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Abstract
Bullous pemphigoid (BP) is an acquired autoimmune disease characterized by subepidermal vesicles and bullae. The etiology for BP is mostly idiopathic with the highest occurrence in elderly patients; however, it is now well-accepted that BP has been triggered by or associated with drug therapy. We present a case of furosemide-induced bullous pemphigoid and review the literature of drug-induced bullous pemphigoid (DIBP).
Introduction

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Bullous pemphigoid (BP) is an acquired autoimmune disease characterized by subepidermal vesicles and bullae. The specific antigens implicated in BP have been identified as BP antigen 2 (BP 180) and BP antigen 1 (BP230), components of the hemidesmosome and lamina lucida of the basement membrane. Histologically, BP demonstrates subepidermal bullous formation with numerous eosinophils. Direct immunofluorescence shows linear deposition of auto-antibodies (IgG) and complement along the basement membrane zone, specifically the hemidesmosome and upper lamina lucida. This is in contrast to the sublamina densa region targeted in epidermolysis bullosa acquisita. Indirect immunofluorescence demonstrates circulating anti-basement membrane zone IgG binding the epidermal side of salt-split human skin. Immunoblotting shows IgG antibodies binding the BP antigen 1 (230kDa) and BP antigen 2 (180 kDa).
Case Report
A 70-year-old Caucasian male presented with a 7-month history of recurrent blisters on bilateral lower legs. At the time of initial evaluation, he was on multiple medications including insulin, amiodarone, digoxin, losartan, metoprolol, lansoprazole, zolpidem, ferrous sulfate, cephalexin, and furosemide. He had been on furosemide on and off for many months, but had recently restarted upon developing blisters. At initial presentation, he was being treated for cellulitis of the lower extremities with cephalexin. His past medical history included diabetes mellitus, hypertension, hypercholesterolemia, coronary artery disease, ischemic dilated cardiomyopathy, and chronic renal insufficiency.
Physical examination revealed multiple tense bullae ranging from 0.5 cm to 1 cm (Figure 1). These were located on bilateral lower legs and were associated with erythema and leg edema. He also had a cellulitis of the lower legs. There was no involvement of the face, oral mucosa, chest, back, or arms. The patient was afebrile. The serum indirect immunofluorescence was negative for circulating pemphigoid-pemphigus antibody.
Diagnosis of furosemide-associated BP was made clinically. Furosemide was discontinued and the patient was switched to bumetanide. His bullous lesions were treated only with topical steroids, while the associated cellulitis was treated with oral and topical antibiotics. The bullous lesions resolved within 11 days and the patient has not had recurrence after 9 months.
Review of Literature
In 1970, the first case of drug-induced BP (DIBP) was reported by Bean et al. (1) This case described an 11-year-old boy who erupted in widespread bullae following salicylazosulfapyridine. This patient required systemic immunosuppressants and had a prolonged recovery course. Since this report, there have been multiple medications reported to cause BP or BP-like eruptions (Table 1). These medications include oral penicillamine, (2) ciprofloxacin, (3) amoxicillin, (4) sulphasalazine, (5) chloroquine, (6) ampicillin, (7) phenacetin, (8) captopril, (9) spironolactone, (10,11) terbinafine, (12) and serratiopeptidase. (13) BP-like eruption has also been reported with topical fluorouracil, (14) topical and oral iodide, (15) subcutaneous enoxaparin, (16) and PUVA phototherapy. (17,18)
[FIGURE 1 OMITTED]
The course of DIBP is not uniform. There appear to be 2 main types of eruptions. (7,19) The first is an acute, self-limited type with rapid resolution after withdrawal of the offending agent. Systemic corticosteroid therapy may not be necessary. This form has been termed “DIBP proper.” The second variant is a more chronic type that seems precipitated by a drug but the course is more consistent with classic, spontaneously occurring disease. This has been termed “drug-triggered BP.”
DIBP seems to demonstrate several features that differ from idiopathic BP. These include positive Nikolsky’s sign, (4,8,20) younger average age of patients, (7,19) distribution of bullae on normal-appearing skin (19) and lower leg areas, target lesions on palms and soles, (19) rapid improvement on systemic steroids, low or no recurrence, and more dense dermal eosinophilic infiltrates. (7,8,19) There may also be increased mucosal involvement, (20) eosinophilia, (21) and involvement of the face. (7)
Morphologic appearance ranges from large, tense bullae on an erythematous urticarial base, (22,23) to moderate involvement of oral mucosa, (6,19,20) to mild forms with a few bullous lesions without erythematous bases, to target lesions, (6,19) to scarred plaques and nodules with bullae or excoriations (papular and nodular pemphigoid). (24) Bullous erythema multiforme-like lesions have also been reported. (4,19)