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Sir, Bullous pemphigoid (BP) is a relatively common autoimmune skin disease characterized by blister formation, eosinophilia, chronicity and a relatively old age of onset (1). Drugs, including penicillin (2), may trigger BP, but this is a far less common event than drug-induced pemphigus vulgaris (1). The literature describes no clinical or laboratory features that distinguish idiopathic and drug-induced BP; however, a detailed patient history is essential. The chronology of drug intake and development of disease, and the observation that patients with drug-induced BP are often younger than patients with idiopathic disease (3) is supportive of this diagnosis. The prognosis of druginduced BP is good, provided that the drug is withdrawn early in the course of the disease (3). CASE REPORT An 80-year-old man with Parkinson’s disease, with no previous atopic diseases or contact dermatitis, but with a known history of adverse cutaneous reactions to penicillin, was mistakenly treated with penicillin for an infection of a traumatic wound. Two MIU penicillin G was given in the emergency room and oral penicillin V (1 MIU) was prescribed. After the first dosage of penicillin V (phenoxymethylpenicillin, Nycomed, Denmark), taken at home, he developed a rash. His family physician stopped penicillin treatment and gave erythromycin instead. Seven days after the last penicillin administration the exanthema became bullous, and the patient was admitted. The previous reaction to penicillin was in the 1950s in Africa. No records about the incident were available, and the patient failed to recall any details. Clinically he had an itchy generalized maculo-papular rash confluent in the loins, over the knees and forearms with scattered widespread large vesicles, small tense bullae with serous exudate and denuded areas at the trunk and extremities. A 4-mm punch biopsy from the chest showed a slightly smudged dermo-epidermal interphase with focal subepidermal blistering. A few eosinophils were scattered within the epidermis, and in the papillary dermis a mixed inflammatory infiltrate of eosinophils, lymphocytes and neutrophils was seen. Direct immunofluorescence showed linear deposits of IgG and C3 along the basement membrane zone, but no deposits of other immunoglobulins including IgE. The histopathological diagnosis was BP. Blood analyses showed elevated CRP (54 mg/ml) and leukocytes (13.6610 9 /l). Eosinophils were increased from 0.41610 9 /l on admission to 1.07610 9 /l during hospitalization. Kidney and liver function were not affected. Specific IgE and histamine release were measured routinely prior to investigation for penicillin allergy (Table I). Total IgE was not measured. Three weeks later the patient was tested. Skin prick tests were performed with penicillin G, benzyl penicilloylpolylysine and minor determinant mixture (BPO-PL & MDM, AllergopenH, Allergopharma, Reinbek, Germany), carbidopa/levodopa, hydroxyzine HCl, paracetamol and erythromycin. All tests were negative. Intradermal tests with penicillin V, BPO-PL, MDM and erythromycin were also negative. Patch tests using routine procedure with Finn chambers on Scanpore were performed with penicillin G, ampicillin trihydrate, amoxicillin trihydrate, dicloxacillin sodium salt hydrate, cefotaxime sodium salt (all at 10% petrolatum). Also, hydroxyzine HCl (1% pet.), cefuroxime (30% pet.), carbidopa/levodopa (25 mg/100 mg, 30% pet.), paracetamol (30% pet.) and erythromycin (10% pet.). The tests were read according to ICDRG guidelines and the positive results are shown in Table II. The patient did not consent to biopsy of the patch test reactions or to any further investigations. In BP, systemic drug challenge is considered to be contraindicated except for vital indications, so no further investigations were performed.

Drug-induced Bullous Pemphigoid with Positive Patch Test and in vitro IgE Sensitization