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International Journal of Endocrinology
Volume 2015 (2015), Article ID 969040, 7 pages
Review Article

Vitamin D and Osteoporosis in HIV/HCV Coinfected Patients: A Literature Review

1Department of Sciences for Health Promotion and Mother-Child Care “G. D’Alessandro”, University of Palermo, Via del Vespro 127, 90127 Palermo, Italy
2Biomedical Department of Internal Medicine and Specialities, University of Palermo, Via del Vespro 141, 90127 Palermo, Italy

Received 11 October 2014; Revised 23 January 2015; Accepted 10 February 2015

Academic Editor: Ling-Qing Yuan

Copyright © 2015 Paola Di Carlo et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Vitamin D deficiency further increases the risk of osteoporosis in HIV-positive patients coinfected with hepatitis C virus (HCV); however, it is still unclear whether HCV-related increased fracture risk is a function of the severity of liver disease. The aim of this review was to identify studies on associative vitamin D deficiency patterns in high-risk populations such as HIV/HCV coinfected patients. We did this by searching MEDLINE and EMBASE databases, from inception to August 2014, and included bibliographies. The final 12 articles selected are homogeneous in terms of age but heterogeneous in terms of sample size, participant recruitment, and data source. Most of the HIV/HCV coinfected patients have less than adequate levels of vitamin D. After reviewing the selected articles, we concluded that vitamin D deficiency should be regarded as a continuum and that the lower limit of the ideal range is debatable. We found that vitamin D deficiency might influence liver disease progression in HIV/HCV coinfected patients. Methodological issues in evaluating vitamin D supplementation as a relatively inexpensive therapeutic option are discussed, as well as the need for future research, above all on its role in reducing the risk of HCV-related fracture by modifying liver fibrosis progression.