Dermatitis herpetiformis was described 100 years ago by Louis Duhring as a relatively rare skin disease characterized by a rash with small blisters and intense itch. Predilection sites are on the elbows, knees and buttocks, but lesions can also be found on the scalp, axillary folds and back. The onset in young adults is usually sudden. Diagnosis is based on biopsy from the uninvolved skin; immunofluorescence shows characteristic granular IgA deposits along the basement membrane. In dermatitis herpetiformis lesions, subepidermal blisters with cellular inflammatory infiltration are found. The rash is gluten-dependent and the improvement in skin lesions occurs slowly; even on a strict gluten-free diet it lasts several months before the patient can stop using dapsone (diaminodiphenyl sulphane) which controls the rash in few days and, therefore, it has been used for years in the treatment of dermatitis herpetiformis [30, 31].
Even though less than 10% of patients with dermatitis herpetiformis have gastrointestinal symptoms suggestive of CD, they all have gluten-sensitive enteropathy ranging from flat mucosa to normal mucosal architecture, but with increased numbers of intraepithelial y8 TCR-bearing T cells. Molecular genetics did not point out any difference between dermatitis herpetiformis and CD. The genetic background of dermatitis herpetiformis is the same as in CD. Both conditions are associated with the class II HLA DQ2 molecule, and especially with DQ alleles A1 0501 and B1 0201. The disease can cluster in families similar to CD. Monozygotic twins, one with dermatitis
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