aINSERM bUPMC Univ Paris 06, UMRS 943 cAP-HP, Hôpital Pitié-Salpêtrière, Service de Maladies Infectieuses et Tropicales dAP-HP, Centre de Diagnostic et de Thérapeutique, Hôtel-Dieu, Paris eAP-HP, Hôpital Avicenne, Service de maladies infectieuses, Bobigny fAP-HP, Hôpital Pitié-Salpêtrière, Service de médecines internes gRheumatology Department, Cochin Hospital, Paris-Descartes University hAP-HP, Hôpital Pitié-Salpêtrière, Service de Rhumatologie and UPMC Univ Paris 06, Paris, France.
AIDS. 2013 Sep 24;27(15):2425-30. doi: 10.1097/QAD.0b013e32836378c3.
Although osteopenia is common in HIV-infected patients, there is by now limited data on the evolution of bone mineral density in this population. We aimed to evaluate the course of osteopenia over a 2-year period in HIV-1-infected men, and to identify risk factors for abnormal bone mineral density (BMD) decline.
HIV-1-infected men on combined antiretroviral therapy (cART) screened in the ANRS 120 Fosivir trial, diagnosed with low BMD (-2.5 ≤T-score <-1), not receiving antiosteoporotic agents, with sequential dual-energy-X ray-absorptiometry (DXA) available at baseline were eligible for this study and had a second DXA performed between months 24 and 36.
We enrolled 94 men with a median age of 46 years [interquartile range (IQR), 41-53], BMI 22 kg/m² (21-25) and a CD4 cell nadir of 164/μl (69-261). They were receiving cART for a median of 7.5 years (5.8-9.5). Over a median interval of 2.6 years (2.3-2.9) between the two DXA tests, the mean change in BMD was -0.5 ± 1.7% per year (P = 0.010) at the lumbar spine and -0.4 ± 1.8% per year (P = 0.033) at the hip. BMD fell by more than the smallest detectable difference (SDD) in, respectively, 25.5 and 27.7% of patients at the lumbar spine and hip. Tenofovir (TDF) exposure was independently associated with a larger decline in BMD at both sites [lumbar spine, OR = 2.4 (1.2-4.9); hip, OR = 2.8 (1.3-5.9)].
Although osteopenia overall modestly changes over 2 years in long-term cART-treated patients, a quarter of patients experienced a significant loss (>1 SDD) associated with TDF exposure.
尽管骨质疏松症在 HIV 感染者中很常见,但目前关于该人群骨密度变化的数据有限。我们旨在评估 HIV-1 感染男性在 2 年内骨质疏松症的发展情况,并确定导致骨密度异常下降的危险因素。
在 ANRS 120 Fosivir 试验中筛选出接受联合抗逆转录病毒治疗(cART)、诊断为低骨密度(-2.5≤T 评分<-1)、未接受抗骨质疏松药物治疗、在基线时可进行连续双能 X 射线吸收法(DXA)检查的 HIV-1 感染男性,符合条件并在 24 至 36 个月之间进行第二次 DXA 检查。
我们纳入了 94 名中位年龄为 46 岁[四分位间距(IQR),41-53]、BMI 为 22kg/m²(21-25)和 CD4 细胞最低点为 164/μl(69-261)的男性。他们接受 cART 的中位时间为 7.5 年(5.8-9.5)。在两次 DXA 检查之间的中位时间为 2.6 年(2.3-2.9),腰椎骨密度的平均年变化率为-0.5±1.7%(P=0.010),髋部骨密度的平均年变化率为-0.4±1.8%(P=0.033)。分别有 25.5%和 27.7%的患者腰椎和髋部的骨密度下降超过最小可检测差异(SDD)。替诺福韦(TDF)暴露与腰椎和髋部骨密度下降均相关[腰椎,OR=2.4(1.2-4.9);髋部,OR=2.8(1.3-5.9)]。
尽管长期接受 cART 治疗的患者在 2 年内骨质疏松症总体上变化不大,但四分之一的患者经历了与 TDF 暴露相关的显著骨密度损失(>1 SDD)。