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Specialist in Family and Community Medicine Service of Internal Medicine Hospital de la Ribera Carretera de Corberá Km 1 s/n. 46600 Alzira, Valencia Spain vpalop{at}hospital-ribera.com
Specialist in Family and Community Medicine Palliative Care Unit Hospital de la Ribera
Specialist in Dermatology Service of Dermatology Hospital de la Ribera
Senior Researcher Medical Management University General Hospital Foundation Valencia University General Hospital
Published Online, October 1, 2003. www.theannals.com, DOI 10.1345/aph.1D033
Case Report. A 74-year-old woman was being treated on a chronic basis with ophthalmic drops of latanoprost, dorzolamide hydrochloride, and timolol maleate for glaucoma. The patient had a history of sulfonamide hypersensitivity, gonarthrosis, nephrolithiasis, repeated urinary infections, and an old duodenal ulcer. Due to exacerbation of the gonarthrosis, the patient was treated with rofecoxib 12.5 mg/d and tramadol 100 mg every 12 hours. Within 5 days of treatment, she noted erythematous lesions with itching on both legs that increased in number and size over time. After 15 days of treatment, the patient developed nausea, vomiting, and epigastric pain. She therefore decided to interrupt rofecoxib treatment. At this point, the patient sought emergency hospital care for the eruption on the legs, which she related to consumption of the above-mentioned drugs.
Physical examination revealed edema and confluent purpuric lesions on both legs (with necrosis of some of them) that failed to disappear in response to pressure. Laboratory tests showed complete blood cell count, biochemistry, and urinary sediment to be normal. On skin biopsy, leukocytoclastic vasculitis was diagnosed. Following withdrawal of rofecoxib and the introduction of corticosteroids, the skin lesions improved within 6 months, leaving residual pigmentary lesions. Tramadol was continued along with treatment of the skin lesions.
Discussion. According to the Naranjo probability scale, the vasculitis reported in our case exhibited a probable causal correlation to rofecoxib administration2: a clear temporal correlation was observed, the condition was unrelated to any concomitant medication, and no alternative cause was able to account for the microvascular disease. Furthermore, the biopsy results and favorable course after rofecoxib withdrawal likewise support the causal relation. Rechallenge with rofecoxib was not contemplated, due to the severity of the reaction.
Although no cases of vasculitis due to rofecoxib have been described in the literature to date, 19 cases of spontaneously reported suspected vasculitis related to rofecoxib have been identified in the World Health Organization database.3 On the other hand, the first case of fatal allergic vasculitis associated with celecoxib, another selective COX-2 inhibitor, has recently been reported.4 The authors suggested that such a reaction could have been triggered by at least 2 mechanisms: an allergic reaction linked to the sulfonamide moiety or activity upon systemic prostacyclin biosynthesis, shifting the metabolism of endothelial eicosanoids toward other vasoactive end products. The latter mechanism appears to be a common feature of the selective COX-2 inhibitors, which could explain vasculitis related to these drugs.5 Unlike celecoxib, rofecoxib does not possess a sulfonamide moiety, and we do not know how the history of sulfonamide hypersensitivity in this patient could have participated in the observed ADR.
References
This article has been cited by other articles:
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  M. Garcia-Cortes, M I. Lucena, P. J Andrade, R. Camargo, and R. Alcantara Is the Naranjo probability scale accurate enough to ascertain causality in drug-induced hepatotoxicity? Ann. Pharmacother., September 1, 2004; 38(9): 1540 - 1541. [Full Text] [PDF]
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