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Vitamin D Boost Does Not Improve Endothelial Function With HIV
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18th Conference on Retroviruses and Opportunistic Infections, February 27-March 2, 2011, Boston
Mark Mascolini
Twelve weeks of vitamin D supplementation in D-deficient people with HIV did not improve endothelial function in the first placebo-controlled trial of this strategy in HIV-positive adults [1]. Results hinted that efavirenz may limit the impact of vitamin D supplements.
Vitamin D insufficiency and deficiency are common in people with HIV as well as the in the general US population [2]. Some research suggests that extra vitamin D may improve endothelium-dependent vasodilation, a predictor of heart disease, in people with vitamin D deficiency. To test that possibility in people with HIV, researchers at four US centers planned this double-blind, placebo-controlled trial.
Study participants were HIV-positive adults from a single center with 25(OH)D levels at or below 20 ng/mL and a viral load below 50 copies after at least 12 weeks on a stable regimen. The researchers randomized them 2-to-1 to 4000 mg of vitamin D3 or placebo daily for 12 weeks. Tablets analyzed after study completion verified that they contained an average 136% of the stated 2000-mg dose. A single technician performed brachial artery dilatation before treatment and at week 12. Measuring 25(OH)D is considered the most accurate way to calculate vitamin D levels.
The 30 people randomized to vitamin D were significantly older than the 15 people randomized to placebo (average 47 versus 40 years, P = 0.009). But the groups did not differ in standard HIV-related measures (including CD4 count, viral load, HIV duration, antiretroviral duration, and type of antiretroviral regimen) or metabolic parameters (including body mass index, lipids, and insulin resistance). Most study participants were black (77% in the vitamin D group and 80% in the placebo group), and most were men (83% in the vitamin D group and 67% in the placebo group).
Vitamin D levels, measured as 25(OH)D, improved significantly in the supplement group from week 0 (9.0 ng/mL) to week 12 (13.3 ng/mL) (P = 0.002). Brachial artery diameter did not differ between the vitamin D group and the placebo group when the study began, and flow-mediated dilation was similar: 2.87% in the supplement group and 2.46% in the placebo group. After 12 weeks, neither brachial artery diameter nor flow-mediated dilation (3.87% and 2.75%) had changed significantly in either group. Absolute change in flow-mediated dilation was +0.55% in the vitamin D supplement group and +0.29% in the placebo group.
Median total cholesterol fell 9.0 mg/dL in the vitamin D supplement group over 12 weeks (P = 0.009), while median non-high-density lipoprotein cholesterol fell 7.0 mg/dL (P = 0.022). But median insulin resistance measured as HOMA-IR rose significantly among vitamin D takers (from 2.1 to 3, P < 0.0001), as did insulin levels (from 10 to 14 microIU/mL) (P = 0.0007). Changes in serum markers of coagulation were similar in the vitamin D and placebo groups, except for an increase in IL-6 in the placebo group.
Vitamin D levels rose by a median 5.0 ng/mL of 25(OH)D in the overall vitamin D group, by 4.6 ng/mL among those taking efavirenz, and by 5.15 ng/mL in people not taking efavirenz. The investigators characterized this as a blunted response in efavirenz takers, though the difference was not statistically significant. An exploratory multivariate analysis to identify predictors of change in 25(OH)D did not identify efavirenz use as an independent predictor.
The failure of vitamin D supplementation to improve flow-mediated dilation or markers of inflammation or coagulation led the investigators to suggest that "the possibility of increased catabolism [breakdown] of 25(OH)D or altered levels of vitamin D binding protein in HIV-infected patients requires further investigation." The researchers also noted that this patient group had worse endothelial function when the study began than other populations of HIV-positive people. They suggested that longer supplementation or a higher dose should be studied.
A retrospective study presented at this meeting and reviewed separately by NATAP found evidence that vitamin D supplementation may lower the risk of type 2 diabetes in adults with HIV [3]. In a randomized trial of 18-to-24-year-olds, vitamin D3 supplementation appeared to offset the negative impact of tenofovir on parathyroid hormone, which stimulates production of vitamin D and thus enhances absorption of calcium from the small intestine [4].
References
1. Longenecker C, Hileman C, Carman T, et al. Vitamin D supplementation and endothelial function among vitamin D-deficient HIV-infected persons: a randomized placebo-controlled trial. 18th Conference on Retroviruses and Opportunistic Infections. February 27-March 2, 2011. Boston. Abstract 829.
2. Dao CN, Patel P, Overton ET, et al. Low Vitamin D among HIV-infected adults: prevalence of and risk factors for low vitamin D levels in a cohort of HIV-infected adults and comparison to prevalence among adults in the US general population. Clin Infect Dis. 2011;52:396-405.
3. Guaraldi G, Zona S, Orlando G, et al. Vitamin D3 supplementation decreases the risk of diabetes mellitus among patients with HIV infection. 18th Conference on Retroviruses and Opportunistic Infections. February 27-March 2, 2011. Boston. Abstract 827.
4. Havens P, Hazra R, Stephensen C, et al. Vitamin D3 supplementation decreases PTH in HIV-infected youth being treated with TDF-containing combination ART: a randomized, double-blind, placebo-controlled multicenter trial: Adolescent Trials Network Study 063. 18th Conference on Retroviruses and Opportunistic Infections. February 27-March 2, 2011. Boston. Abstract 80.
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