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Funding sources: Grants‐in‐Aid for Scientific Research and Strategic Research Basis Formation Supporting Project from the Ministry of Education, Culture, Sports, Science and Technology of Japan; Health and Labour Sciences Research Grants; Grants for Research on Measures for Intractable Diseases from the Ministry of Health, Labour and Welfare of Japan. This work was also supported by grants from the Uehara Memorial Foundation, the Nakatomi Foundation, the Kaibara Morikazu Medical Science Promotion Foundation, the Japan Lydia O’Leary Memorial Foundation, the Cosmetology Research Foundation, the Japanese Dermatological Association (Shiseido Award), the Fukuoka Foundation for Sound Health, and Galderma K.K. (Galderma Award). Conflicts of interest: none declared. Madam, Brunsting–Perry type pemphigoid is characterized clinically by recurrent blisters and vesicles and histopathologically by subepidermal blisters. The blisters are limited to the head, face, neck and upper trunk and leave atrophic scars on healing.1 It is a matter of debate whether Brunsting–Perry type pemphigoid is a variant of pemphigoid1, 2 or of epidermolysis bullosa acquisita.3, 4 In support of the former notion, some previous reports suggested that the target antigen in Brunsting–Perry type pemphigoid was BP180 and that the clefts of the bullae were located at the lamina lucida, based on an ultrastructural study.1, 2, 5 In support of the latter notion, some patients with Brunsting–Perry type pemphigoid had autoantibodies against type VII collagen, and the clefts of the bullae were located at the sublamina densa area.3, 4 Moreover, there are also reports of autoantigen targets other than BP180 and type VII collagen in Brunsting–Perry type pemphigoid; for example, Honoki et al.6 reported on a patient with autoantibodies against a 145‐kDa antigen combined with type VII collagen. We report here the first case of Brunsting–Perry type pemphigoid with autoantibodies toward laminin‐332, BP230 and desmoplakins.
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Fukuda et al. (2011) studied this question.
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