PUVA induced bullous pemphigoid in a patient with psoriasis.

A bullous eruption in a patient with psoriasis was first described by Bloom in 1929 (as cited by Weber) (1). Since then there have been several reports of bullous pemphigoid occurring during the treatment of psoriasis, especially after ultraviolet (UV) B exposure. Comorbidity of these two diseases without treatment has also been reported (2,3). Psoriasis is one of the most common chronic inflammatory skin diseases. Its etiopathogenesis is unknown, but nonspecific inflammatory processes and specific immunologic factors have been described. Autoimmune processes occurring within the epidermis and immunologic responses to exogenous infectious agents are suspected as causes, but not confirmed. In contrast, bullous pemphigoid (BP) represents a distinct autoimmune disease in which basement membrane zone (BMZ) molecules are most affected (4). BP is an autoimmune subepidermal bullous disease with circulating autoantibodies against BP antigen 1 (230kDa) and BP antigen 2 (180kDa). Antigen 2 is a transmembrane glycoprotein located in the hemidesmosomes and is the major antigenic target in this disorder (5,6). The BP180 NC16a domain is considered to be the most immunogenic site (7). The occurrence of BP in patients with psoriasis has occasionally been reported (8). Although the pathogenetic mechanism of comorbidity of psoriasis vulgaris and BP is unclear, a common immunogenetic mechanism might be involved (9). Most previously reported cases attributed the occurrence of BP in psoriasis to photochemotherapy and phototherapy (PUVA, UVA, UVB311nm), topical treatment with anthralin, tar, and as a result of systemic application of anti-TNF antibodies (10). The role of PUVA therapy in the development of BP remains unknown. George at al. suggested that such changes may trigger the development of antibodies which may later cross-react with proteins, such as the BP antigen, causing a bullous eruption to appear. The possibility that PUVA induces the alteration of immunologic reactivity of Thelper and T-suppressor cells, allowing the development of autoantibodies against native proteins, has also been raised (6,11). A 55-year-old woman was referred to our department with a ten days history of bullous lesions, erosions, and exacerbated plaque psoriasis. Psoriasis was diagnosed in 1994, and various systemic and topical therapies (in combination or as single treatment)