Dear Editor, Linear immunoglobulin A bullous dermatosis (LABD) is a relatively rare autoimmune blistering disease characterized clinically by the presence of small tense blisters and immunologically by the presence of immunoglobulin (Ig)A at the dermal-epidermal junction.1 Idiopathic, systemic disease-related and drugrelated types of this disorder have been described so far. 1,2 We report the first case of LABD possibly associated with mefenamic acid, which is well known to induce commonly fixed drug eruptions.A 69-year-old Japanese woman presented with multiple blisters and erosions on her trunk, hip and thighs. She first noticed the skin eruption after taking mefenamic acid for 7 days for treatment of a common cold and the skin lesions were only a few blisters at the beginning. She visited a dermatology practitioner and a diagnosis of fixed drug eruption by mefenamic acids was made. Thus, she was given an oral antihistaminic drug and topical corticosteroid ointment. However, the eruption exacerbated and she was then referred to our clinic. Physical examination revealed some tense bullae and edematous erythema with vesiculobullae and erosions arranged annularly on her trunk, hip, thighs and upper extremities (Fig 1a,b). Mucosal lesions were not found in mucous membranes and there were no scars and milia. History taking revealed that the patient had experienced a similar eruption after taking mefenamic acids approximately 7 years before visiting us. Histological examination showed a subepidermal blister with a dense inflammatory infiltrate of lymphocytes, neutrophils and eosinophils in the edematous superficial dermis. Acantholysis and papillary abscess were not seen. All the laboratory data obtained were within normal limits.Direct immunofluorescent study revealed linear deposits of IgA and IgG at the basement membrane zone (BMZ) (Fig 1c,d). Indirect immunofluorescence found anti-BMZ antibodies: IgA (titer 1:160) and IgG (titer 1:160). Also, indirect immunofluorescence on 1 mol⁄ L NaCl-split human skin sections demonstrated that both IgA and IgG antibodies reacted with the epidermal side of the split (data not shown). Immunoblot analysis with human epidermal extracts failed to detect a clear band (data not shown). Enzyme-linked immunosorbent assays (ELISA) for both BP180 and BP230 were negative.We made a diagnosis of LABD based on clinical observations and immunological results. Also, we suspected mefenamic acid as a causative drug. We started treatment of 25 mg ⁄ day prednisone and the patient showed good response when we tapered prednisone.Linear IgA bullous dermatosis is an acquired immune-mediated subepidermal blistering disease characterized by circulating IgA autoantibodies, and now the soluble 120-kDa (LAD-1) ⁄ 97-kDa (LABD97) ectodomain of BP180 is the major target of the IgA antibodies. This condition is currently classified as a pemphigoid disease, which also includes bullous pemphigoid, pemphigoid gestationis and mucous membrane pemphigoid.3 It is well known that LABD sometimes shows an antigenic het...