The functional and histological liver alterations induced by amiodarone treatment have been well known for some time and often consist in isolated increases in transaminase levels during long-term treatment. Secondary phospholipidosis was observed in these cases, an alteration which suggests the presence of toxic damage. Reports in the literature also indicate acute liver intoxication, including a number of fatal cases. This paper reports the finding of acute alterations of laboratory parameters indicative of hepatocytonecrosis with alterations of protein synthesis capacity following the first dose of the drug and which regressed after its suspension. On the basis of a review of the literature the authors propose that, in addition to a dose-dependent toxic mechanism, immunogenic or idiosyncratic mechanisms may also play a role in the onset and manifestation of acute liver intoxication by amiodarone.