Acad Emerg Med 2002 Jan;9(1):75-7
Department of Emergency Medicine and Institute for Environmental Medicine, University of Pennsylvania Medical Center, Philadelphia, PA, USA.
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PMID: 11772674, UI: 21633511
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Ann Pharmacother 2001 Sep;35(9):1143-4
PMID: 11573872, UI: 21457799
Ann Pharmacother 2001 Sep;35(9):1142-3
PMID: 11573870, UI: 21457797
Ann Pharmacother 2001 Sep;35(9):1053-5
Institute of Internal Medicine, University of Siena, Italy. Giordanon@unisi.it
OBJECTIVE: To report a case of acute hepatitis resulting from the use of cyproterone acetate, an adjuvant treatment for prostate cancer. CASE SUMMARY: An 87 year-old white man, admitted to surgery for prostate cancer, received cyproterone acetate 300 mg/d orally and developed acute hepatitis, which initially was diagnosed clinically. A liver biopsy showed changes suggestive of acute cholestatic hepatitis. Cyprotorone was stopped immediately, and the patient was subsequently treated with corticosteroids. He then improved rapidly. DISCUSSION: Cyproterone acetate is thought to be well tolerated, but some authors have reported severe hepatic reactions, in particular acute hepatitis, fatal fulminant hepatic failure, and hepatocellular carcinoma. The above-mentioned hepatotoxicity represents an idiosyncratic drug reaction, probably due to the hepatomitogen action of cyproterone, causing an increase of hepatocytes expressing placental glutathione S-transferase, which are considered preneoplastic elements. CONCLUSION: This case suggests the possibility of hepatotoxicity from cyproterone.
PMID: 11573856, UI: 21457783
Ann Pharmacother 2001 Sep;35(9):1049-52
Department of Gastroenterology, Nahariya Hospital, B. Rappaport Faculty of Medicine, Technion, Israel. reshgs@naharia.health.gov.il
OBJECTIVE: To report the occurrence of nimesulide-induced acute hepatitis confirmed by biopsy and an in vitro lymphocyte toxicity assay. CASE SUMMARY: A 54-year-old Arabic woman treated with nimesulide for chronic low back pain was admitted to the hospital with acute hepatitis confirmed by biopsy. Her liver function test results returned to normal within one month after nimesulide discontinuation. An in vitro lymphocyte toxicity assay confirmed that the liver injury was due to nimesulide exposure. DISCUSSION: A case of acute hepatitis secondary to nimesulide, confirmed by biopsy and a laboratory in vitro assay, is described. Although the occurrence of clinically significant liver damage due to nonsteroidal antiinflammatory drugs (NSAIDs) is low, the enormous consumption of these drugs has made them an important cause of liver damage. Nimesulide, a relatively new NSAID commonly used in Europe, with a relative selectivity to cyclooxygenase type 2, can cause a wide range of liver injuries, from mild abnormal liver function to severe liver injuries. These effects are usually reversible on discontinuation of the drug, but occasionally can progress to fatal hepatic failure. CONCLUSIONS: Drug-induced acute hepatitis is a well-recognized adverse effect of many drugs, including nimesuilde. Identification of a drug as a cause for this life-threatening disease is important because the discontinuation of it may be life saving. This article confirms the occurrence of nimesulide-induced hepatitis. It also highlights the importance of monitoring liver function test results after initiating therapy with such a drug.
PMID: 11573855, UI: 21457782
Arch Dermatol 2002 Jan;138(1):129-31
PMID: 11790188, UI: 21650097
Arch Dermatol 2002 Jan;138(1):29-32
Department of Dermatology, Instituto Portugues Oncologia, 4200 Porto, Portugal. osvaldo.correia@netc.pt
BACKGROUND: Toxic epidermal necrolysis (TEN) is a rare but severe adverse drug disease, characterized by extensive skin and mucosal detachment with participation of different immunoinflammatory pathways, in particular with early participation of activated CD8+ T lymphocytes. OBJECTIVE: To further study the potential role of T lymphocytes in the early phase of keratinocyte necrosis. DESIGN: Prospective study. SETTING: University hospitals. PATIENTS: Thirteen patients with clinical and histopathologic criteria of TEN and 6 patients with second-degree burns. MAIN OUTCOME MEASURES: Measurement of soluble interleukin (IL) 2 receptor (sIL-2R) and IL-1alpha in serum samples and fluid of recent blisters. RESULTS: In the blister fluid of patients with TEN, we found significantly higher levels of sIL-2R than in patients with burns, whereas IL-1alpha levels were higher in the blister fluid of burned patients. No significant differences were found in serum samples of patients with TEN and burns, in either sIL-2R or IL-1alpha. In TEN we also found significantly higher levels of sIL-2R in the blister fluid compared with serum samples, pointing to a predominantly local production contrasting with the low concentration of sIL-2R in the blister fluid of burned patients. CONCLUSIONS: Our findings of elevated sIL-2R levels in blister fluid of patients with TEN are probably related to a local down-regulation of an immunologically mediated cytotoxic reaction and further support the involvement of activated T lymphocytes in the early blisters of TEN.
PMID: 11790164, UI: 21650073
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