Background: Early highly active antiretroviral therapy (HAART) is recommended for HIV-1–infected infants. There are limited data on lipid changes during infant HAART.
Methods: Nonfasting total (TC), low density lipoprotein (LDL) and high density lipoprotein (HDL) cholesterol and triglycerides (TG) were measured at 0, 6 and 12 months. Correlates of lipid levels and changes post-HAART were assessed using linear regression.
Results: Among 115 infants, pre-HAART median age was 3.8 months, CD4% was 19% and weight-for-age Z score was –2.42. Pre-HAART median lipid levels were: TC, 108.7 mg/dL; LDL, 42.5 mg/dL; HDL, 29.4 mg/dL and TG, 186.9 mg/dL. Few infants had abnormally high TC (6.2%) or LDL (5.6%), but many had low HDL (76.5%) or high TG (69.6%). Higher pre-HAART weight-for-age and height-for-age Z scores were each associated with higher pre-HAART TC (P = 0.04 and P = 0.01) and LDL (P = 0.02 and P = 0.008). From 0 to 6 months post-HAART, TC (P < 0.0001), LDL (P < 0.0001) and HDL (P < 0.0001) increased significantly, and 23.1% (P = 0.002), 14.0% (P = 0.2), 31.3% (P < 0.0001) and 50.8% (P = 0.2) of infants had abnormally high TC, high LDL, low HDL and high TG, respectively. Changes in TC and HDL were each associated with higher gain in weight-for-age Z score (P = 0.03 and P = 0.01) and height-for-age Z score (P = 0.01 and P = 0.007). Increased change in LDL was associated with higher gain in height-for-age Z score (P = 0.03). Infants on protease inhibitor–HAART had smaller HDL increase (P = 0.004).
Conclusions: Infants had substantive increases in lipids, which correlated with growth. Increases in HDL were attenuated by protease inhibitor–HAART. It is important to determine clinical implications of these changes.
From the *Department of Paediatrics and Child Health, University of Nairobi, Nairobi, Kenya; Departments of †Medicine, ‡Biostatistics, §Global Health, and ¶Pediatrics, University of Washington; and ‖Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, WA.
Data presented previously at the 18th Conference on Retroviruses and Opportunistic Infections, Abstract #703, Boston, MA, March, 2011.
A.L. conceived the study, led clinical study management and data collection, analyzed and interpreted data and wrote the article. S.B.-N., D.W., K.T., B.A.R. and G.C.J-S. also contributed to study design, data analysis and interpretation and writing. E.N. led clinical study implementation and data collection. L.D. contributed data analysis and interpretation. A.M. provided critique of intellectual content and interpretation of data. All authors participated in critical review and final approval of the article.
The Optimizing HIV-1 Therapy Study was supported by the National Institute of Child Health and Human Development grant 2 R01 HD023412. Field site support was provided by the University of Washington Center for AIDS Research International Core, an NIH funded program (P30 AI027757), which is supported by the following NIH Institutes and Centers (NIAID, NCI, NIMH, NIDA, NICHD, NHLBI and NCCAM). A.L. was supported by the NIH Research Grant # D43 TW000007, funded by the Fogarty International Center. S.B.-N. was supported by 2 R01 HD023412. K.T. was supported by the NIH grants P30 AI027757 and 2 R01 HD023412. G.C.J.-S. was supported by NIH grant K24 HD054314. The authors have no other funding or conflicts of interest to disclose.
Address for correspondence: Sarah Benki-Nugent, MS, PhD, Department of Global Health, University of Washington, Box 359931, 325 9th Ave., Seattle, WA 98104. E-mail: firstname.lastname@example.org.