LAUSR

101 superficial perivascular infiltration of lymphocytes and eosinophils (figure 1E). Direct immunofluorescence (DIF) revealed the linear deposition of IgG and C3 along the basement membrane zone (BMZ) (figure 1F). Indirect IF (IIF) revealed IgG deposition on the epidermal side of 1-M NaCl-split skin sections. At the time, the serum anti-BP180 antibody level was increased (49.0 U/mL), however, no eosinophilia was detected. Ultimately, she was diagnosed with LPP based on the clinical course and the histological and IF findings. The dose of PSL was increased to 10 mg/day; thereafter, the symptoms completely disappeared. The patient showed hyperkeratotic plaques of the palms and soles, in addition to common LPP lesions. Involvement of the palms and/or soles is uncommon in LP patients. The clinical appearance of the present patient resembled that of palmoplantar LP (PPLP), a rare localized variant of LP that occasionally shows additional skin involvement [2]. To our knowledge, there have only been two reported cases of LPP with palmoplantar keratoderma [3, 4]. We therefore consider the clinical features of the present patient to be rare. In the present case, a slight increase in the anti-BP180 antibody level was detected when the severe lichenoid lesions appeared. The anti-BP180 antibody level then showed a marked increase when the blistering lesions developed. A previous report showed that anti-BP180 antibodies were detected in most cases of LPP in which molecular studies were performed [5]. Furthermore, reactivity to proteins of 130, 200, 230 and 240 kDa was also observed [5]. However, the anti-BP180 antibodies were detected in only three of 22 patients with mucosal LP [6]. The precise pathogenesis of LPP remains unknown. Previous reports suggest that the inflammation in LP lesions may result in epitope spreading and production of autoantibodies against the BMZ [7, 8]. Sekiya et al. reported an LPP case with autoantibodies to BP180, in which no autoantibodies were detected before the development of blistering lesions [9]. In contrast, in patients in which oral LP developed 5-12 years after the onset of autoimmune subepidermal blistering disease, it is suggested that the immune response extends from autoantibodies to BP180 to an additional pathogenic T-cell response [10]. In our case, we hypothesize that damage to the basal keratinocytes in the LP lesions might have induced exposure of the sequestered antigens of BP180 and the production of anti-BP180 autoantibodies.