IgA antiepidermal transglutaminase antibodies in dermatitis herpetiformis: a significant but not complete response to a gluten-free diet treatment

Funding sources: The study and the Celiac Disease Study Group were financially supported by the Competitive Research Funding of Tampere University Hospital (grants 9N062, 9P008 and 9P060), the Competitive State Research Financing of the Expert Area of Tampere University Hospital (grant 9R018) and Seinäjoki Central Hospital (VTR16), the Academy of Finland and Sigrid Juselius Foundation. Conflicts of interest: none declared. Dear Editor, Dermatitis herpetiformis (DH) is a blistering skin disease accompanied by intensive itching, and is currently recognized as an extraintestinal manifestation of coeliac disease. The majority of patients with DH have subclinical villous atrophy in the small bowel, identical to that which occurs in coeliac disease, and the remainder show signs of mucosal inflammation. The small bowel mucosa and rash in DH respond to a strict gluten‐free diet (GFD) treatment.1 Patients with DH show pathognomonic IgA deposits in dermal papillae.2 In 2002, Sardy et al.3 demonstrated that epidermal transglutaminase (TG3) colocalizes with dermal IgA deposits and proposed that TG3 is the autoantigen in DH. Previously, Dieterich et al.4 showed that tissue transglutaminase (TG2) is the autoantigen in coeliac disease in which TG2 colocalizes with deposited IgA in the small bowel mucosa.5