Vitamin D deiciency and its relation to bone mineral density and liver ibrosis in HIV-HCV coinfection

Background: Fractures and cirrhosis are major causes of morbidity and mortality among HIV-HCV-coinfected individuals. It is not known whether vitamin D deiciency is associated with these outcomes. Methods: Between 2005 and 2007, 116 HIV-HCVcoinfected individuals underwent dual-energy X-ray absorptiometry within 1 year of a liver biopsy. 25-Hydroxyvitamin D (25OHD) and parathyroid hormone were measured from archived samples. Low bone mineral density (BMD) was deined as BMD=2 standard deviations lower than age-, sex- and race-matched controls (Z-score =-2.0) at the total hip, femoral neck or lumbar spine. Histological ibrosis staging was assessed according to the METAVIR system (0 [no ibrosis] to 4 [cirrhosis]). Results: The cohort was 87% African-American and 63% male. The median age (IQR) was 49.9 years (46.5-53.3). A total of 89% had a CD4+ T-cell count <200 cells/mm3 and 64% were receiving HAART. The median 25OHD was 19 ng/ ml (IQR 11.0-26.0). Hypovitaminosis D (25OHD=15 ng/ml) was present in 41% and secondary hyperparathyroidism, deined by parathyroid hormone <65 pg/ml, was present in 24%. In total, 27% had low BMD (Z-score -2) at the spine, femoral neck or total hip, and 39% had signiicant hepatic ibrosis (METAVIR=2). In multivariate analysis, vitamin D deiciency was not associated with signiicant ibrosis or with BMD at any site. Conclusions: Vitamin D deiciency was highly prevalent in this mostly African-American HIV-HCV-coinfected population, but was not related to BMD or liver disease severity. These data suggest that efforts to increase vitamin D levels in this population may not improve bone or liver outcomes.