Vitamin D Insufficiency/Deficiency in HIV-Infected Inner City Youth

Abstract

Background: High prevalence of vitamin D deficiency among HIV-infected individuals has been reported in many studies. Increasing evidence for vitamin D’s role in innate and cell-mediated immunity suggests that vitamin D insufficiency or deficiency is worrisome particularly for HIV-infected individuals who are already at increased risk of infection. It is unknown whether vitamin D deficiency and supplementation will have any effects on HIV infection, including CD4 counts/CD4% and HIV plasma RNA. Method: Serum vitamin D levels, 25-hydroxyvitamin D (25-(OH)D), were obtained from 160 HIV-infected youth, aged 2 to 26 years as part of routine care. The HIV plasma RNA and CD4 counts were compared between patients with normal vitamin D and vitamin D insufficiency/deficiency. Individuals whose vitamin D level was ≤35 ng/mL received vitamin D3 supplementation. We compared the HIV plasma RNA, absolute CD4 counts, and CD4% in pre– and post–vitamin D supplementation. Categorical comparisons between the groups were examined using a nonparametric Fisher exact test, while continuous variables, pre– and post–vitamin D supplementation, were examined using a parametric paired samples t test. Results: The majority (152 of 160; 95%) of our patients were African American. Only 8 (5%) of 160 had normal vitamin D. Of the 160 patients with HIV, 37 (23.1%) had vitamin D insufficiency (25-(OH)D level between 21 and 35 ng/mL) and 11 of 160 (71.9%) had vitamin D deficiency (25-(OH)D level ≤20 ng/mL). Absolute CD4 counts averaged lower in patients who have severe vitamin D deficiency (25-(OH)D ≤10 ng/mL; mean 574.41 ± 306.17 cells/mm3) compared to those who had higher vitamin D level (mean 701.15 ± 444.19 cells/mm3). The CD4% were also lower (mean 25.12% ± 12.5%) in those who have severe vitamin D deficiency compared to those whose vitamin D level was ≥11 ng/mL (mean 29.47% ± 11.62%). The HIV plasma RNA was similar in all the groups. Our patients who were prescribed tenofovir (TDF) and/or efavirenz (EFV) did not have different vitamin D levels than patients who were prescribed other antiretroviral (ARV) medications. Only 60 (39.5%) of the 152 patients who received vitamin D supplement showed improvement in vitamin D level. Of the 60 patients, 10 (16.7%) had normalized vitamin D level (25-(OH)D level > 35 ng/mL). We did not see any significant change in the absolute CD4 counts or CD4%. Conclusions: A higher prevalence of vitamin D insufficiency/deficiency was found in our study compared to the previous large cohorts. However, patients who were prescribed TDF/EFV did not have lower vitamin D levels. Inadequate sunlight exposure in temperate latitudes and the cloud effect of the Great Lakes as well as large number of African American participants who live in the inner city area with poverty and poor diet may combine to explain these results. The effect of ARV medications on vitamin D may be washed out by the numerous other factors affecting vitamin D in our patients. Severe vitamin D deficiency seemed to be related to lower CD4 counts and CD4% but not related to HIV plasma RNA. Vitamin D supplementation did not increase CD4 counts/CD4% in our study.