Abstract

We read with interest the article by Plunkett et al1Plunkett RW Chiarello SE Beutner EH Linear IgA bullous dermatosis in one of two piroxicam-induced eruptions: a distinct direct immunofluorescence trend revealed by the literature.J Am Acad Dermatol. 2001; 45: 691-696Abstract Full Text PDF PubMed Scopus (41) Google Scholar reporting 2 cases of proxicam-induced bullous eruptions, one of which was linear IgA bullous dermatosis (LABD). We would like to add our experience of one patient who had LABD provoked by acetaminophen, which has not been reported as an inducing agent before. A 42-year-old woman presented with pruritic erythematous macules and blisters extending from her legs to her back and head. She indicated that she had received acetaminophen (500 mg, twice daily) for upper respiratory tract infection 2 days before the onset of the lesions. Examination revealed confluent tense vesicles and bullae overlying sharp-bordered erythematous macules and papules (Fig 1). Nikolsky's sign was not present. Mucous membranes were spared. Her white blood cell count reached 12.5 × 109/L, and eosinophils were increased (40%; total count, 4 × 109/L). Routine histologic examination of a new lesion revealed a subepidermal bulla, filled with serous fluid and fibrin. In the dermis, there was a dense infiltration of neutrophils, eosinophils, and lymphocytes, which were pronounced in perivascular areas. Neutrophilic abscess formation was determined in the papillary dermis. Direct immunofluorescence of perilesional skin was strongly positive for IgA in a linear pattern at the basement membrane zone, consistent with LABD (Fig 2). Fig. 2Dense IgA deposition in basement membrane zone.View Large Image Figure ViewerDownload Hi-res image Download (PPT)IgG, IgM, and C3 were not present. Fibrin deposition was observed in the junctional separation area. We treated the patient with oral dapsone (150 mg/d) and topical prednicarbate cream. During the next 4 days, no new lesions developed. When complete resolution of lesions was achieved on the 15th day of the treatment, acetaminophen (500 mg/d) was reinstituted. On the second day of the acetaminophen challenge, multiple blisters and vesicles, essentially of the same severity and localization seen at initial presentation, developed. Acetaminophen was discontinued and dapsone was reinstituted. In 3 days, complete resolution of lesions occurred. Although most of the recent case reports focus on drug-induced LABD cases, the idiopathic form may be just as common. Drug-induced LABD has been reported in association with vancomycin, somatostatin, rifampin, captopril, trimethoprim, sulfamethoxazole, phenytoin, atorvastatin, piroxicam, lithium carbonate, amiodarone, cyclosporine, interleukin 2, cefamandole naftate, diclofenac, glibenclamide, furosemide, and vigabatrin.1Plunkett RW Chiarello SE Beutner EH Linear IgA bullous dermatosis in one of two piroxicam-induced eruptions: a distinct direct immunofluorescence trend revealed by the literature.J Am Acad Dermatol. 2001; 45: 691-696Abstract Full Text PDF PubMed Scopus (41) Google Scholar, 2Kuechle M Stegemeir E Maynard B Gibson LE Leiferman KM Peters MS Drug-induced linear IgA bullous dermatosis: report of six cases and review of the literature.J Am Acad Dermatol. 1994; 30: 187-192Abstract Full Text PDF PubMed Scopus (193) Google Scholar, 3König C Eickert A Scharfetter-Kochanek K Krieg T Hunzelmann N Linear IgA bullous dermatosis induced by atorvastatin.J Am Acad Dermatol. 2001; 44: 689-692Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar Both idiopathic and drug-induced LABD are heterogeneous in clinical presentation.4Geissman C Beylot-Barry M Doutre MS Beylot C Drug-induced linear IgA bullous dermatosis.J Am Acad Dermatol. 1995; 32: 296Abstract Full Text PDF Scopus (36) Google Scholar Drug-induced LABD may appear by breaking self-tolerance to the implicated potential antigens located in the lamina lucida and sub-lamina densa regions by a hapten-mediated process. An alternative explanation for the pathogenesis of the drug-induced LABD is the structural modification of protein molecules or the emergence of a previously hidden antigenic determinant by the drug leading to an immune response.5Klein PA Callen JP Drug-induced linear IgA bullous dermatosis after vancomycin discontinuance in a patient with renal insufficiency.J Am Acad Dermatol. 2000; 42: 316-323Abstract Full Text Full Text PDF PubMed Google Scholar Although in idiopathic LABD the course is more severe, drug-induced LABD cases can be treated by the withdrawal of the implicated drug.2Kuechle M Stegemeir E Maynard B Gibson LE Leiferman KM Peters MS Drug-induced linear IgA bullous dermatosis: report of six cases and review of the literature.J Am Acad Dermatol. 1994; 30: 187-192Abstract Full Text PDF PubMed Scopus (193) Google Scholar As Plunkett et al1Plunkett RW Chiarello SE Beutner EH Linear IgA bullous dermatosis in one of two piroxicam-induced eruptions: a distinct direct immunofluorescence trend revealed by the literature.J Am Acad Dermatol. 2001; 45: 691-696Abstract Full Text PDF PubMed Scopus (41) Google Scholar suggested for the drug-induced cases, we observed no IgG deposition in our case and, to our knowledge, this is the first report of LABD induced by acetaminophen.

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