Low bone mineral density (BMD) is a significant comorbidity in HIV. However, studies evaluating vitamin D supplementation on bone health in this population are limited. This study investigates changes in bone health parameters after 12 months of supplementation in HIV-infected youth with vitamin D insufficiency.
This is a randomized, active-control, double-blind trial investigating changes in bone parameters with 3 different vitamin D3 doses [18,000 (standard/control dose), 60,000 (moderate dose), and 120,000 IU/monthly (high dose)] in HIV-infected youth 8–25 years old with baseline serum 25-hydroxyvitamin D (25(OH)D) concentrations <30 ng/mL. BMD and bone turnover markers were measured at baseline and 12 months.
One hundred two subjects enrolled. Over 12 months, serum 25(OH)D concentrations increased with all doses, but the high dose (ie, 120,000 IU/monthly) maintained serum 25(OH)D concentrations in an optimal range (≥30 or ≥20 ng/mL) throughout the study period for more subjects (85% and 93%, respectively) compared with either the moderate (54% and 88%, respectively) or standard dose (63% and 80%, respectively). All dosing groups showed some improvement in BMD; however, only the high-dose arm showed significant decreases in bone turnover markers for both procollagen type 1 aminoterminal propeptide (−3.7 ng/mL; P = 0.001) and Β-CrossLaps (−0.13 ng/mL; P = 0.0005).
High-dose vitamin D supplementation (120,000 IU/mo) given over 12 months decreases bone turnover markers in HIV-infected youth with vitamin D insufficiency, which may represent an early, beneficial effect on bone health. High vitamin D doses are needed to maintain optimal serum 25(OH)D concentrations.
*Department of Pediatrics and Medicine, Divisions of Infectious Diseases, Medical University of South Carolina, Charleston, SC;
†Department of Pediatrics, Division of Infectious Diseases, Emory University School of Medicine, Atlanta, GA;
‡Department of Pediatrics, Division of Infectious Diseases, Case Western Reserve University, Rainbow Babies & Children's Hospital, Cleveland, OH; and
§Department of Medicine, Division of Endocrinology, Metabolism and Lipids.
Correspondence to: Allison Ross Eckard, MD, Divisions of Infectious Diseases, Medical University of South Carolina, 135 Rutledge Avenue, Suite 1217, Charleston, SC 29425 (e-mail: firstname.lastname@example.org).
This work was made possible by the National Institute of Child Health and Development at the National Institutes of Health (K23 HD069199 to ARE; R01 HD070490 to GAM; and K12 HD072245 to AC), Case Western Reserve University's Center for AIDS Research (P30 AI36219), Emory University's Center for AIDS Research (P30 AI050409), Emory+Children's Pediatric Research Center (Immunology and Flow Cytometry Cores), Clinical and Translational Science Award and the Clinical and Translational Science Collaborative of Cleveland (UL1TR000439) from the National Center for Advancing Translational Sciences (NCATS) component of the National Institutes of Health and NIH roadmap for Medical Research. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
Data were presented in part at the Conference on Retroviruses and Opportunistic Infections; Abstract 859; February 25, 2016; Boston, MA.
A.R.E. has received research funding from Bristol-Myers Squibb, Cubist Pharmaceuticals, and GlaxoSmithKline and has served as an advisor and speaker for Gilead. A.R.E. has received research funding from Bristol-Myers Squibb, Cubist Pharmaceuticals, and GlaxoSmithKline and has served as an advisor and speaker for Gilead. G.A.M. serves as a consultant for Bristol-Myers Squibb, ViiV/GlaxoSmithKline, Gilead, Pfizer, and ICON and has received grant funding from Bristol-Myers Squibb, ViiV/GlaxoSmithKline, Merck, AstraZeneca, and Gilead. The remaining authors have no conflicts of interest to disclose.
ClinicalTrials.gov Identifier: NCT01523496.
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Received June 22, 2017
Accepted August 28, 2017