you, and services can be expensive: in different cities, an appointment costs 1500-5000 R. Most people feel better after the tenth appointment.

    What in the end

    1. Short-term stress is a normal physiological response that helps to survive in emergency situations.
    2. Chronic stress is harmful to health because it weakens the body and increases the likelihood of developing the disease in people with a predisposition.
    3. Chronic stress can provoke and exacerbate symptoms of many diseases, but does not cause allergies or hives by itself.

    Scientists have created the world’s first allergy vaccine.Read on UKR.NET

    The blister looks like a nettle burn: a pale raised skin with redness around it, which can last from a few minutes to 24 hours. Blisters, as a rule, itch very much, sometimes a person even complains of a burning sensation in the place of their formation.

    Urticaria can be accompanied by angioedema (up to 40% of cases), but such edema can occur in some people on its own.

    What is chronic urticaria?

    Chronic urticaria is characterized by daily or occasional blistering and / or angioedema for 6 or more.weeks. This skin condition can persist for 1-5 years, sometimes longer.

    It is classified as spontaneous or induced and both types can coexist in the same patient.

    What is chronic spontaneous urticaria and how does it manifest itself?

    This is a chronic disease that does not have a specific cause or trigger. It is also called chronic idiopathic urticaria.

    Such urticaria appears as blisters (urticaria) on the skin of the whole body and these manifestations last 6 or more weeks with or without angioedema.The manifestations are itchy and interfere with daily activities at school or at work.

    Symptoms of this disease may disappear after a few months. However, in about 50% of cases, they periodically appear within 3-5 years. And in 20% of cases, they can persist for more than 10 years.

    Urticaria most often occurs as a result of the influence of a biologically active substance – histamine – on the H1 -receptors, which are located on the cells of the vascular endothelium. As a result, fluid is released from the vascular bed and a blister forms.Histamine also affects sensory nerve endings, which leads to itching and redness of the skin.

    Who most often suffers from chronic urticaria?

    The disease most often occurs in adults between the ages of 20 and 40. Most studies report that women suffer from it almost twice as often as men.

    In the children’s category, it more often affects older children and adolescents.

    What is the most common cause of chronic spontaneous urticaria?

    In most cases, this trigger factor cannot be identified.Possible causes:

    Autoimmune diseases

    Acute or chronic infections

    Pseudoallergy

    Thyroid diseases

    Diseases of the gastrointestinal tract and other

    The approach to the treatment of chronic spontaneous urticaria may include any: causes

    Avoiding any known aggravating factors such as NSAIDs

    Antihistamines

    Omalizumab

    Cyclosporine

    Corticosteroids

    What is omalizumab?

    Omalizumab is a humanized monoclonal antibody that binds to circulating immunoglobulin E (IgE) and reduces the release of inflammatory mediators from mast cells and basophils.Thus, preventing the formation of blisters on the skin with chronic urticaria.

    Currently, Omalizumab is recommended by the International Protocols for the treatment of severe chronic urticaria, allergic asthma for patients over 12 years of age as an adjunctive therapy to antihistamines.

    It is given as a subcutaneous injection once every 4 weeks.

    What is the role of omalizumab in the treatment of urticaria?

    This antibody is intended for use as a second-line therapy for the treatment of chronic, spontaneous urticaria that is refractory to antihistamines.Many patients also fail to respond to a range of other systemic treatments, including systemic steroids and immunomodulatory drugs.

    How does Omalizumab work for hives?

    Immunoglobulin E (IgE) plays an important role in the development of an allergic reaction. Although the disease often does not develop due to the action of an allergen, IgE plays an important role in its development.

    Omalizumab was developed to recognize and adhere to a specific structure on IgE present in the blood.This prevents the binding of high affinity IgE receptors (FcεRI) on the surface of mast cells and basophils, thus reducing the release of inflammatory mediators and the formation of urticaria on the skin.

    What are the side effects of Omalizumab?

    About 10% of patients who received this drug complained of headache and local reactions (swelling, redness, pain and itching at the injection site).

    An allergist will help you to prescribe medications and choose the dosage.Do not hesitate with treatment – contact a specialist today.

    What is the difference between hives and rashes

    Many people call hives any rash. Of course, hives are also skin rashes, but not every rash is hives.

    If you are concerned about the condition of your skin, it is important to know when the rash on it is hives and when it is a manifestation of other skin conditions.

    In this article, we will look at the difference between hives and other types of rashes.And also – we will determine the symptoms, causes and treatment of each of these conditions.

    How to tell if the rash is hives

    Urticaria – itchy, flat, raised, pale pink blisters that look like blisters from a nettle burn. They can be large or small, red, or the same color as your skin.

    Blisters can appear and pass quickly or remain on the skin for a long time.

    Manifestations of the disease can be observed throughout the body or only in one or two localized areas.

    Symptoms and Causes

    Itching that accompanies urticaria can be intense or mild, prolonged or short-term. Often the appearance of blisters caused by the disease is preceded by itching. In other cases, blisters and itching appear at the same time.

    Urticaria usually looks like a collection of blisters that can occur anywhere on the body. Its manifestations can be tiny, pinpoint, or much more. They can also vary in size and shape.

    In some cases, individual blisters coalesce to form very large itchy areas. The skin surrounding the area where the rash appears may appear red, swollen, or irritated.

    The blister usually disappears within 24 hours, but it may appear elsewhere. The rash can remain on the body or recur for weeks, months, or even years.

    Causes of urticaria

    Acute urticaria that lasts less than 6 weeks can be caused by the release of too much or increased histamine in the body.Also, acute urticaria is a common manifestation of a true allergic reaction.

    Allergies are believed to be the main cause of blistering. It can occur if you have eaten or drunk something. Or have had contact with an environmental factor to which you are allergic.

    Other factors causing urticaria may include:

    In some cases, the causes of the rash may remain undetected.

    Symptoms and causes of rash

    Urticaria rash may mimic the skin manifestations in other infectious and autoimmune diseases.

    Skin rashes can be completely different:

    • scaly, red, moist in appearance;
    • as blisters, ulcers or scars;
    • painful, itchy and / or hot to the touch;
    • sometimes – edematous.

    Depending on the underlying cause, the rash may be localized in one area or spread throughout the body.

    Rash as a symptom

    A fairly large number of skin diseases are accompanied by a rash:

    How is urticaria treated

    Antihistamines are the first line of treatment for both acute and chronic urticaria.And although the disease often disappears on its own so that there is no relapse, it is important to determine what exactly is causing it. And based on certain factors, already choose the right treatment.

    The main measures in the treatment of urticaria are:

    1. Identification and elimination of its main causes.
    2. Avoiding contact with factors that cause the development of symptoms, namely: sunlight in case of solar urticaria, cold in cases of cold, food, etc.
    3. Use of medicines recommended by an allergist.

    Hives, like any rash, can last for hours, days, weeks, or longer.

    Chronic, long-term urticaria may require more aggressive drug treatment. Such as biologics and immunosuppressants.

    However, again, all these strategies are determined by the doctor.

    When to see a doctor

    If you have long-term hives or any other rash, be sure to see an allergist or dermatologist.They can help you determine the cause of the symptom and provide an effective course of treatment.

    Hives and any other rash may be the result of an allergic reaction or medical emergency.

    Seek medical attention immediately if, in addition to a worsening of your skin, any of the following symptoms occur:

    Like adults, any type of rash can develop in newborns and young children. This can be caused, for example, by a bug bite or the influence of foods new to children.

    If your child has a rash and you are not sure where it is, call the pediatrician. Especially if you notice at least one of the symptoms listed above.

    Key remarks:

    Hives and other types of skin rashes have a wide variety of causes and are very common.

    Urticaria is a type of rash, although not every rash resembles it. Both skin conditions can be acute or chronic.

    It is important to try to determine the root cause of your hives or other rash, this will help you choose the best treatment.

    Breathing problems associated with urticaria may require immediate medical attention.

    90,000 Clinical Study Urticaria: Rituximab – Clinical Trials Registry
    Acceptability

    Criteria:

    Main inclusion criteria: – Chronic urticaria is defined as symptoms> 50% days or 3 days per week for a longer period. more than 12 weeks – Previous requirement for persistent or repeated use of corticosteroids OR requirement for immunomodulatory treatment for urticaria (e.g. hydroxychloroquine, sulfasalazine, dapsone, cyclosporine, intravenous immunoglobulins, etc.)OR persistent symptoms lasting at least 6 months with no response, at least the maximum approved dosages of 2 different antihistamines – Chronic therapy with stable doses of antihistamines for at least 4 weeks. Patients may be taking more than one antihistamine or taking combinations of antihistamines and leukotriene receptor antagonists – High baseline pruritus score (at least 2 on a 3-point scale) – No clear definition of the underlying etiology of urticaria.- Evidence of underlying autoimmunity, confirmed by clinical and laboratory criteria – Concomitant use of hydroxychloroquine, sulfasalazine or dapsone is permitted if doses are stable for at least 12 weeks – Negative serum pregnancy test (for women of childbearing age) – Men and women with reproductive potential must agree to use an acceptable method birth control during treatment and for twelve months (1 year) after completion of treatment.- Absence of planned elective surgery for at least 6 months Main exclusion criteria: – concomitant use of corticosteroids – Current use of immunosuppressants (cyclosporine, IVIG, methotrexate, cyclophosphamide). Any such medication will be discontinued for at least 6 weeks. before watching. – Treatment with any investigational agent within 4 weeks of screening or 5 half-lives of the investigational drug, whichever is longer – Received live vaccine within 4 weeks prior to randomization – Previous treatment with Rituximab (Mabthera® / Rituxan®) – Previous therapy antibodies – History of severe allergic or anaphylactic reactions to humanized or murine monoclonal antibody preparations – Known history of HIV seropositivity (testing will be done at screening) – History of hepatitis B and / or hepatitis C (Hep BsAg and Hep C Ab can be obtained from screening) – History of recurrent significant infection or recurrent bacterial infection History of infection – Known active bacterial, viral, fungal, mycobacterial, or other infections (including tuberculosis or atypical mycobacterial disease, but excluding fungal infections of the nail bed) – Any serious episode of infection or requiring hospitalization IV treatment.antibiotics within 4 weeks after screening or oral antibiotics within 2 weeks before screening – known immunodeficiency syndrome, hypogammaglobulinemia, etc. – Systemic lupus erythematosus – Pregnancy (negative serum pregnancy test will be performed for all women fertile potential within 7 days after treatment ) or breastfeeding – Malignant neoplasms within the last five years, except for adequately treated basal or squamous cell skin cancer or cervical cancer in situ.- Atopic dermatitis – Clinically significant diseases (cardiovascular, including poorly controlled hypertension or ischemic heart disease, pulmonary, metabolic, renal, hepatic, psychiatric) or clinical laboratory findings that give reasonable suspicion of a disease or condition that contraindicates the use of the investigated drug or could affect the interpretation of results or put the patient at high risk of complications of treatment – Plans or need for vaccination against live viruses during the study (eg, Flu-Mist TM)

    Floor:

    All

    Minimum age:

    18 years old

    Maximum age:

    pizza z oliwkami

    Healthy volunteers:

    No

    Allergist in Novosibirsk | Make an appointment with an allerologist at EuroMed Clinic

    Allergists of EuroMed Clinic in Novosibirsk strongly recommend contacting them for advice:

    • For various types of allergic dermatoses.The most common types of allergic dermatoses include Quincke’s edema, toxicoderma, urticaria, eczema and atopic dermatitis;
    • For allergic hay fever, conjunctivitis and rhinosinusitis;
    • With recurrent sinusitis and chronic tonsillitis, frequent tonsillitis and acute respiratory infections;
    • For repeated pneumonia, chronic bronchitis and bronchial asthma;
    • When infected with herpesvirus infection, cytomegalovirus and Epstein-Barr virus;
    • With the manifestation of human papillomavirus infection on the skin and mucous membranes;
    • For various types of pyoderma: acne, hydradenitis and recurrent boils;
    • When resistance to drug exposure occurs in chronic urogenital infection;
    • With recurrent candidiasis occurring on the skin and mucous membranes;
    • For chronic fatigue syndrome;
    • With a syndrome of increased ESR;
    • With diagnosed fever of unknown origin.

    Also, an appointment with an allergist will be required after completing corticosteroid treatment, radiation therapy, or chemotherapy. Finally, the doctor of the EuroMed Clinic medical center will help you restore the functioning of the immune system mechanisms during long-term healing of traumatic and postoperative wounds.

    Any immunological condition can be conventionally attributed to one of three groups:

    1. State of immunodeficiency.
      • Primary – genetically determined or hereditary;
      • Secondary – acquired;
      • Physiologically determined – pregnancy or age (children or the elderly).
    2. Diseases of an allergic nature.
    3. Diseases of an autoimmune nature.

    Main activities of an allergist

    The allergist deals with the treatment of allergic diseases and immunodeficiency conditions.Autoimmune diseases are treated mainly by rheumatologists.

    Allergic diseases are characterized by increased sensitivity to certain substances to which the organisms of most people do not have a pathological or increased reaction. For example, some allergy sufferers are diagnosed with an allergic reaction to mold, animal epidermis or house dust. Others have an allergic reaction to certain foods.

    According to the International Health Organization, about a third of the world’s population suffers from one or another allergic reaction.Moreover, in recent years, the number of allergy sufferers has been steadily increasing, which is due to a whole range of factors: abuse of drugs and artificially created vitamin complexes, constant stress, the emergence of new allergens, an unfavorable lifestyle, unhealthy diet, environmental degradation.

    What is an immunodeficiency state?

    The immunodeficiency state can be diagnosed for the first time already in childhood.The secondary (acquired) state of immunodeficiency is much more common than the primary one, and it is much more difficult to treat it.

    Reasons for acquired immunodeficiency:

    • Lack of sleep, stress, overwork;
    • Parasitic, viral, bacterial infections of a chronic and acute nature;
    • Metabolic disorders;
    • Pathogenic effects of household and industrial poisons, household chemicals, food and cosmetic dyes, etc.;
    • Result of exposure to antibiotic therapy, chemotherapy, or immunosuppressive therapy;
    • The impact of certain physical factors – increased background radiation, microwave exposure, etc.;
    • Mechanical and thermal injuries;
    • Consequence of chronic diseases;
    • Consequence of malignant neoplasms.

    The main groups of clinical syndromes arising in the immunodeficiency state:

    1. Infectious group.
    2. Allergic group.
    3. Autoimmune group.
    4. Neoplastic group – the appearance of neoplasms.

    Immunodeficiency is characterized by a decrease in anti-infectious resistance (resistance), which leads to an increase in the total number of inflammatory diseases of a viral or bacterial nature and the frequency of their occurrence.

    Most often, with immunodeficiency, the following diseases occur:

    • Bronchitis, pneumonia, otitis media, sinusitis, tonsillitis and pleurisy;
    • Acne, hydradenitis, furunculosis;
    • Mycoses of the skin and mucous membranes;
    • Various viral, urogenital and parasitic infections.

    Diagnostic features

    EuroMed Clinic has everything you need to confirm or deny your concerns regarding immunity or allergies. In particular, the medical center has the ability to perform the following tests:

    1. The amount of total and specific immunoglobulins E in the blood;
    2. Immunological studies;
    3. Other studies required to determine the causes of immune pathologies.Their volume will be determined for you by your attending physician, an allergist-immunologist.

    Treatment details

    It is important to clearly understand that to restore normal immunity, just taking immunostimulating and antiallergic drugs is not enough. Firstly, their appointment requires caution and balance, and secondly, these drugs will not be able to give a positive result if the primary causes of the pathology are not eliminated. To do this, it is necessary to eliminate contact with allergens, sanitize foci of chronic infection, normalize the work of the digestive, endocrine and nervous systems, change the diet and lifestyle.