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Fulminant Liver Failure Associated with Clarithromycin

Chief Resident, Department of Internal Medicine, University Hospital, Basel, Switzerland

Markus H Heim, MD

Head, Hepatology Unit, Division of Gastroenterology, University Hospital, Basel

Urs Eriksson, MD

Resident, Division of Intensive Care, University Hospital, Basel

Stephan Marsch, MD

Head, Division of Intensive Care, University Hospital, Basel

Luigi Terracciano, MD

Head, Liver Pathology Unit, Department of Pathology, University Hospital, Basel

Stephan Krähenbühl, MD PhD

Head, Division of Clinical Pharmacology & Toxicology, University Hospital, Basel

Reprints: Stephan Krähenbühl MD PhD, Clinical Pharmacology & Toxicology, University Hospital, Petersgraben 4, CH-4031 Basel, Switzerland, FAX 41-61-265 45 60, E-mail kraehenbuehl{at}uhbs.ch

OBJECTIVE: To report a patient developing fulminant liver failure while being treated with clarithromycin for pneumonia.

CASE SUMMARY: A 58-year-old white woman developed fulminant liver failure while being treated with the macrolide antibiotic clarithromycin for pneumonia. Comedication included N-acetylcysteine, atenolol, and isradipine. Other causes of liver failure, such as viral hepatitis, autoimmune hepatitis, toxins, and heart failure, were excluded by appropriate diagnostic means. All drugs were stopped, and the patient was transferred to another hospital for liver transplantation. She recovered spontaneously within several days, making transplantation unnecessary. A liver biopsy obtained 10 days after the initial presentation revealed centroacinar necrosis and beginning fibrous reorganization, compatible with recent centroacinar damage.

DISCUSSION: Since no other cause could be identified, liver injury was considered to be drug related. Fulminant liver failure has not previously been described with concomitant use of atenolol and N-acetylcysteine. Although isradipine has been associated with hepatocellular injury, there are no reports of fulminant liver failure with this agent, and our patient had been treated for >2 years without signs of toxicity. The most likely cause of liver failure in this patient was, therefore, clarithromycin, which undergoes hepatic metabolism and has been reported to cause fulminant hepatic failure. A second possibility is an interaction between clarithromycin and isradipine, potentially increasing the hepatic toxicity of isradipine.

CONCLUSIONS: Clarithromycin may be a cause of fulminant liver failure either alone or by inhibiting the metabolism of other drugs.

Key Words: clarithromycin, fulminant liver failure, isradipine

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