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Low Vitamin D Not Linked to Bone Density or Liver Fibrosis in HIV/HCV Group
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First International Workshop on HIV and Aging, October 4-5, 2010, Baltimore
Mark Mascolini
Although more than 40% of 116 people coinfected with HIV and hepatitis C virus (HCV) had low vitamin D levels in a prospective cohort study, low D did not correlate with either bone mineral density or liver fibrosis [1]. Researchers from Johns Hopkins University believe their findings "suggest that efforts to increase vitamin D levels in this population may not improve bone or liver outcomes."
The cohort included 116 HIV/HCV-coinfected people recruited from the Hopkins HIV clinic or a clinical practice in Baltimore from 2005 through 2007. All cohort members had a DEXA scan for bone mineral density within 1 year of liver biopsy. The investigators defined low D levels as 25OHD at or below 15 ng/mL; low bone mineral density as a value 2 or more standard deviations lower than values for age-, gender-, and race-matched controls at the total hip, femoral neck, or lumbar spine; liver fibrosis as a Metavir score of 2 or greater; and secondary hyperparathyroidism as a parathyroid hormone (PTH) level above 65 pg/mL. (Hyperparathyroidism is marked by excessive PTH production, which controls calcium, phosphorus, and vitamin D levels in blood and bone. People with secondary hyperparathyroidism produce extra PTH in an attempt to compensate for low calcium levels caused by low vitamin D or poor absorption of calcium from the intestines.)
Seventy-three of 116 cohort members (63%) were men, 101 (87%) were African American, 69 (59%) were injection drug users, 70 (60%) smoked, and 53 (46%) abused alcohol. Median age of the study group was 49.9 years (interquartile range [IQR] 46.5 to 53.3). Fifty-eight people were taking antiretrovirals, and 77 had a viral load below 400.
Median vitamin D (measured as 25OHD) stood at 19 ng/mL (IQR 11 to 26), and 48 cohort members (41%) had a 25OHD level at or below 15 ng/mL. Forty-five people (39%) had fibrosis, 31 (27%) had low bone mineral density, and 28 (24%) had secondary hyperparathyroidism.
The researchers found a modest inverse correlation between PTH and 25OHD levels: the lower the PTH, the higher the vitamin D (r2 = 0.046, P = 0.02). But prevalence of secondary hyperparathyroidism was similar in people with normal (22%) and low (29%) bone mineral density (P = 0.46). When the investigators divided cohort members into those with no fibrosis (Metavir 0 and 1) and those with fibrosis (Metavir 2, 3, and 4), prevalence of secondary hyperparathyroidism was similar in people with and without fibrosis (P = 0.41).
Although Z scores indicated below-normal bone mineral density in the cohort, median Z scores did not approach the study-defined cutoff for low bone mineral density, a score at or below -2. Median scores were -0.42 (IQR -1.12 to +0.25) at the hip, -0.09 (IQR -0.84 to +0.47) at the femoral neck, and -0.95 (IQR -1.83 to +0.16) at the lumbar spine. Median 25OHD levels were similar in people with and without low bone mineral density (P = 0.63).
Lack of correlation between low vitamin D levels and liver fibrosis or low bone mineral density underlines the difficulty in understanding what to make of low D levels in people with HIV. Todd Brown, senior author of this study, noted during the workshop that "if you look for vitamin D deficiency, you will find it, and if you supplement with vitamin D, you will increase levels. But whether you're doing anyone a favor is still an open question."
Reference
1. El-Maouche D, Mehta SH, Sutcliffe C, et al. Relation between vitamin D deficiency and bone mineral density and liver fibrosis in HIV/HCV co-infection. First International Workshop on HIV and Aging. October 4-5, 2010. Baltimore. Abstract P_17.
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