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Amiodarone hepatotoxicity: Prevalence and clinicopathologic correlations among 104 patients
Author(s) -
Lewis James H.,
Ranard Richard C.,
Caruso Anthony,
Jackson Lawrence K.,
Mullick Florabel,
Ishak Kamal G.,
Seeff Leonard B.,
Zimmerman Hyman J.
Publication year - 1989
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840090504
Subject(s) - amiodarone , medicine , phospholipidosis , asymptomatic , toxicity , liver injury , pulmonary toxicity , drug , gastroenterology , hepatitis , cardiology , pharmacology , atrial fibrillation , phospholipid , membrane , biology , genetics
The prevalence of apparent amiodarone‐related hepatic injury in 104 patients followed prospectively is compared to that reported in the literature. Asymptomatic elevation of serum aminotransferase levels was detected in approximately one‐fourth of the patients, a figure similar to the average of reported cases. The frequency of extrahepatic organ toxicity was increased in patients with elevated levels. Symptomatic “hepatitis” developed in 3% of this series and in less than 1% of cases in the litérature. Evidence of hepatic phospholipidosis and the development of pseudoalcoholic liver injury is most likely due to the biochemical effects of the drug and to possible metabolic idiosyncrasy, respectively. Serial blood enzyme measurements, as recommended by the manufacturer, may offer some protection against the development of more serious liver injury. However, levels of amiodarone may persist in various tissues for weeks to months following withdrawal, and stopping the drug does not guarantee the prompt reversal of any organ toxicity. Accordingly, the risks posed and benefits offered by amiodarone should be carefully weighed prior to discontinuing the drug, as the risk of sudden cardiac death may outweigh the hazards of ongoing hepatic, pulmonary or other toxicity.