UNLABELLED: We evaluated the influence of long-term HIV infection and its treatment on distal tibia and radius microstructure. Premenopausal eumenorrheic HIV-positive women displayed trabecular and cortical microstructure alterations, which could contribute to increased bone fragility in those patients. INTRODUCTION: Bone fragility is an emerging issue in HIV-infected patients. Dual-energy X-ray absorptiometry (DXA) quantified areal bone mineral density (BMD) predicts fracture risk, but a significant proportion of fracture risk results from microstructural alterations. METHODS: We studied the influence of long-term HIV infection on bone microstructure as evaluated by high-resolution peripheral quantitative computed tomography (HR-pQCT) in 22 HIV-positive (+ve) premenopausal eumenorrheic women and 44 age- and body mass index (BMI)-matched HIV-negative (-ve) controls. All subjects completed questionnaires regarding calcium/protein intakes and physical activity, and underwent DXA and HR-pQCT examinations for BMD and peripheral skeleton microstructure, respectively. A risk factor analysis of tibia trabecular density using linear mixed models was conducted. RESULTS: In HIV+ve women on successful antiretroviral therapy (undetectable HIV-RNA, median CD4 cell count, 626), infection duration was 16.5 ± 3.5 (mean ± SD) years; median BMI was 22 (IQR, 21-26) kg/m². More HIV+ve women were smokers (82 versus 50 %, p = 0.013). Compared to controls, HIV+ve women had lower lumbar spine (spine T-score -0.70 vs -0.03, p = 0.014), but similar proximal femur BMD. At distal tibia, HIV+ve women had a 14.1 % lower trabecular density and a 13.2 % reduction in trabecular number compared to HIV-ve women (p = 0.013 and 0.029, respectively). HR-pQCT differences in distal radius were significant for cortical density (-3.0 %; p = 0.029). CONCLUSIONS: Compared with HIV-ve subjects, premenopausal HIV+ve treated women had trabecular and cortical bone alterations. Adjusted analysis revealed that HIV status was the only determinant of between group tibia trabecular density differences. The latter could contribute to increased bone fragility in HIV+ve patients.
UNLABELLED: We evaluated the influence of long-term HIV infection and its treatment on distal tibia and radius microstructure. Premenopausal eumenorrheic HIV-positivewomen displayed trabecular and cortical microstructure alterations, which could contribute to increased bone fragility in those patients. INTRODUCTION: Bone fragility is an emerging issue in HIV-infectedpatients. Dual-energy X-ray absorptiometry (DXA) quantified areal bone mineral density (BMD) predicts fracture risk, but a significant proportion of fracture risk results from microstructural alterations. METHODS: We studied the influence of long-term HIV infection on bone microstructure as evaluated by high-resolution peripheral quantitative computed tomography (HR-pQCT) in 22 HIV-positive (+ve) premenopausal eumenorrheic women and 44 age- and body mass index (BMI)-matched HIV-negative (-ve) controls. All subjects completed questionnaires regarding calcium/protein intakes and physical activity, and underwent DXA and HR-pQCT examinations for BMD and peripheral skeleton microstructure, respectively. A risk factor analysis of tibia trabecular density using linear mixed models was conducted. RESULTS: In HIV+ve women on successful antiretroviral therapy (undetectable HIV-RNA, median CD4 cell count, 626), infection duration was 16.5 ± 3.5 (mean ± SD) years; median BMI was 22 (IQR, 21-26) kg/m². More HIV+ve women were smokers (82 versus 50 %, p = 0.013). Compared to controls, HIV+ve women had lower lumbar spine (spine T-score -0.70 vs -0.03, p = 0.014), but similar proximal femur BMD. At distal tibia, HIV+ve women had a 14.1 % lower trabecular density and a 13.2 % reduction in trabecular number compared to HIV-ve women (p = 0.013 and 0.029, respectively). HR-pQCT differences in distal radius were significant for cortical density (-3.0 %; p = 0.029). CONCLUSIONS: Compared with HIV-ve subjects, premenopausal HIV+ve treated women had trabecular and cortical bone alterations. Adjusted analysis revealed that HIV status was the only determinant of between group tibia trabecular density differences. The latter could contribute to increased bone fragility in HIV+ve patients.
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