Vitamin D deficiency has been described in HCV-infected patients [1
] and HIV-infected individuals [15
], but it is unknown whether vitamin D deficiency in these high-risk populations results in adverse health consequences. In this middle-aged, predominately African-American cohort of HIV–HCV-coinfected individuals, we found a high prevalence of vitamin D deficiency (41%), hepatic fibrosis (39%) and low BMD (27%); however, vitamin D deficiency was not related to hepatic fibrosis or low BMD.
Vitamin D plays an important role in bone metabolism and vitamin D deficiency has been associated with lower BMD in Caucasian populations [16
]. In African-American men and women, however, lower vitamin D levels have not been associated with low BMD [18
], despite the fact that average vitamin D levels are lower than Caucasians, because of decreased vitamin D synthesis [19
], reduced vitamin D intake [20
] and other socioeconomic and genetic factors [21
]. Racial differences in the effect of vitamin D on bone health have been highlighted in a recent case-control study from the Women’s Health Initiative, which showed a detrimental effect of lower 25OHD levels on fractures in Caucasian women, but a protective effect (that is lower 25OHD levels [≤20 ng/ml] associated with a lower risk of fracture) in African-American women [22
]. A potential mechanism explaining this phenomenon is that African-Americans could be more resistant to the bone-resorbing effects of PTH [23
We also found no relation between vitamin D deficiency and hepatic fibrosis. Vitamin D deficiency could play a role in inflammation and fibrosis through release of inflammatory and profibrogenic cytokines [6
] and indeed has been linked to severe fibrosis in HCV-infected patients [1
]. In addition, vitamin D deficiency has also been postulated to cause an unfavourable response to HCV antiviral therapy [1
]. Further studies to assess the role of vitamin D in liver disease should examine the longitudinal relation between vitamin D levels, supplementation and progression of fibrosis, particularly with respect to differential effects by race.
Our study has a few limitations. Because it was cross-sectional, we cannot conclude that vitamin D deficiency would not potentially have an adverse effect on BMD or fibrosis in this cohort of HIV–HCV-coinfected individuals. We did not have fracture history on these individuals; however, follow-up for future fracture events could add information on the clinical significance of low BMD in this population. In addition, our sample size was relatively small, and the study could potentially have been underpowered to detect small differences in BMD and fibrosis by vitamin D deficiency status. With a sample size of 116, prevalence of vitamin D deficiency of 41% and standard deviation in Z-score of 1.0 (at all three sites), we would have 80% power to detect a difference in mean Z-score between those with and without vitamin D deficiency of 0.34. However, even at the hip where the observed difference in mean Z-score between those with and without vitamin D deficiency was the largest (estimated mean difference −0.06; SE 0.20), if the observed effects of vitamin D were real, it would not be clinically significant.
In conclusion, vitamin D deficiency was prevalent among predominately African-American, HIV–HCV-coinfected individuals but was not related to BMD or fibrosis. It is questionable whether vitamin D supplementation in such populations would provide any benefits, and whether African-Americans have vitamin D thresholds different from Caucasians. Further studies examining the effect of vitamin D supplementations in African-Americans with multiple comorbidities should assess potential benefits or harms of vitamin D replacement.