In HIV-infected adults, we and others have shown that vitamin D deficiency is independently associated with increased carotid intima-media thickness (cIMT), a surrogate marker for cardiovascular disease (CVD). This study explored for the first time the relationship between vitamin D and CVD risk in HIV-infected youth.
This is a cross-sectional assessment of cIMT, inflammation, metabolic markers and vitamin D status in HIV-infected youth and healthy controls. We measured serum 25-hydroxyvitamin D (25(OH)D), fasting lipids, insulin, glucose, inflammatory markers and cIMT.
Thirty HIV-infected subjects and 31 controls were included. Among HIV-infected subjects, median age was 11 years (37% males; 73% black; similar to controls). HIV-infected subjects’ mean (standard deviation) serum 25(OH)D was 24 (35) ng/mL; 70% had 25(OH)D <20 ng/mL (deficient), 23% between 20–30 ng/mL (insufficient) and 7% >30 ng/mL (sufficient); proportions were similar to controls (P = 0.17). After adjusting for season, sex and race, there was no difference in serum 25(OH)D between groups (P = 0.11). Serum 25(OH)D was not significantly correlated with cIMT, inflammatory markers or lipids. Serum 25(OH)D was negatively correlated with body mass index, insulin resistance, HIV duration, and cumulative use of antiretroviral therapy, non- and nucleoside reverse transcriptase inhibitors.
Most HIV-infected youth have vitamin D deficiency or insufficiency. Despite no direct association between serum 25(OH)D and cIMT, there were notable associations with some CVD risk factors, particularly inverse correlation with insulin resistance. Studies are needed to determine whether CVD risk, including insulin resistance, could be improved with vitamin D supplementation.
From the *Emory University School of Medicine; †Children’s Healthcare of Atlanta, Atlanta, GA; and ‡Case Western Reserve University and Rainbow Babies and Children’s Hospital, Cleveland, OH.
The study was funded by an independent research grant from GlaxoSmithKline Collaborative Study Group, as well as supported by research grants to G.A.M. (R01HD070490) and A.R.E (1K23HD069199) from the National Institutes of Health and National Institute of Child Health and Development. The funding agencies had absolutely no role in study design, data collection or analysis.
G.A.M. serves as a consultant and has received research funding from Bristol-Myers Squibb, GlaxoSmithKline, Gilead, Merck, Tibotec and Abbott. G.A.M. currently chairs a DSMB for a Pfizer-funded study. A.R.E. has received research funding from Bristol-Myers Squibb, Cubist Pharmaceuticals and GlaxoSmithKline. The authors have no other funding or conflicts of interest to disclose.
Address for correspondence: Grace A. McComsey, MD, Department of Pediatric Infectious Diseases, Rainbow Babies and Children’s Hospital, 11100 Euclid Avenue, Cleveland OH, 44106. E-mail: email@example.com.