LETTERS from Archives of IM: Venlaxafine-Associated Hepatitis

[Robert Marshall <marshalr@OHSU.EDU>]

   LETTERS
   
  Venlafaxine-Associated Hepatitis
  
   Annals of Internal Medicine, 1 Jun 99
   
   To the Editor: Venlafaxine is a second-generation antidepressant agent
   approved for use in the United States in 1993 (1, 2). It is a derivative of
   phenethylanine and is structurally unrelated to first- and other
   second-generation antidepressant agents. Elevations of liver enzyme levels
   has rarely been described (2). We report the first case of acute hepatitis
   after venlafaxine administration.
   
   A 44-year-old woman was seen for acute hepatitis on 23 March 1998. Results
   of liver function tests done in September 1997 at the time of the
   introduction of venlafaxine therapy (150 mg/d) were normal. For several
   months the patient had also been taking lormetazepam and trazodone for her
   depression. She had undergone hysterectomy in 1996 for a fibroma. On 9 March
   1998, blood tests were performed by her general practitioner because of
   severe asthenia. Findings included an alanine aminotransferase level of 1082
   U/L (normal, <56 U/L) and an aspartate aminotransferase level of 661 U/L
   (normal, <40 U/L).
   
   When the patient was seen in our institution on 30 March, a similar
   perturbation in liver function test results was observed. Results of
   serologic tests for hepatitis, iron studies, antimitochondrial, and
   anti-smooth-muscle antibodies were normal or negative. Abdominal
   ultrasonography showed no abnormalities. Examination of a percutaneous liver
   biopsy specimen obtained on 9 April revealed well-demarcated zone 3
   confluent necrosis, with some inflammation and clumps of perivenular Kupffer
   cells containing lipid-rich ceroid pigment. The portal tracts were
   unaffected (Figure[20]). Venlafaxine therapy was then progressively
   discontinued because of the risk for withdrawal symptoms (3). The patient
   continued to receive lormetazepam and trazodone. Liver function test results
   progressively improved and returned to normal 4 months after discontinuation
   of venlafaxine therapy. The result of a second serologic test for hepatitis
   C performed in July 1998 was also negative.
   
   We believe that there was a causal association between venlafaxine and
   hepatitis because the histologic findings supported drug-related
   hepatotoxicity, other causes of hepatitis were excluded, discontinuation of
   venlafaxine therapy led to recovery, and venlafaxine can increase liver
   aminotransferase levels. Liver function test results should therefore be
   regularly monitored in patients receiving venlafaxine.
   
   Yves Horsmans, MD
   Michel De Clercq, MD
   Christine Sempoux, MD
   Cliniques Universitaires Saint Luc
   1200 Brussels, Belgium
   
   Reference
   
   1. Holliday SM, Benfield P. Venlafaxine. A review of its pharmacology and
   therapeutic potential in depression. Drugs. 1995;49:280-94.
   
   2. Morton WA, Sonne SC, Verga MA. Venlafaxine: a structurally unique and
   novel antidepressant. Ann Pharmacother. 1995;29:387-95.
   
   3. Johnson H, Bouman WP, Lawton J. Withdrawal reaction associated with
   venlafaxine. BMJ. 1998;317:787.
   
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