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. 2017 Mar;9(1):52-67.
doi: 10.1007/s40506-017-0109-9. Epub 2017 Feb 23.

Bone Loss in HIV Infection

Caitlin A Moran  1   2 , M Neale Weitzmann  3   4 , Ighovwerha Ofotokun  1   2
Affiliations

Bone Loss in HIV Infection

Caitlin A Moran et al. Curr Treat Options Infect Dis. 2017 Mar.

Abstract

Human immunodeficiency virus (HIV) infection is an established risk factor for low bone mineral density (BMD) and subsequent fracture, and treatment with combination antiretroviral therapy (cART) leads to additional BMD loss, particularly in the first 1-2 years of therapy. The prevalence of low BMD and fragility fracture is expected to increase as the HIV-infected population ages with successful treatment with cART. Mechanisms of bone loss in the setting of HIV infection are likely multifactorial, and include viral, host, and immune effects, as well as direct and indirect effects of cART, particularly tenofovir disoproxil fumarate (TDF) and the protease inhibitors (PIs). Emerging data indicate that BMD loss following cART initiation can be mitigated by prophylaxis with either long-acting bisphosphonates or vitamin D and calcium supplementation. In addition, newer antiretrovirals, particularly the integrase strand transfer inhibitors and tenofovir alafenamide (TAF), are associated with less intense bone loss than PIs and TDF. However, further studies are needed to establish optimal bone sparing cART regimens, appropriate screening intervals, and preventive measures to address the rising prevalence of fragility bone disease in the HIV population.

Keywords: HIV; bisphosphonates; combination antiretroviral therapy; immune reconstitution; osteopenia; osteoporosis.

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Conflict of interest statement

Conflicts of Interest Dr. Caitlin A. Moran, Dr., M. Neale Weitzmann, and Dr. Ighovwerha Ofotokun declare no conflicts of interest.

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