A Case of Alcoholic Cirrhosis in a Teetotaler

1University of Michigan, Ann Arbor, Ml

Meeting: Hospital Medicine 2010, April 8-11, Washington, D.C.

Abstract number: 220

Case Presentation:

An 82‐year‐old female with a history of hypertension and paroxysmal atrial fibrillation presented as a transfer to our institution She presented with fatigue, a 10‐pound weight loss, and right upper quadrant abdominal pain lasting for 3 months. Her initial WBC count was 24,000, and alkaline phosphatase was elevated, prompting cholecystectomy with incidental finding of ascites and the appearance of cirrhosis. A liver biopsy was done and read as alcoholic cirrhosis. The patient and her daughter both confirmed that she never drank any alcohol. She developed acute renal failure requiring dialysis, right‐sided pneumonia, hepatic encephalopathy, and persistent leukocytosis. A noncontrast CT scan showed a hyperdense liver. The patient's prior liver testing was obtained, which showed minimal transaminitis delected 6 months prior to the onset of symptoms (AST 42, ALT 45, alkaline phosphatase 103). Labs here showed elevated AST (peak 51), normal ALT, and elevated alkaline phosphatase (range 269‐455) The patient continuec to have leukocytosis (WBC 19,000‐31,000), which was evaluated with paracentesis x 2, lumbar puncture, bone marrow biopsy, and lagged WBC scan, which did not identify the source of WBC elevation. A detailed medication history was obtained. The patient had been on amiodarone at 200 mg daily since September 2005 (approximately 4 years ‐ 292 g total). The pathology results were reread in our hospital showing cirrhosis with numerous Mallory bodies, suggestive of alcohol‐induced hepatitis. The pathologist believed that this was a result of amiodarone use given Ihe history. She was discharged to a rehabilitation center with requirement for chronic hemodialysis due to renal failure.


This case had many of the familiar elements of alcoholic hepatitis in a patient with baseline cirrhosis, such as leukocytosis, high AST‐to‐ALT ratio, and biopsy suggestive of alcoholic hepatitis and cirrhosis. However, a reliable clinical history of no alcohol use and the medication history led to an alternate diagnosis of pseudo‐alcoholic cirrhosis due to amiodarone. A hyperdense liver noted on CT scan can be a marker of excessive iodine deposition. This is known as phosholipidosis but is more a marker of amiodarone use than of disease. The patient's leukocytosis was unexplained, but this may have been from amiodarone‐induced hepatitis. Nonalcoholic fatty liver disease leading to cryptogenic cirrhosis cannot be excluded in this case, but the pathology strongly supporting an alcohol‐induced pattern and the lack of other risk factors for fatty liver (not diabetic, not obese) makes this less likely.


Amiodarone can cause several forms of liver disease (acute hepatitis, cholestasis, granulomatous hepatitis)\, but these are generally seen with higher doses or shortly after starting amiodarone. Low‐dose chronic amiodarone is a cause of cirrhosis with a pseudo‐alcoholic pattern and may carry a poor prognosis because of continued inflammation from deposited amiodarone in the liver.

Author Disclosure:

A. Berg, none.

To cite this abstract:

Berg A. A Case of Alcoholic Cirrhosis in a Teetotaler. Abstract published at Hospital Medicine 2010, April 8-11, Washington, D.C. Abstract 220. Journal of Hospital Medicine. 2010; 5 (suppl 1). https://www.shmabstracts.com/abstract/a-case-of-alcoholic-cirrhosis-in-a-teetotaler/. Accessed March 30, 2020.

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