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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...

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Dear Editor, Morphea typically develops over the trunk in an asymmetrical pattern. The dose of methotrexate (MTX) when used in combination with prednisolone (PSL) for juvenile morphea ranges 0.3-0.4 mg/kg per week. 1 We have successfully used lower dose MTX in combination with PSL for the treatment of Figure 1. (a,b) Whitish and sclerotic plaques on bilateral lateral and medial malleoli with characteristic violaceous border (lilac ring). (c,d) Atrophic erythema on the dorsum of bilateral hands and feet. (e) No nail fold capillary changes. (f,g) A biopsy specimen from right lateral malleolus with lymphocytic perivascular infiltration in the reticular dermis, thickened collagen bundles expanding into the entire dermis and the subcutaneous fat, resulting in the disappearance of eccrine glands (hematoxylin-eosin, original magnifications: [f] 940; [g] 9100). (h) After 13 months, skin indurations had nearly disappeared. (a-d, h) The sclerotic lesions are surrounded by broken lines.

Postherpetic neuralgia (PHN) is the most common complication following acute varicella zoster virus infection. PHN is associated with chronic severe pain and is resistant to conservative management treatments. The purpose of this study was to evaluate the effect of 0.3-millisecond multi-pulsed 1064-nm Nd:YAG laser treatment on PHN. Five subjects were treated with 2 - 3 sessions at 2-week interval. After the treatments, reduced visual analog scale (VAS) scores were noted in all patients. Treatments showed no adverse or intolerant effects and all patients felt warmth and comfort during the therapy. We first reported treating PHN patients using 0.3-millisecond multi-pulsed 1064-nm laser Nd:YAG. The results showed remarkable improvements in pain. This laser treatment could be an alternative choice for PHN patients with intractable neuralgia