Amiel C, Ostertag A, Slama L, Baudoin C, N'Guyen T, Lajeunie E, Neit-Ngeilh L, Rozenbaum W, De Vernejoul M C
Department of Infectious Disease, Hôpital Tenon, Paris, France.
J Bone Miner Res. 2004 Mar;19(3):402-9. doi: 10.1359/JBMR.0301246. Epub 2003 Dec 22.
Osteoporosis has be reported to be a complication of active antiretroviral therapy of HIV infection. We studied 148 HIV-infected men stratified according to their treatment. Our data show that these patients have an average 9% decreased BMD, irrespective of their treatment. Low body mass index and high resorption markers were associated with low bone density.
Osteoporosis has been reported in HIV-infected (HIV+) patients, and it has been suggested that it may be linked to protease-inhibitor treatments (PI).
To assess this risk and to investigate its putative link with treatments, we compared the bone density of HIV+ men, who were either receiving treatment (including PI [PI+], n = 49; without PI [PI-], n = 51) or untreated (UT, n = 48). We included 81 age-matched control HIV-negative (HIV-) males (age, 40 +/- 8 years).
BMD adjusted for age (Z-score) was lower in the HIV+ patients at the lumbar spine (HIV+: -1.08 +/- 1.21, HIV-: -0.06 +/- 1.26, p < 0.001) and the femoral neck (HIV+: -0.39 +/- 1.05, HIV-: 0.25 +/- 0.87, p < 0.001). The prevalence of osteoporosis was 16% in HIV+ and 4% in HIV- subjects (p < 0.01). In the HIV+ subjects, the Z-score was correlated only to body mass index (r = 0.27 at lumbar spine and 0.35 at femoral neck). Untreated HIV+ patients had a negative Z-score (-0.82 +/- 1.15 for the lumbar spine), which was not different from the one of treated HIV+ patients. In the PI+ and PI- groups, the Z-score did not depend on the presence of lipodystrophy or the proportion of fat in the abdomen and legs measured by DXA. Markers of bone remodeling were measured in the 132 HIV+ and 35 HIV- subjects. Compared with controls, HIV+ patients had lower bone alkaline phosphatase and higher urinary cross-laps/Cr, which was negatively correlated with the Z-score at both the femoral neck (r = -0.22) and lumbar spine (r = -0.21). TNFalpha was increased in untreated compared with treated HIV+ subjects and was not correlated to the Z-score.
Our cross-sectional study does not show any deleterious effect of the treatment but does indicate a decrease in bone density in HIV+ patients irrespective of the treatment. This low bone density is in part related to the low body weight and is associated with increased bone resorption.
据报道，骨质疏松是人类免疫缺陷病毒（HIV）感染积极抗逆转录病毒治疗的一种并发症。我们对148名感染HIV的男性根据其治疗情况进行了分层研究。我们的数据显示，这些患者的骨密度平均降低了9%，无论其治疗情况如何。低体重指数和高吸收标志物与低骨密度相关。
据报道，HIV感染（HIV+）患者中存在骨质疏松，有人认为这可能与蛋白酶抑制剂治疗（PI）有关。
为评估这种风险并研究其与治疗的假定联系，我们比较了接受治疗（包括PI[PI+]，n = 49；不包括PI[PI-]，n = 51）或未治疗（UT，n = 48）的HIV+男性的骨密度。我们纳入了81名年龄匹配的HIV阴性（HIV-）男性对照（年龄，40±8岁）。
经年龄调整的骨密度（Z评分）在HIV+患者的腰椎处较低（HIV+：-1.08±1.21，HIV-：-0.06±1.26，p < 0.001），在股骨颈处也较低（HIV+：-0.39±1.05，HIV-：0.25±0.87，p < 0.001）。HIV+患者中骨质疏松的患病率为16%，HIV-受试者中为4%（p < 0.01）。在HIV+受试者中，Z评分仅与体重指数相关（腰椎处r = 0.27，股骨颈处r = 0.35）。未治疗的HIV+患者Z评分为阴性（腰椎处为-0.82±1.15），与接受治疗
