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Author Notes:

Allison Ross Eckard, MD, Associate Professor of Pediatrics and Medicine, Divisions of Infectious Diseases, Medical University of South Carolina, 135 Rutledge Ave, Suite 1217, Charleston, SC 29425; Phone: 843-792-9909; Fax: 843-792-5127; eckarda@musc.edu.

The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

ARE has received research funding from Bristol-Myers Squibb, Cubist Pharmaceuticals, and GlaxoSmithKline and has served as an advisor for Gilead.

ARE has received research funding from Bristol-Myers Squibb, Cubist Pharmaceuticals, and GlaxoSmithKline and has served as an advisor and speaker for Gilead.

GAM 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.

All other declare no conflicts of interest.

These data were presented at the 19th Vitamin D Workshop, March 2016, Boston, MA (abstract #52).

Subjects:

Research Funding:

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], National Institutes of Health/Clinical Research Center Grant [8G12MD007602-27 to Morehouse School of Medicine].

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 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.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Biochemistry & Molecular Biology
  • Endocrinology & Metabolism
  • HIV
  • Vitamin d metabolites
  • Vitamin d binding protein
  • Cholecalciferol supplementation
  • Randomized-controlled trial
  • Pediatrics and adolescents
  • Vitamin D
  • HUMAN-IMMUNODEFICIENCY-VIRUS
  • INTIMA-MEDIA THICKNESS
  • CARDIOVASCULAR RISK-FACTORS
  • PERINATALLY ACQUIRED HIV
  • PLACEBO-CONTROLLED TRIAL
  • D DEFICIENCY
  • ANTIRETROVIRAL THERAPY
  • 25-HYDROXYVITAMIN D
  • YOUNG-ADULTS
  • GENERAL-POPULATION

Effects of Cholecalciferol Supplementation on Serum and Urinary Vitamin D Metabolites and Binding Protein in HIV-infected Youth

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Journal Title:

Journal of Steroid Biochemistry and Molecular Biology

Volume:

Volume 168

Publisher:

, Pages 38-48

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Vitamin D insufficiency is widespread in HIV-infected patients. HIV and/or antiretroviral therapy (ART), particularly efavirenz (EFV), may interfere with vitamin D metabolism. However, few data from randomized, controlled trials exist. Here, we investigate changes in vitamin D metabolites and binding protein (VDBP) after 6 months of supplementation in a randomized, active-control, double-blind trial investigating 2 different monthly cholecalciferol (vitamin D 3 ) doses [60,000 (medium) or 120,000 (high) IU/month] vs. a control arm of 18,000 IU/month in 8–25 year old HIV-infected youth on ART with HIV-1 RNA < 1000 copies/mL and baseline 25-hydroxycholecalciferol (25(OH)D 3 ) ≤30 ng/mL. A matched healthy uninfected group was enrolled in a similar parallel study for comparison. Changes after 6 months were analyzed as intent-to-treat within/between groups [control group (low dose) vs. combined supplementation doses (medium + high)]. At 6 months, 55% vs. 82% of subjects in control and supplementation groups, respectively, reached 25(OH)D 3 ≥30 ng/mL (P = 0.01) with no difference between medium and high doses (both 82% ≥30 ng/mL). There were few differences for those on EFV vs. no-EFV, except serum VDBP decreased in EFV-treated subjects (both within- and between-groups P ≤ 0.01). There were no significant differences between the HIV-infected vs. healthy uninfected groups. The major finding of the present study is that cholecalciferol supplementation (60,000 or 120,000 IU/month) effectively raises serum 25(OH)D 3 in the majority of HIV-infected subjects, regardless of EFV use. Notably, response to supplementation was similar to that of uninfected subjects.

Copyright information:

© 2017 Elsevier Ltd

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