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Ibuprofen-Induced Bullous Leukocytoclastic Vasculitis Kimberly A

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Ibuprofen-Induced Bullous Leukocytoclastic Vasculitis Kimberly A continuing medical education Ibuprofen-Induced Bullous Leukocytoclastic Vasculitis Kimberly A. Davidson, King of Prussia, Pennsylvania Franziska Ringpfeil, MD, Philadelphia, Pennsylvania Jason B. Lee, MD, New York, New York GOAL To discuss a case of ibuprofen-induced bullous leukocytoclastic vasculitis (LCV) OBJECTIVES Upon completion of this activity, dermatologists and general practitioners should be able to: 1. List the drugs implicated as causative agents of bullous eruptions. 2. Discuss the diagnosis of suspected drug-related bullous eruptions. 3. Describe the distinguishing characteristics that separate bullous LCV from other bullous eruptions. CME Test on page 308. This article has been peer reviewed and ACCME to provide continuing medical ed- approved by Michael Fisher, MD, Professor ucation for physicians. of Medicine, Albert Einstein College of Albert Einstein College of Medicine Medicine. Review date: March 2001. designates this educational activity for a This activity has been planned and im- maximum of 1.0 hour in category 1 credit plemented in accordance with the Essen- toward the AMA Physician’s Recognition tials and Standards of the Accreditation Award. Each physician should claim only Council for Continuing Medical Education those hours of credit that he/she actually through the joint sponsorship of Albert spent in the educational activity. Einstein College of Medicine and Quadrant This activity has been planned and HealthCom, Inc. The Albert Einstein produced in accordance with ACCME College of Medicine is accredited by the Essentials. A dramatic case of ibuprofen-induced bullous including bullous erythema multiforme, bullous leukocytoclastic vasculitis (LCV) is described in fixed drug eruption, linear IgA bullous dermatosis, a patient with a history of prior sensitization to and bullous pemphigoid. The distinctive histo- ibuprofen, a common household nonsteroidal anti- pathologic changes of leukocytoclastic vasculitis inflammatory drug (NSAID) that has few reported readily distinguish this bullous eruption from adverse skin reactions. Bullous LCV is a relatively the others. rare clinical presentation of LCV, which requires differentiation from other blistering diseases, eukocytoclastic vasculitis (LCV) has many dif- ferent clinical manifestations, including Ms. Davidson is from Jefferson Medical College, Thomas Jefferson University, King of Prussia, Pennsylvania. Dr. Ringpfeil is macules, papules, nodules, vesicles, bullae, and L 1 from Jefferson Medical College, Thomas Jefferson University, ulcers. The etiology of LCV is just as protean, which Philadelphia, Pennsylvania. Dr. Lee is from the Ackerman includes various infections, cryoglobulinemia, con- Academy of Dermatopathology, New York, New York. nective tissue diseases, and drugs.2 Bullae are a rela- Ms. Davidson is a medical student. Dr. Ringpfeil is an Assistant tively rare clinical presentation of LCV, which Professor in the Department of Dermatology and Cutaneous Biology. Dr. Lee is an Associate. requires differentiation from other blistering diseases, Reprints: Jason B. Lee, MD, 145 E 32nd St, 10th Floor, New York, including drug-induced blistering eruptions. A dra- NY 10016. matic case of ibuprofen-induced bullous LCV is VOLUME 67, APRIL 2001 303 IBUPROFEN-INDUCED BULLOUS LCV Figure 2. Close-up view of the bullae. turia. Complete blood count, blood urea nitrogen level, creatinine level, and liver function test results were all within normal limits. A punch biopsy revealed an intraepidermal blis- tering process (Figure 3) with a superficial and mid- Figure 1. Multiple bullae with surrounding purpura on dermal perivascular and interstitial infiltrate the thigh. composed of neutrophils and their nuclear dust. There were extravasated red blood cells and fibrin described in a patient with a history of prior sensiti- deposition around some of the vessels (Figure 4). Di- zation to ibuprofen, a common household non- rect immunofluorescence revealed deposits of IgM steroidal anti-inflammatory drug (NSAID) with few and IgA within the vessel walls consistent with reported adverse skin reactions. immune-complex–mediated vasculitis. A diagnosis of ibuprofen-induced bullous LCV was made based on Case Report the history and the temporal association with pres- A 65-year-old African American woman presented ence of no other etiology of LCV. The hepatitis A to the emergency department with a 5-day history of titer was assumed to be convalescent, as the patient a progressively worsening blistering eruption on the had no current or recent symptoms of hepatitis. The legs and arms bilaterally without systemic symptoms. patient was treated with oral prednisone starting at The patient had diabetes mellitus and hypertension, 60 mg a day and tapering over the subsequent 3 weeks. for which she was on insulin, furosemide, amlodip- The eruption cleared within that period. Some of the ine, enalapril, and potassium for the past several bullae healed with mild scarring. years. The only new medication she reported was Advil®, which she ingested 2 days prior to the erup- Comment tion, despite her history of an allergic rash to ibupro- Diverse heterogeneous bullous eruptions can be fen in the past. The patient was unaware that Advil induced by drugs, which include bullous erythema contained ibuprofen. On physical examination, she multiforme (EM), toxic epidermal necrolysis (TEN), had multiple tense hemorrhagic bullae with bullous fixed drug eruption, pseudoporphyria, bullous surrounding purpura on the lower extremities and lichen planus, and bullous LCV, as well as autoim- forearms bilaterally (Figures 1 and 2). There were few mune bullous diseases such as linear IgA bullous flaccid bullae, vesicles, and erosions on the extrem- dermatosis, pemphigus vulgaris, pemphigus foliaceus, ities. There was no mucosal involvement. The bullous pemphigoid, and epidermolysis bullosa ac- patient was afebrile, and her overwhelming com- quisita. A wide variety of drugs have been implicated plaint was pain. The laboratory studies were as the causative agents for these diverse group of bul- remarkable for elevated sedimentation rate and pos- lous eruptions (Table), but some drugs have been itive antibody titer for hepatitis A but not B and C. more frequently associated with specific eruptions Serial urinalysis results showed no evidence of hema- (eg, vancomycin and linear IgA bullous dermatosis, 304 CUTIS® IBUPROFEN-INDUCED BULLOUS LCV Figure 3. Biopsy specimen showing an intraepidermal Figure 4. Fibrin deposition within a vessel with neu- blister (H&E, original magnification ϫ50). trophils and eosinophils present around the vessel (H&E, original magnification ϫ400). sulfonamides and TEN, penicillamine and pemphigus fixed drug eruption is usually associated with a mixed- vulgaris). There are no specific tests that may pin- cell infiltrate of inflammatory cells (ie, with point a drug as the culprit. Therefore, most reported neutrophils and eosinophils), while EM is usually as- drug-induced eruptions are based on circumstantial sociated with lymphocytes and rarely with eosinophils evidence in which there is usually a history of inges- or neutrophils. In bullous EM, however, the conflu- tion of the suspected drug with resolution of the erup- ent necrosis of the epidermis is chemotactic for tion when the suspected drug is withdrawn. The neutrophils, and, thus adding to the difficulty in patch tests and in vitro tests, such as the lymphocyte distinguishing it from bullous fixed drug eruption. transformation test, macrophage migration inhibi- Bullous LCV also may be difficult to distinguish tion, and mast cell degranulation test, may support clinically from the aforementioned eruptions,16 but the association between the eruption and the sus- the histopathologic features readily distinguish bul- pected drug,3-7 but they do not provide definitive lous LCV from the other eruptions. Bullous LCV is evidence of the connection. A positive rechallenge a type III hypersensitivity reaction in which immune test with the suspected drug provides more definitive complex deposition in postcapillary venules results evidence that the drug is the culprit. The potential in a destructive inflammatory venulitis. The detrimental outcome to the patient, however, limits endothelial injury caused by immune-complex de- the use of the rechallenge test. position results in activation of the complement The clinical, histopathologic, and, in cases of au- cascade, resulting in an influx of inflammatory cells, toimmune bullous diseases, direct and indirect im- including eosinophils and neutrophils, which release munofluorescent characteristics can distinguish the proteolytic enzymes that damage the vessel walls.17,18 different types of drug-induced bullous eruptions. As the process progresses, leukocytoclasis, fibrinoid Clinically, at times, however, the eruptions are diffi- necrosis, and fibrin deposition within and around the cult to distinguish from one another, especially among affected vessels eventuate. Rarely, either an in- widespread bullous EM, fixed drug eruption, TEN, traepidermal or a subepidermal blister may form, the linear IgA bullous dermatosis, and bullous pem- former due to spongiosis and/or ballooning (intra- phigoid.8-10 Lyell demonstrated this difficulty in his cellular edema) of the epidermis, and the latter due landmark reports on TEN in which he erroneously to pronounced edema in the superficial dermis.19 A included a widespread bullous fixed drug eruption.11,12 subepidermal blister is more commonly encountered
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