A case of anti‐laminin γ1 (p200) pemphigoid developed after dipeptidyl peptidase‐4 inhibitor administration

Abstract

AbstractA 73‐year‐old man with diabetes mellitus was referred to our department for ultraviolet treatment for erythematous skin lesions with itching. On dipeptidyl peptidase‐4 inhibitor (DPP‐4i) sitagliptin (Januvia®) for diabetes mellitus, the erythematous skin lesions appeared and spread to the whole body. At the initial visit, erythema multiforme‐like skin lesions with crusts were observed on the trunk and extremities, and the patient was suspected to have drug eruption. Histopathology demonstrated eosinophilic infiltration in the superficial dermis and inflammatory cell infiltration in the epidermis. Sitagliptin was discontinued, and erythematous lesions improved with oral prednisolone. Thereafter the patient was treated with phototherapy and  betamethasone sodium phosphate infusion for residual prurigo. However, blistering skin lesions appeared 5 months later. Histopathological findings were subepidermal blisters with eosinophilic abscess, and bullous pemphigoid was suspected. CLEIAs for autoantibodies to desmoglein 1 (Dsg1), Dsg3 and BP180 were negative. Direct immunofluorescence showed linear depositions of immunoglobulin G (IgG) and C3 at the epidermal basement membrane zone, and indirect immunofluorescence detected IgG anti‐epidermal basement membrane zone antibodies, reacting with the dermal side of 1M NaCl‐split normal human skin. IgG antibodies reacted with 200 kDa laminin γ1 (p200) by immunoblotting using dermal extracts. These results indicated that this patient was diagnosed with anti‐laminin γ1 (p200) pemphigoid developed after DPP‐4i administration. Although reports of DPP‐4i‐related bullous pemphigoid have accumulated, cases of anti‐laminin γ1 (p200) pemphigoid developed after DPP‐4i administration are rarely reported.