Abstract
H2 receptor antagonists can rarely cause idiosyncratic drug reactions leading to acute hepatitis. Famotidine, however, is considered a relatively safe drug with regards to hepatotoxicity. We report a case of a 47 year old male with a history of hepatitis C who developed acute hepatitis on the third day of hospitalization with a dramatic rise in his liver enzymes from normal values at the time of admission. The acute rise in liver enzymes made us consider an adverse drug reaction and famotidine was discontinued. Subsequently his liver enzymes came back to normal in seven days. Thus, physicians should consider famotidine induced hepatitis as a possible etiology of acute liver dysfunction.
Highlights
Drug-induced hepatic injury is a very common cause of hepatitis in adults
Hepatotoxicity can occur with many drugs through a variety of mechanisms and can present with an array of clinical presentations ranging from asymptomatic mild biochemical abnormalities to an acute illness that resembles viral hepatitis [2,3]
Current H2 receptor antagonists have been very rarely associated with idiosyncratic drug reactions leading to liver failure
Summary
Drug-induced hepatic injury is a very common cause of hepatitis in adults. Drug hepatotoxicity is the most common cause of fulminant liver failure in the United States [1]. Current H2 receptor antagonists have been very rarely associated with idiosyncratic drug reactions leading to liver failure. A 47 year old male with a past history of asymptomatic chronic Hepatitis C diagnosed 4 years ago, on no home medications, came to the hospital with chief complaints of right upper quadrant abdominal pain and vomiting for one day. His vital signs on admission were stable. (Figure 1) No further investigations were done on the patient as the temporal association of the administration of famotidine and elevation in liver enzymes combined with the response demonstrated after discontinuation of famotidine was very significant in this case The liver enzymes started improving from the day and were back to normal within the 7 days. (Figure 1) No further investigations were done on the patient as the temporal association of the administration of famotidine and elevation in liver enzymes combined with the response demonstrated after discontinuation of famotidine was very significant in this case
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