www.pneumonologia.viamedica.pl PRACA ORYGINALNA 52 CASE REPORT Correspondence address: Correspondence address: Correspondence address: Correspondence address: Correspondence address: Krzysztof Gomulka M.D., Department of Internal Diseases, Geriatrics and Allergy, Medical University in Wroclaw, Traugutta St. 57/59, 50–417 Wroclaw, Poland, tel.: +48 71 733 2400, e-mail: kgomulka@wp.pl Received on 08 August 2010 Copyright © 2011 Via Medica ISSN 0867–7077 Krzysztof Gomułka 1 , Danuta Kuliczkowska 1 , Maria Cisło 2 , Zdzisław Woźniak 3 , Bernard Panaszek 1 1 Department of Internal Diseases, Geriatrics and Allergy, Medical University in Wrocław, Poland Head: Prof. B. Panaszek M.D., Ph.D. 2 Department of Dermatology, Venereology and Allergy, Teaching Hospital No 1 in Wrocław, Poland Head: Prof. E. Baran M.D., Ph.D. 3 Department of Pathology, Medical University in Wrocław, Poland; Head: Prof. J. Rabczyński M.D., Ph.D. Drug-induced hypersensitivity syndrome: a literature review and a case report Abstract Drug-induced hypersensitivity syndrome (DIHS) is characterised by fever, rash and an involvement of the internal organs, mainly the liver, myocardium, kidneys or lungs, which may develop within 1–8 weeks after exposure to the offending drug. An increase in body temperature is generally the first sign, followed by erythematous skin eruptions, although the severity of skin changes does not parallel the severity of internal organ involvement. It is believed that anti-epileptic drugs (particularly carbamazepine), antibiotics and allopurinol are the commonest causes of DIHS. The pathomechanism of the syndrome is unclear, although defects in the detoxification of reactive drug metabolites and genetic predisposition have been implicated. The diagnosis of DIHS is based on the characteristic manifestations triggered by the drug and may be supported by eosinophilia, elevated markers of inflammation and abnormal organ function tests, such as liver function tests. Management involves immediate discontinuation of all suspected drugs and initiation of glucocorticosteroids. We report the case of a 72 year-old female who developed manifestations of DIHS after about four weeks of treatment with an anti-epileptic drug (carbamazepine) for sensory axonal polyneuropathy. Discontinuation of the offending drug and initiation of systemic glucocorticosteroids resulted in resolution of the clinical manifestations. Key words: drug-induced hypersensitivity syndrome, carbamazepine, hepatitis Pneumol. Alergol. Pol. 2011; 79, 1: 52–56 Introduction Drug-induced hypersensitivity syndrome (DIHS) is characterised by a skin rash, elevated temperature and an involvement of the internal organs (mainly the liver and kidneys) with a pro- ved causal relationship between the drug and the manifestations. Bocquet et al. [cited in: 1–3] extended the de- finition and introduced the term DRESS (drug rash with eosinophilia and systemic symptoms). The most commonly implicated drugs include anti- epileptic drugs (mainly carbamazepine, phenyto- in, phenobarbitol, lamotrigine), antibiotics (mino- cycline, b-lactams, sulfonamides), antiviral agents (abacavir, nevirapine), dapsone, sulfasalazine, and allopurinol [3–6]. Callot et al. [cited in: 7] observed DIHS follo- wing treatment with diltiazem and mexiletine. The pathomechanism of the syndrome is unclear, al- though it is arbitrarily assumed that the drug-in- duced manifestations are associated with cytochro- me P450 dysfunction and the presence of biologi- cally reactive drug metabolites in the circulation [5, 7]. These metabolites may activate macropha- ges, eosinophils and T cells, which results in the release of cytokines, mainly IL-5 [3, 4]. Recent bi- bliographical data also suggests a possible reacti- vation of certain viruses in the course of DIHS, such as herpesvirus (HHV-6, HHV-7), Epstein-Barr virus (EBV) or cytomegalovirus (CMV), which is associated with the replication of viral DNA by the stimulated immunocompetent cells [2–5, 8]. The first manifestations of DIHS usually develop wi-