Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Email this article to a Colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to My Articles & Searches Download to citation manager Citing Articles via HighWire Citing Articles via Google Scholar Articles by Teitelbaum, M. Search for Related Content PubMed Citation Articles by Teitelbaum, M. General Topics in Psychiatry

Severe and Moderate Hypertriglyceridemia Secondary to Citalopram and Fluoxetine

Key Words: Citalopram • Fluoxetine • Hypertriglyceridemia

TO THE EDITOR: Hypertriglyceridemia is a common problem of familial etiology. Acute causes include medication side effect, genetic predisposition, diabetes mellitus, obesity, and alcohol or substance abuse.^1–3 Mild elevation can have long-term cardiovascular consequences. Severe hypertriglyceridemia can lead to acute life- threatening events such as pancreatitis. Selective serotonin reuptake inhibitors (SSRIs) are reported to occasionally have mild effects on cholesterol and triglyceride level elevation, per package inserts. However, there are no reports of severe hypertriglyceridemia specifically linked to citalopram⁴ (per direct communication with Forest Pharmaceuticals, Inc.). I report here a case of severe hypertriglyceridemia without apparent causal risk factors other than the use of citalopram, with lesser elevation following prior fluoxetine use.

Case Report

Mr. A., a 46-year-old man, presented in 1996 without medical problems except for dysthymia, major depression, and obsessive-compulsive traits, in full remission, on fluoxetine (20 mg daily). Triglyceride levels from February and October 1996 were 509 mg/dl and 490 mg/dl, respectively (see Table 1). Previous labwork reports were unavailable, but there was suspicion that fluoxetine was related. Mr. A.'s only other medication was zolpidem on an as- needed basis. There were no indications of diabetes mellitus, obesity, or excess alcohol use. Further consultation with the primary care physician was recommended.

View this table: [in this window] [in a new window]

TABLE 1. Liquid profile progression

The fluoxetine dosage was increased to 20 and 30 mg on alternate days in 1997 and 30 mg daily in 1998. Although recommended, further labwork was not drawn. Zolpidem was discontinued. Mirtzapine (30 mg daily) was started for sleep and antidepressant augmentation, but it was later changed to an as-needed insomnia treatment.

In June 1999, a change was made because of persistent libido reduction and suspected triglyceride elevation. Over 1 month fluoxetine was discontinued and citalopram was started.

Mild depressive symptoms recurred in July, leading to an increase in citalopram from 20 mg to 30 mg daily. Symptoms were in full remission within weeks. Side effects were denied, although labwork had still not been drawn.

In September 1999, fasting labwork was drawn, with normal liver enzymes and glucose in addition to an extremely elevated triglyceride level of 846 mg/dl. Mr. A. denied physical complaints, describing having started an exercise program in the absence of weight gain. Alcohol use was still minimal without other routine medications. His triglyceride elevation was confirmed 9 days later with a fasting level of 877 mg/dl. The citalopram was discontinued over 3 days.

At this time, pre-antidepressant lipid profiles from 1993 and 1994 were located. Respective triglyceride levels were 200 mg/dl and 211 mg/dl.

Alprazolam (0.25 mg) was added as-needed for anxiety while continuing with intermittent mirtazapine (30 mg) for insomnia. No other medications were used over the 3-week interval until the fasting lipid profile was repeated (577 mg/dl). Another level was performed 24 days after (692 mg/dl), although at a different laboratory than the 1996–October 1999 tests. The primary care physician recommended gemfibrozil (600 mg daily) to treat hypertriglyceridemia, while fluoxetine (20 mg daily) was restarted for recurrent depression. Mr. A.'s last lipid profile, drawn within 1 week of these medications being started, reflected almost full triglyceride normalization (223 mg/dl).

DISCUSSION

There are no apparent variables outside of fluoxetine and citalopram use that explain the hypertriglyceridemia. Baseline levels were generally in a normal range. Elevation was seen only after administration of these medications. Significant elevation was seen with fluoxetine use, and severe elevation was seen with citalopram use. The triglyceride level decreased on discontinuation of citalopram, although in a nonlinear fashion. The third postcitalopram triglyceride level included newly introduced variables (fluoxetine was added 6 days and gemfibrozil 7 days prior) and reflected a return to baseline. It is unlikely that these medications significantly influenced the lipid levels in this time span.⁵

Of significance, Mr. A. had no complaints or risk factors to aid in the diagnostic process. There is no known etiology to explain the hypertriglyceridemia, which raises the importance of labwork with antidepressant use. Additional studies may be required for clarification of the risk for SSRI-induced hypertriglyceridemia.

REFERENCES

1. Scheen AJ: How I investigate hypertriglyceridemia. Rev Med Liege 1998; 53:103–105[Medline]
2. Hozumia Y, Kawano M, Miyata M: Severe hypertriglyceridemia caused by tamoxifen- treatment after breast cancer surgery. Endocr J 1997; 44:745–749[Medline]
3. Suga S, Tamasawa N, Kinpara I, et al: Identification of homozygous lipoprotein lipase gene mutation in a woman with recurrent aggravation of hypertriglyceridemia induced by pregnancy. J Intern Med 1998; 243:317– 321[CrossRef][Medline]
4. Muldoon C: The safety and tolerability of citalopram. Int Clin Psychopharmacol 1996; 11:35–40
5. Jeng J, Jeng C, Sheu W, et al: Gemfibrozil treatment of hypertriglyceridemia: improvement on fibrinolysis without change of insulin resistance. Am J Heart 1997; 134:565– 571[Medline]

This article has been cited by other articles:

				M. Teitelbaum Severe Hypertriglyceridemia Secondary to Venlafaxine and Fluoxetine Psychosomatics, October 1, 2001; 42(5): 440 - 441. [Full Text]

Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Email this article to a Colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to My Articles & Searches Download to citation manager Citing Articles via HighWire Citing Articles via Google Scholar Articles by Teitelbaum, M. Search for Related Content PubMed Citation Articles by Teitelbaum, M. General Topics in Psychiatry

Get information about faster international access.

Privacy Policy

Copyright © 2000 Academy of Psychosomatic Medicine. All rights reserved.

Home | Search | Current Issue | Past Issues | Subscribe | All APPI Journals | Help | Contact Us