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 chronic, and they tend to come and go, mostly in short periods of time in response to the amount of gluten ingested.The bullae found in the skin affected by dermatitis herpetiformis are subepidermal and have rounded lateral borders.The jejunal mucosa may show partial villous atrophy, but the changes tend to be milder than in coeliac disease.The main autoantigen of dermatitis herpetiformis is epidermal transglutaminase (eTG), a cytosolic enzyme involved in cell envelope formation during keratinocyte differentiation.[7] Various research studies have pointed out different potential factors that may play a larger or smaller role in the development of dermatitis herpetiformis.These antibodies cross-react with eTG, and IgA/eTG complexes deposit within the papillary dermis to cause the lesions of dermatitis herpetiformis.[7] Gliadin proteins in gluten are absorbed by the gut and enter the lamina propria where they need to be deamidated by tissue transglutaminase (tTG).Thus, the B cell presents the foreign peptide (modified gliadin) but produces antibodies specific for the self-antigen (tTG).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.As with ordinary celiac disease, IgA against transglutaminase disappears (often within months) when patients eliminate gluten from their diet.[31] Topical steroid medications are also sometimes used in combination with dapsone and a gluten-free diet to alleviate the itchiness associated with the rash.The risks of developing complications from dermatitis herpetiformis decrease significantly if the affected individuals follow a gluten-free diet.Individuals of Northern European descent are most likely to be affected and estimates of the rates of DH in British and Finnish populations range from 30 in 100,000 to 75 in 100,000 people, respectively.[6] There is a slight male predominance in DH for unknown reasons and it is associated with celiac disease and the haplotypes HLA-DQ2 and, less commonly, HLA-DQ8.A researcher suggested in 1979 that the mysterious skin disease was DH based on these symptoms and this regimen of self-treatment.
Cross-reactivity hypothesis for the onset of dermatitis herpetiformis in people with celiac disease
Micrograph of dermatitis herpetiformis: Subepidermal vesicles, with papillary neutrophil microabcesses, with neutrophil, eosinophil and lymphocytes infi ltrates in the superfi cial dermis. However, the histopathology is unspecific in approximately 35–40% of the cases,
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and direct immunofluorescence is needed, showing deposition of IgA in the papillary dermis in a granular or fibrillar pattern.
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