Bone Loss in HIV Infection
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...
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Publicado no: | Curr Treat Options Infect Dis |
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2017
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Acesso em linha: | https://ncbi.nlm.nih.gov/pmc/articles/PMC5388454/ https://ncbi.nlm.nih.gov/pubmed/28413362 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1007/s40506-017-0109-9 |
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pubmed-53884542018-03-01 Bone Loss in HIV Infection Moran, Caitlin A. Weitzmann, M. Neale Ofotokun, Ighovwerha Curr Treat Options Infect Dis Article 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. 2017-02-23 2017-03 /pmc/articles/PMC5388454/ /pubmed/28413362 http://dx.doi.org/10.1007/s40506-017-0109-9 Text en |
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Article Moran, Caitlin A. Weitzmann, M. Neale Ofotokun, Ighovwerha Bone Loss in HIV Infection |
description |
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. |
author |
Moran, Caitlin A. Weitzmann, M. Neale Ofotokun, Ighovwerha |
author_facet |
Moran, Caitlin A. Weitzmann, M. Neale Ofotokun, Ighovwerha |
author_sort |
Moran, Caitlin A. |
title |
Bone Loss in HIV Infection |
title_short |
Bone Loss in HIV Infection |
title_full |
Bone Loss in HIV Infection |
title_fullStr |
Bone Loss in HIV Infection |
title_full_unstemmed |
Bone Loss in HIV Infection |
title_sort |
bone loss in hiv infection |
container_title |
Curr Treat Options Infect Dis |
publishDate |
2017 |
url |
https://ncbi.nlm.nih.gov/pmc/articles/PMC5388454/ https://ncbi.nlm.nih.gov/pubmed/28413362 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1007/s40506-017-0109-9 |
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1819112384315260928 |