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Herpetiform dermatitis duhring. Dühring dermatitis herpetiformis - Elemzések

Signs and symptoms[ edit ] Its characteristic rash resembles herpes and is the basis of its clinical name Dermatitis herpetiformis is characterized by intensely itchychronic papulovesicular eruptions, usually distributed symmetrically on extensor surfaces buttocks, back of neck, scalp, elbows, knees, back, hairline, groin, or face.

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The condition is extremely itchy, and the desire to scratch may be overwhelming. The rash rarely occurs on other mucous membranes, excepting the mouth or lips. The symptoms range in severity from mild to serious, but they are likely to disappear if gluten ingestion is avoided and appropriate treatment is administered. Dermatitis herpetiformis symptoms are chronicand they tend féregpaszta oroszlánhoz come and go, mostly in short periods of time in response to the amount of gluten ingested.

However, herpetiform dermatitis duhring with DH often have no gastrointestinal symptoms even if they have associated intestinal damage. In the herpetiform dermatitis duhring stage, the patient may notice a slight discoloration of the skin at the site where the lesions appear. In the next stage, the skin lesions transform into obvious vesicles and papules that are likely to occur in groups. Healing of the lesions is the last stage of the development of the symptoms, usually characterized papillómák a szemhéj árán a change in the skin color.

This may result in areas of the skin turning darker or lighter than the color of the skin on the rest of the body. Because of the intense itching, patients usually scratch, which may lead to the formation of crusts.

Pathophysiology[ edit ] Cross-reactivity hypothesis for the onset of dermatitis herpetiformis in people with celiac disease In terms of pathology, the first signs of the condition may be observed within the dermis. The changes that may take place at herpetiform dermatitis duhring level may include edemavascular dilatationand cellular infiltration.

It is common for lymphocytes and eosinophils to be seen. The bullae found in the skin affected by dermatitis herpetiformis are subepidermal and have rounded lateral borders.

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When looked at under the microscopethe skin affected by dermatitis herpetiformis presents a collection of neutrophils. They have an increased prevalence in the areas where the dermis is closest to the epidermis.

The jejunal mucosa may show partial villous atrophybut the changes tend to be milder than in coeliac disease. The main autoantigen of dermatitis herpetiformis is epidermal transglutaminase eTGa cytosolic enzyme involved in cell envelope formation during keratinocyte differentiation.

The fact that eTG has been found in precipitates of skin-bound IgA from skin affected by herpetiform dermatitis duhring condition has been used to conclude that dermatitis herpetiformis may be caused by a deposition of both IgA and eTG within the dermis.

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It is estimated that these deposits may resorb after ten years of following a gluten-free diet. Moreover, it is suggested that this condition is closely linked to genetics. This theory is based on the arguments that individuals with a family history of gluten sensitivity who still consume foods containing gluten are more likely to develop the condition as a result áttétes petefészekrák the formation of antibodies to gluten.

These IgA deposits may disappear after long-term up to ten years avoidance of dietary gluten. Neutrophil recruitment results in a very rapid onset of inflammation.

Dermatitisz herpetiformisz

Therefore, co-infection with microbes that carry PAMPs may be necessary for the initial onset of symptoms in herpetiform dermatitis duhring sensitivity, but would not be necessary for successive encounters with gluten due to the production of memory B and memory T cells discussed below.

Dermatitis herpetiformis may be characterised based on inflammation in the skin and gut. Inflammation in the gut is similar to, and linked to, celiac disease. These T cells become activated and polarised into type I helper T Th1 cells. Th1 cells reactive towards gliadin have been discovered, but none against tTG. Thus, the B cell presents the foreign peptide modified gliadin but produces antibodies specific for the self-antigen tTG.

Once the B cell becomes activated, it differentiates into plasma cells that secrete autoantibodies against tTG, which may be cross-reactive with epidermal transglutanimase eTG. Class A antibodies IgA deposit in the gut. This will trigger endocytosis of the tTG-IgA complex, resulting in the activation of macrophages.

Macrophages secrete more IL-8, propagating the neutrophil-mediated inflammatory response. The purportedly cross-reactive autoantibodies may migrate to the skin in dermatitis herpetiformis.

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IgA deposits may form if the antibodies cross-react with epidermal transglutanimase eTG. Some herpetiform dermatitis duhring have eTG-specific antibodies instead of tTG-specific cross-reactive antibodies and the relationship between dermatitis herpetiformis and celiac disease in these patients is not fully understood.

Macrophages may be stimulated to secrete IL-8 by the same process as is seen in the gut, causing neutrophils to accumulate at sites of high eTG concentrations in the dermal papillae of the skin.

Duhring dermatitiszének jellemzői

Neutrophils produce pus in the dermal papillae, generating characteristic blisters. IL accumulation at the blisters may intensify itching sensations. Symptoms of dermatitis herpetiformis are often resolved if patients avoid a gluten-rich diet. Micrograph of dermatitis herpetiformis: Subepidermal vesicles, with papillary neutrophil microabcesses, with neutrophil, eosinophil and lymphocytes infi ltrates in the superfi cial dermis.

Additionally, the concomitant diagnosis of Celiac disease can be made without the need for a small-intenstinal biopsy if an individual has biopsy-confirmed dermatitis herpetiformis as well as supporting serologic studies elevated levels of IgA tissue transglutaminase antibodies, IgA epidermal transglutaminase antibodies, or IgA endomysial antibodies.

As with ordinary celiac disease, IgA against transglutaminase disappears often within months when patients eliminate gluten from their diet. Thus, for both groups of patients, it may be necessary to restart gluten for several weeks before testing may be done reliably.

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InCutis reported an eruption labelled gluten-sensitive dermatitis which is clinically indistinguishable from dermatitis herpetiformis, but lacks the IgA connection, [27] similar to gastrointestinal symptoms mimicking coeliac disease míg a condylomát kezelik without the diagnostic immunological markers. Avoidance of gluten will reduce any associated helminthoglypta california damage [15] [25] and the risk of other complications.

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It can be very difficult to maintain a strict gluten-free diet, however, as contamination with gluten is common in many supposedly gluten-free foods and restaurants. Dapsone is an effective initial treatment in most people and is the initial drug of choice to alleviate the rash and itching.

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Itching is typically reduced within 2—3 days, [15] [29] however, dapsone treatment has no effect on any intestinal damage that might be present. Dapsone is an antibacterialand its role in the treatment of DH, which is not caused by bacteriais poorly understood. It may cause adverse effects, especially hemolytic anemiaso regular blood monitoring is required.