Coelho, S

Figueiredo, A

Mariano, A

Reis, JP

Tellechea, O

Repositório Institucional dos Hospitais da Universidade de Coimbra

© 2006 The International Society of Dermatology International Journal of Dermatology 2006, 45, 982–983995Correspondence4 Simonart T, Noel JC, Van Vooren JP, et al. Role of viral agents in the pathogenesis of Kaposi’s sarcoma. Dermatology 1998; 196: 447–449.5 Guttman-Yassky E, Cohen A, Kra-Oz Z, et al. Familial clustering of classic Kaposi’s sarcoma. J Infect Dis 2004; 189: 2023–2026.6 Monti M, Mancini LL, Ceriani R, et al. Iatrogenic Kaposi’s sarcoma and HCV infection. J Eur Acad Dermatol Venereol 2004; 18: 191–193.7 Montella M, Serraino D, Crispo A, et al. Infection with human herpes virus type 8 in an area at high prevalence for hepatitis C virus infection in southern Italy. J Viral Hepat 2004; 11: 268–270.45Correspondence95 96Vancomycin-associated linear IgA bullous dermatosis mimicking toxic epidermal necrolysisDear Sir,Linear IgA bullous dermatosis (LABD) is an auto-immunevesiculobullous disease with an often misleading clinicalpicture. Although most reported cases are idiopathic, drug-induced disease may rarely occur. Both forms of LABD haveindistinguishable clinical, histological, and immunofluores-cence features. The clinical presentation is heterogeneous andcan resemble dermatitis herpetiformis, bullous pemphigoid,cicatricial pemphigoid, pemphigus vulgaris, erythema multi-forme, lichen planus, and rarely toxic epidermal necrolysis(TEN). Identification of linear IgA deposition at the basementmembrane zone on direct immunofluorescence is essentialto diagnosis. We describe an exuberant case of LABD toVancomycin presenting as TEN.Case reportA 67-year-old woman was transferred to our departmentbecause of a bullous dermatosis of 3 days’ evolution. Thepatient had been hospitalized in another hospital for 2 weeksowing to pneumonia and received a 10-day course of vanco-mycin, subsequently substituted for meropenem. Cutaneouslesions started abruptly 3 days after stopping vancomycin,presenting as tense bullae with a symmetric distribution on thearms, hands (Fig. 1), breasts, back, lower legs, buttocks, andperineum. Most of the bullae had a surrounding erythema, andon the trunk were associated with annular maculo-papules.There was no mucous or ocular involvement. The patientcomplained of a burning sensation and denied pruritus. Duringthe following 72 h extensive erosions progressed (Fig. 2)with a positive Nikolsky sign obtained at their periphery.The patient was on chronic prednisolone (30 mg/day) owingto rheumatoid arthritis, and besides being blind had no otherrelevant medical antecedents. We diagnosed TEN. The patientwas in good general condition and the relevant laboratorialchanges were leucocytosis (19.5 g/L) with 93% neutrophilsand anemia (8.3 g/dL). Oral prednisolone and meropenem weremaintained and endovenous methylprednisolone (500 mg) wasadministered. On the next day the patient had maintained agood general condition although new lesions had occurredand there was progression of erosions covering 40% of bodysurface. Microscopic examination of the frozen section ofa blister roof showed a normal epidermis. Toxic epidermalnecrolysis was therefore excluded and linear IgA bullousdermatosis to vancomycin seemed the probable diagnosis.This was confirmed by direct immunofluorescence (DIF) onperilesional skin, which revealed a linear IgA deposition atthe basement membrane zone. Histology of the lesionalskin exposed a subepidermal blister with a superficial dermalinflammatory infiltrate composed of polymorphonuclearFigure 1 Hand with tense bullae within erythematous plaquesFigure 2 Back showing annular maculo-papules and major exfoliation leaving areas of denudated skinInternational Journal of Dermatology 2006, 45, 982–983 © 2006 The International Society of Dermatology996 Correspondenceneutrophils, mononuclear cells, and some interspersedeosinophils. Prednisolone was maintained at the same dosageand topical betametasone was initiated. Five days afterbeginning the dermatosis no new lesions had developed andthe eruption had completely resolved in 2 weeks withoutscarring. Meropenem was suspended on the ninth day ofdermatosis owing to the favorable pulmonary evolution.DiscussionThe interest of this case report is the unusual clinical presen-tation suggesting TEN. Although vancomycin is the mostfrequently involved agent in drug-induced LABD, this formof presentation has been rarely reported.1–4 A similar case wasdescribed with phenytoin,5 and there are a few reports ofidiopathic LABD mimicking Stevens–Johnson syndrome6 andTEN.7,8 When the later is suspected the microscopic examina-tion of the frozen section of a blister roof is helpful to confirmfull-thickness epidermal necrosis. On drug-induced disease, ifthe suspected agent is interrupted a spontaneous remission oflesions is noticed and IgA deposits will also disappear. Thisevolution is not observed in the idiopathic form.Polymorphous clinical and immunopathologic featuresof this dermatosis can be partially explained by the differenttarget antigens identified on Western blotting, namely collagentype VII9 and antigens of 97 kDa and 230 kDa.10This case demonstrates the benignity of drug-induced LABD,even in cases presenting as a severe bullous eruption.Sónia Coelho, MDOscar Tellechea, MD, PhDJosé Pedro Reis, MDAngelina Mariano, MDAmérico Figueiredo, MD, PhDUniversity Hospital, Coimbra, PortugalReferences1 Mofid MZ, Costarangos C, Bernstein B, et al. Drug-induced linear immunoglobulin A bullous disease that clinically mimics toxic epidermal necrolysis. J Burn Care Rehabil 2000; 21: 246–247.2 Hughes AP, Callen JP. Drug-induced linear IgA bullous dermatosis mimicking toxic epidermal necrolysis. Dermatology 2001; 202: 138–139.3 Dellavalle RP, Burch JM, Tayal S, et al. Vancomycin-associated linear IgA bullous dermatosis mimicking toxic epidermal necrolysis. J Am Acad Dermatol 2003; 48: S56–S57.4 Waldman MA, Black DR, Callen JP. Vancomycin-induced linear IgA bullous disease presenting as toxic epidermal necrolysis. Clin Exp Dermatol 2004; 29: 633–636.5 Tran D, Kossard S, Shumack S. Phenytoin-induced linear IgA dermatosis mimicking toxic epidermal necrolysis. Australas J Dermatol 2003; 44: 284–286.6 Schneck B, Termeer C, Mockenhaupt M, et al. Linear IgA dermatosis in an adult with clinical signs of Stevens-Johnson syndrome. Hautarzt 1999; 50: 288–291.7 Abreu A, Bowers K, Mattson DH, et al. Linear IgA bullous dermatosis in association with multiple sclerosis. J Am Acad Dermatol 1994; 31: 797–799.8 Buchvald J, Filo V, Horvathova J. IgA-linear dermatosis imitating Lyell syndrome. Bratisl Lek Listy 1987; 88: 211–217.9 Wakelin SH, Allen J, Zhou S, et al. Drug-induced linear IgA disease with antibodies to collagen VII. Br J Dermatol 1998; 138: 310–314.10 Paul C, Wolkenstein P, Prost C, et al. Drug induced linear IgA disease: Target antigens are heterogeneous. Br J Dermatol 1997; 136: 406–411.45CorrespondenceTuberculosis – CSVVPanayiotis S.G. et al.96 98Cutaneous small vessel vasculitis and pulmonary tuberculosis: an unusual associationCutaneous small vessel vasculitis (CSVV) may present as“palpable” purpura, erythema, urticaria, bullae, or skininfraction leading to ulceration. Causative factors vary.1Mycobacterium tuberculosis is a rather uncommon etiologicagent for CSVV. Our case report deals with the infrequentcoexistence of pulmonary tuberculosis (PT) and CSVV.2A 39-year-old Greek man presented to our hospitalwith a 3-month history of an eruption located mainly on thelegs, which began with the appearance of erythema progress-ing to sparse palpable purpuric macules. Medical historyrevealed a low-grade fever, a slight nonproductive cough anda weight loss of 5–8 kg over the last 5 months. There was non-associated medication use. Initial investigations showed anerythrocyte sedimentation rate of 68 nm/h and a white cellcount of 12,650-cells /mL. Blood chemistries and urine anal-ysis were normal. Antinuclear antibodies, anti-DNA, anti-Sm, anti-Ro, anti-La, anticardiolipin, lupus anticoagulant,cytoplasmic, and perinuclear antineutrophil antibodieswere all negative. C-reactive protein, cryoglobulins, and com-plement levels were found within normal ranges. Immu-noglobulins fraction revealed a slight elevation of IgG andIgA. The viral serology was negative for hepatitis B, C, andacquired human immunodeficiency virus. Chest X-raysshowed calcificated lymph nodes and a few confluent opac-ities in the upper pulmonary segments. The skin purified pro-tein derivative (PPD) test was positive (indurations of 14 mm)and the Ziehl – Nielsen staining of the sputum was positivefor acid-fast bacilli. Sputum culture eventually grewMycobacterium tuberculosis. Skin biopsy from a recentpurpuric lesion showed perivascular polymorphonuclearinfiltration in the upper dermis with extravasation of eryth-rocytes, fibrinoid necrosis of dermal vessels and presence of

Vancomycin-associated linear IgA bullous dermatosis mimicking toxic epidermal necrolysis.

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