Clopidogrel
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Liver damage: case report A 78-year-old man developed liver damage during treatment with clopidogrel for ST-elevation myocardial infarction (STEMI). The man, who had STEMI, successfully been treated by alteplase. Thereafter, he had undergone angiography and angioplasty on the left anterior descending artery (LAD) with a drug-eluting stent on the next day. Later, he was discharged home in a stable condition and started on medications including clopidogrel 75mg tablet daily [route not stated], aspirin [ASA], carvedilol, captopril, pantoprazole and warfarin. Forty days after the angioplasty, he again presented with complaints of itching, icterus and decreased appetite. He did not have a recent history of abdominal pain, fever, weight loss, nausea, vomiting, urine or stool discoloration, or bleeding from any site in the body. Also, he did not have a past drug history. On physical examination, he did not appear ill or toxic, his vital signs were found to be stable with good general condition except icterus and loss of appetite. No abnormalities were found on cardiac and neurological examinations. The abdomen was soft without a sign of ascites or organomegaly and stigmata of chronic liver disease. Therefore, a gastrointestinal consultation was requested. The serological and immunological tests for hepatitis A, B, C, and E, and tumor markers were found to be negative. Abdominopelvic ultrasound revealed no lesions. Magnetic resonance cholangiopancreatography (MRCP) showed normal wall thickness and appearance of the gall bladder, without any lesions or filling defects with normal size and shape of the intrahepatic and extrahepatic biliary tracts. The pancreatic ducts were observed as normal. In view of the lack of anatomical lesions, a differential diagnosis of liver injury with a hepatocellular, cholestatic, or mixed pattern because of autoimmunity or drug-induced was considered. While considering his recent echocardiography, which showed improvement in his cardiac function without the presence of clots in the left ventricle, his medications were stopped due to the possibility to cause liver damage. So, unspecified statins were discontinued initially, followed by captopril and, lastly, warfarin. Regardless of discontinuation of medications, no improvement in his laboratory conditions were noted; however, an elevation in bilirubin level was observed with symptoms of jaundice. Therefore, the man’s clopidogrel treatment was switched to ticagrelor. Eventually, over the next 2 weeks, his jaundice improved and the laboratory results were found to be normal. Based on presenting symptoms and investigational findings, a diagnosis of clopidogrel-induced liver damage was confirmed [time to reaction onset not stated]. Thereafter, his medications other than clopidogrel were re-started slowly with 1 week of intervals in between and over a follow-up period of 2 months with normal general condition and laboratory findings. Eslami V, et al. Clopidogrel-induced liver damage: A case report and review of the literature. Clinical Case Rep
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