cephalosporins*

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Cephalosporins* Cholestatic jaundice: first report For 6 days, a 36-year-old woman with a history of acute bacterial infections received 1M cefazolin Ig once daily, oral cefadroxil Ig bid, as well as a 500mg mefenamic acid suppository once daily for acute febrile salpingitis. The patient did not drink alcohol, had no evidence of liver disease, diabetes, or allergy and was taking no drugs. Within 4 days she became afebrile and symptomless, but 2 days later she noted alcoholic stools with dark urine followed by increasing jaundice. She was admitted to hospital in good general condition without acute distress. Investigations revealed a normal liver, gallbladder and spleen but liver biopsy showed cenJrilobular cholestasis, mild portal infiltration with some eosinophils, but no evidence of liver cell necrosis. Haemoglobin was 13.4 gJdl with leucocyte counts of 7700-8800/1'1 « 7% eosinophils). Serum amylase was transiently elevated at 1150 U/L, but there was no evidence of pancreatitis. The patient received prednisone 40mg daily for 5 weeks, but on withdrawal of the corticosteroid her condition deteriorated. As an outpatient, she then received cholestyramine 15mg daily and phenobarbitone for 4 weeks and her condition gradually returned to normal. Subsequent skin tests with penicillin G, ampicillin, cefazolin and cefadroxil were negative, but a lymphocyte transformation stimulation test for cefazolin was This ·first reported case of typical intrahepatiC cholestasis with cepha\osporins eQuId have been caused by hypersensitivity rather than IOxic mechanisms affecting the liver tissue. Rechal1enge was considered unethicaL ·\n)mann. R. rt aL Lanc"1 2: 336 (7 Aug 1982) 0157-7271/82/0917-0003/0$01.00/0 © AOISPress Reactions 17 Sep 1982 3

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Page 1: Cephalosporins*

Cephalosporins*

Cholestatic jaundice: first report For 6 days, a 36-year-old woman with a history of acute bacterial infections received 1M cefazolin Ig once daily, oral cefadroxil Ig bid, as well as a 500mg mefenamic acid suppository once daily for acute febrile salpingitis. The patient did not drink alcohol, had no evidence of liver disease, diabetes, or allergy and was taking no drugs. Within 4 days she became afebrile and symptomless, but 2 days later she noted alcoholic stools with dark urine followed by increasing jaundice. She was admitted to hospital in good general condition without acute distress. Investigations revealed a normal liver, gallbladder and spleen but liver biopsy showed cenJrilobular cholestasis, mild portal infiltration with some eosinophils, but no evidence of liver cell necrosis. Haemoglobin was 13.4 gJdl with leucocyte counts of 7700-8800/1'1 « 7% eosinophils). Serum amylase was transiently elevated at 1150 U/L, but there was no evidence of pancreatitis. The patient received prednisone 40mg daily for 5 weeks, but on withdrawal of the corticosteroid her condition deteriorated. As an outpatient, she then received cholestyramine 15mg daily and phenobarbitone for 4 weeks and her condition gradually returned to normal. Subsequent skin tests with penicillin G, ampicillin, cefazolin and cefadroxil were negative, but a lymphocyte transformation stimulation test for cefazolin was po~itive. This ·first reported case of typical intrahepatiC cholestasis with cepha\osporins eQuId have been caused by hypersensitivity rather than IOxic mechanisms affecting the liver tissue. Rechal1enge was considered unethicaL ·\n)mann. R. rt aL Lanc"1 2: 336 (7 Aug 1982)

0157-7271/82/0917-0003/0$01.00/0 © AOISPress Reactions 17 Sep 1982 3