Psychosomatics 42:440-441, October 2001
© 2001 The Academy of Psychosomatic Medicine
Severe Hypertriglyceridemia Secondary to Venlafaxine and Fluoxetine
Marshall Teitelbaum, M.D., Palm Beach Gardens, FL
Key Words: Venlafaxine • Fluoxetine
To the Editor: Chronic hypertriglyceridemia is a commonly seen disorder of familial etiology. This elevation is associated with cardiovascular consequences over time. Acute elevation in the serum triglyceride level can be caused by medication side effect, dietary changes, genetic predisposition, diabetes mellitus, obesity, and alcohol/substance abuse.1–5 Sudden severe increases in the serum triglyceride level can lead to more immediate medical consequences, such as pancreatitis. Selective serotonin-reuptake inhibitors (SSRIs) can occasionally have mild (statistically insignificant) effects on cholesterol and triglyceride level elevation per package inserts. There is only one case report of severe hypertriglyceridemia directly linked to SSRI or venlafaxine administration, however.6 I report here another case of severe elevation of serum triglycerides without apparent acute causal risk other than the separate use of fluoxetine and extended-release venlafaxine.
Case Report
Mr. B. is a 42-year-old white male who presented in May 2000 with severe social phobia associated with panic attacks, agoraphobia, and depressive disorder NOS. Paroxetine had been tried prior to our consultation and discontinued due to side effects. Routine nonfasting labwork, although requested to be drawn in a fasting state, was drawn on the same day as the assessment with the results indicative of a normal comprehensive metabolic panel, complete blood count, and thyroid profile. The lipid panel reflected slight elevation (triglyceride level of 261 mg/dL, cholesterol level of 215 mg/dL, and cholesterol:HDL ratio of 5.24), although the nonfasting nature of the test could have affected the outcome. Medical risk factors included mild obesity and tobacco use (one pack per day cigarette use) without the use of any regular medications or supplements except for a multivitamin. Alprazolam (0.25 mg up to three times/day) and fluoxetine (gradually increasing to 20 mg/day over 1 week) were recommended, with a taper of the alprazolam thereafter. The lipid profile was to be rechecked while fasting within 6 months.
Over this timeframe, fluoxetine was well tolerated, including an increase to 40 and 20 mg on alternate days. As of October 2000, Mr. B. described 80%–90% benefit in symptoms. The repeat testing of his lipid profile did not occur until December 2000, however.
Upon receiving the results (triglyceride level of 604 mg/dL, invalidating LDL results due a level over 400 as per the Quest Diagnostics laboratory report), I recommended fluoxetine discontinuation. Venlafaxine extended-release was begun 2 weeks later, increasing the daily dose weekly by 37.5 mg with a 37.5-mg daily starting dose, thus leading to a 150-mg daily dose by late January 2001. Mr. B. described symptom remission to be approximately 85% of that received while taking fluoxetine. Although well tolerated, a repeat lipid profile in late February 2001 demonstrated further triglyceride elevation (1,090 mg/dL) with a normal amylase level of 65 u/l.
The venlafaxine extended-release dose was discontinued over 10 days with the recommendation to use only alprazolam on a regular basis.
Labwork was rechecked 2 weeks after venlafaxine discontinuation. The triglyceride level was reduced to a safe level of 154 mg/dL, although still having an elevated total cholesterol and cholesterol:HDL ratio as he had initially (225 mg/dL and 6.25, respectively).
Discussion
Mr. B. is a 42-year-old male who developed acute significant hypertriglyceridemia apparently as a result of exposure to fluoxetine and later to venlafaxine extended-release, both within moderate dosage ranges while working effectively and without other variables or noticeable side effects. The abnormality was incidentally found because labwork was retested after having mildly elevated baseline readings. The initial elevation was fortunate, as monitoring likely would not have occurred otherwise.
This is the second such case reported by this clinician over the past 18 months,6 thus raising concern about the etiology, incidence, and potential underreporting and secondarily hidden risks for venlafaxine and SSRI-induced acute hypertriglyceridemia. Both cases included fluoxetine as the first antidepressant medication used upon discovery of the abnormality. Consequently, it is necessary to consider that fluoxetine and/or norfluoxetine may in some manner prime hepatic triglyceride manufacturing to increase in an ongoing delayed fashion either directly, as a rebound phenomena, or as a predisposing factor prior to the use of another antidepressant medication.
In summary, it is possible that routine monitoring of lipid profiles needs to occur with the use of venlafaxine or an SSRI even in individuals without physical complaints, obvious side effects, or histories of abnormal lipid profiles. There is no known reason to explain this induced effect or the specific physiologic etiology. Further investigation is warranted.
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Teitelbaum M: Severe and moderate hypertriglyceridemia secondary to citalopram and fluoxetine. Psychosomatics 2000; 41:448-449[Free Full Text]
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