LAUSR

Dyshidrosiform pemphigoid (DP) is regarded as a unique type of bullous pemphigoid (BP) with vesiculobullous eruptions localized to the palms and soles, which clinically resembles dyshidrosiform eczema. Some cases of BP due to programmed cell death protein-1 (PD-1) inhibitor have been reported. Here, we report a case of DP after the administration of the PD-1 inhibitor, nivolumab, with histopathological features that differ from those of idiopathic DP. A 69-year-old man had received chemotherapy for Stage III gastric cancer for two years before discontinuation because of side effects. Computed tomography showed the tumour to be shrinking. Nivolumab had been administered for three months before his first consultation with us. After the seventh administration, oedematous erythema on the palms and soles, and stomatitis appeared. He reported pain, but not pruritus, on the palms and soles. The patient had been treated for hypertension and type 2 diabetes mellitus, but had not taken any diuretics, -blockers, or dipeptidyl peptidase-4 inhibitors. Our initial examination revealed multiple oedematous erythematous lesions, vesicles and small bullae, some of which had coalesced, with tenderness on the palms and soles (figure 1A). His eosinophil count was 120/ L (1% of white blood cells), and no eosinophilia was observed during the subsequent process. The patient was treated with topical glucocorticoids and the nivolumab was stopped. Six days later, the lesions became bullae, 5 to 20 mm in diameter (figure 1B), some of them haemorrhagic. Small, disseminated erythematous lesions appeared on the trunk. At the time, the serum anti-BP180 antibody level was elevated (58.7 U/mL; reference range: <9 U/mL). Histopathological examination of a bulla on the sole revealed subepidermal blistering and perivascular inflammatory cell infiltration containing eosinophils. Some eosinophilic bodies were seen in the lesional epidermis (figure 1C, D). Direct immunofluorescence showed linear C3 deposition at the dermo-epidermal junction (figure 1E). Nivolumab-induced DP was diagnosed. We initiated treatment with oral prednisolone at 20 mg/day and minocycline at 200 mg/day. Ten days later, new blisters stopped forming. Anti-BP180 antibody was elevated to 297 U/mL a month later, and the prednisolone was tapered gradually because the skin manifestations had shown clinical improvement. Anti-BP180 antibody dropped to 69 U/mL two months later, and the erosions re-epithelialized with pigmentation at four months after the A