On 15 April 1999, a 78-year-old man was admitted to our hospital with icteric acute hepatitis. His medical history revealed Parkinson disease that was being treated with levodopa and pergolide and a major depression episode that had been treated with electroconvulsive therapy 2 months before admission. On 6 March, he had begun receiving venlafaxine at an initial dosage of 37.5 mg/d; this was increased to 150 mg/d on 9 April. Abdominal ultrasonography showed no anatomic abnormalities. In sharp contrast to his previous normal liver chemistry analysis, his liver function at admission showed the following abnormalities: alanine aminotransferase level, 3.97 µkat/L (normal < 1.08 µkat/L); aspartate aminotransferase level, 4.36 µkat/L (normal < 0.62 µkat/L); -glutamyltransferase level, 12.17 µkat/L (normal < 1.42 µkat/L); alkaline phosphatase level, 11.33 µkat/L (normal < 2.27 µkat/L); total bilirubin level, 87 µmol/L (normal < 17.1 µmol/L); and direct bilirubin level, 86 µmol/L (normal < 5.5 µmol/L). Serologic tests for hepatitis A, B, and C yielded negative results.

While venlafaxine therapy was progressively discontinued (the patient still received his regular therapy), the patient’s health gradually improved. This improvement is supported by the fact that his liver function test results returned to normal within 5 weeks.

We conclude that it is well justified to identify venlafaxine as the culprit in the patient’s acute liver toxic insult. We excluded all other possible causes of toxic hepatic injury, and liver function returned to normal after discontinuation of venlafaxine therapy. We concur with Horsmans and colleagues and strongly support their recommendation that patients taking venlafaxine be regularly monitored for liver function.