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DOI: 10.1177/0115426505020006668
Alterations in Lipid Profiles in HIV-Infected Patients Treated With Protease Inhibitor Therapy Are Not Influenced by Diet![]() ![]() ,![]()
* Department of Public Health and Nutrition
Infection Unit, Tufts University School of Medicine, Boston, Massachusetts; Correspondence: Christine Wanke, MD, Tufts University School of Medicine, 150 Harrison Avenue, Jaharis 266, Boston, MA 02111. Electronic mail may be sent to christine.wanke{at}tufts.edu. Background: The use of protease inhibitor (PI) –based highly active antiretroviral therapy (HAART) in patients infected with human immunodeficiency virus (HIV) has been linked to alterations in lipid profiles. Methods: Longitudinal cohort study. Lipid profiles were evaluated pre- and post-PI therapy in 49 HIV-infected patients. Diet was also evaluated to determine any contribution to alterations in lipid levels. Results: Pre- and post-PI-based HAART samples were examined from 42 men and 7 women, mean age 40.6 years. Mean CD4 count pre-PI was 242 ± 205 cells/mm3; HIV RNA was 4.2 log10 copies/mL; body mass index (BMI) was 24.7 ± 3.6 kg/m2; body fat was 17.1 ± 9.1 kg by bioelectrical impedance analysis (BIA), dietary intake was 2654 ± 732 kcal/day. Post-PI samples were collected 5.7 ± 1.66 months after starting therapy. CD4 counts increased to 384 ± 323 cells/mm3 and RNA decreased 1 log post-PI. Post-PI BMI (25.2 kg/m2), percent body fat (17.4%) and caloric intake (2656 kcal/day) were unchanged. Pre-PI total cholesterol (TC) in men was 167.6 ± 42.4 mg/dL; TC increased (190.4 ± 47.9 mg/dL) post-PI (p < .0001). Pre-PI triglycerides (TG) were 154.5 ± 109.4 mg/dL; TG increased post-PI (266.1 ± 363.6 mg/dL, p < .03). Low-density lipoprotein (LDL) -C was 97.8 ± 31 mg/dL pre-PI and rose to 107.1 ± 34.7 mg/dL post-PI (p < .05). High density lipoproteins (HDLs) were below desired levels before initiation of PI therapy and remained low. Conclusions: PI therapy significantly alters lipid profiles in HIV-infected patients. Dietary intake did not contribute to changes in lipid profile. More longitudinal studies are needed to demonstrate whether these alterations contribute to additional cardiovascular risk.
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