The goal of this study was to compare the effectiveness of fish oil, fenofibrate, gemfibrozil, and atorvastatin on reducing triglyceride (TG) levels among a large cohort of HIV-infected patients in clinical care.
Retrospective observational cohort study.
The primary endpoint was absolute change in TG levels measured using the last TG value pretreatment and the first TG value posttreatment. A pre–post quasi-experimental design was used to estimate the change in TG because of initiating fish oil. Linear regression models examined the comparative effectiveness of treatment with fish oil versus gemfibrozil, fenofibrate, or atorvastatin for TG reduction. Models were adjusted for baseline differences in age, sex, race, CD4+ cell count, diabetes, body mass index, protease inhibitor use, and time between TG measures.
A total of 493 patients (mean age, 46 years; 95% male) were included (46 patients receiving gemfibrozil; 80, fenofibrate; 291, atorvastatin; and 76, fish oil) with a mean baseline TG of 347 mg/dL. New use of fish oil decreased TG [ΔTG, −45 mg/dL; 95% confidence interval (CI): −80 to −11] in the pre–post study. Compared with fish oil (reference), fibrates were more effective (ΔTG, −66; 95% CI: −120 to −12) in reducing TG levels, whereas atorvastatin was not (ΔTG, −39; 95% CI: −86 to 9).
In HIV-infected patients in routine clinical care, fish oil is less effective than fibrates (but not atorvastatin) at lowering TG values. Fish oil may still represent an attractive alternative for patients with moderately elevated TGs, particularly among patients who may not want or tolerate fibrates.
*Department of Pharmaceutical Outcome and Policy, University of Florida, Gainesville, FL;
†US Food and Drug Administration, Silver Spring, MD;
‡Department of Medicine (HC, MK) and Department of Biostatistics (EB), University of Washington, Seattle, WA;
§Department of Medicine, University of Alabama, Birmingham, AL;
‖Department of Medicine, University of California, San Diego, CA;
¶Department of Medicine, University of North Carolina, Chapel Hill, NC; and
#Department of Medicine, University of California, San Francisco, CA.
Correspondence to: Heidi M. Crane, MD, MPH, University of Washington, Harborview Medical Center, 325 9th Avenue, Box 359931, Seattle, WA 98106 (e-mail: email@example.com).
Supported by AHRQ Grant R21HS019516, the American Heart Association Grant-in-Aid Grant 09050129 G, the CNICS Grant R24 AI067039, and the University of Washington Center for AIDS Research NIAID Grant P30 AI027757. The funding agreements ensured the authors' independence in design and conduct of the study; collection, management, analysis, and interpretation of the data; and preparation, review, and approval of the manuscript.
Presented at the 27th International Conference on Pharmacoepidemiology and Therapeutic Risk Management, August 16, 2011, Chicago, IL.
M.A.M. is employed by the Food and Drug Administration. This study represents the opinions of the authors and not those of the Food and Drug Administration. C.W.M. has consulted for Virco. M.J.M. has consulted for BMS, Gilead, and Merk; is receiving grant funding from BMS, Pfizer, and Definicare; and has received grant funded from Tibotec. S.N. is receiving grant funding from Pfizer, Bristol-Myers Squibb, and Merck. J.H.W. has consulted for BMS, Gilead, and Definicare and is receiving grant funding from BMS, Pfizer, Definicare, Tibotec, and Gilead. The remaining authors have no conflicts of interest to disclose.
Received February 22, 2012
Accepted July 13, 2013