Histopathologic analysis of suspected amiodarone hepatotoxicity

• Published in: Human pathology Vol. 21; no. 1; pp. 59 - 67
• Main Authors: Lewis, James H., Mullick, Florabel, Ishak, Kamal G., Ranard, Richard C., Ragsdale, Bruce, Perse, Randy M., Rusnock, Eileen J., Wolke, Anita, Benjamin, Stanley B., Seeff, Leonard B., Zimmerman, Hyman J.
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 1990; Elsevier
• Subjects: Adolescent; Adult; Aged; Aged, 80 and over; Amiodarone - adverse effects; amiodarone hepatotoxicity; Biological and medical sciences; Cardiovascular system; Chemical and Drug Induced Liver Injury; Diagnosis, Differential; drug-induced liver disease; Female; Humans; Liver - pathology; Liver - ultrastructure; Liver Diseases - diagnosis; Liver Diseases - pathology; Liver Diseases, Alcoholic - diagnosis; Liver Diseases, Alcoholic - pathology; Male; Medical sciences; Middle Aged; Pharmacology. Drug treatments; pseudo-alcoholic hepatitis; pseudo-alcoholic hepatitis; amiodarone hepatotoxicity; drug-induced liver disease; Human; Pathology; Liver function; Treatment; Toxicity; Liver; Cardiovascular disease
• ISSN: 0046-8177; 1532-8392
• DOI: 10.1016/0046-8177(90)90076-H

This analysis of the morphology of suspected amiodarone (AD) liver disease is based on a study of liver specimens from 17 individuals. Changes similar to alcoholic liver injury were commonly seen. Steatosis, both macrovesicular and microvesicular, was the most frequent histopathologic feature. Ballooming of hepatocytes, Mallory bodies, and fibrosis were also common. Other changes included nuclear unrest, acidophilic bodies, foam cells, glycogenated nuclei, and portal inflammation. Characteristic lamellar lysosomal inclusion bodies representing phospholipidosis were found in two of 14 specimens studied ultrastructurally. These changes of pseudoalcoholic hepatitis and/or phospholipidosis were present in liver specimens from asymptomatic, anicteric patients with mild elevations in serum aminotransferase or alkaline phosphatase values with or without hepatomegaly, as well as in patients with clinically overt symptoms of hepatotoxicity. Phospholipidosis appears to be a generalized systemic effect of cationic amphophilic compounds, such as AD. The cytotoxic pseudoalcoholic changes appear to be an independent phenomenon in susceptible patients, whom we speculate may have been unable or less able to metabolize AD through normal pathways. The true incidence of hepatic injury from AD remains to be determined from prospective evaluations of pretreatment and follow-up liver biopsies.