Department of Medicine, Division of Endocrinology, Lenox Hill Hospital, New York, NY, USA.
Department of Medicine, Division of Endocrinology, College of Physicians & Surgeons, Columbia University, New York, NY, USA.
J Bone Miner Res. 2020 Jul;35(7):1274-1281. doi: 10.1002/jbmr.4005. Epub 2020 Mar 26.
Bone remodeling is reduced in hypoparathyroidism, resulting in increased areal bone mineral density (BMD) by dual-energy X-ray absorptiometry (DXA) and abnormal skeletal indices by transiliac bone biopsy. We have now studied skeletal microstructure by high-resolution peripheral quantitative computed tomography (HR-pQCT) through 4 years of treatment with recombinant human PTH(1-84) (rhPTH[1-84]) in 33 patients with hypoparathyroidism (19 with postsurgical disease, 14 idiopathic). We calculated Z-scores for our cohort compared with previously published normative values. We report results at baseline and 1, 2, and 4 years of continuous therapy with rhPTH(1-84). The majority of patients (62%) took rhPTH(1-84) 100 μg every other day for the majority of the 4 years. At 48 months, areal bone density increased at the lumbar spine (+4.9% ± 0.9%) and femoral neck (+2.4% ± 0.9%), with declines at the total hip (-2.3% ± 0.8%) and ultradistal radius (-2.1% ± 0.7%) (p < .05 for all). By HR-pQCT, at the radius site, very similar to the ultradistal DXA site, total volumetric BMD declined from baseline but remained above normative values at 48 months (Z-score + 0.56). Cortical volumetric BMD was lower than normative controls at baseline at the radius and tibia (Z-scores -1.28 and - 1.69, respectively) and further declined at 48 months (-2.13 and - 2.56, respectively). Cortical porosity was higher than normative controls at baseline at the tibia (Z-score + 0.72) and increased through 48 months of therapy at both sites (Z-scores +1.80 and + 1.40, respectively). Failure load declined from baseline at both the radius and tibia, although remained higher than normative controls at 48 months (Z-scores +1.71 and + 1.17, respectively). This is the first report of noninvasive high-resolution imaging in a cohort of hypoparathyroid patients treated with any PTH therapy for this length of time. The results give insights into the effects of long-term rhPTH(1-84) in hypoparathyroidism. © 2020 American Society for Bone and Mineral Research.
甲状旁腺功能减退症会导致骨重建减少,从而通过双能 X 射线吸收法(DXA)增加面积骨密度(BMD),并通过髂骨活检出现异常的骨骼指数。我们现在通过高分辨率外周定量 CT(HR-pQCT)研究了骨骼微结构,对 33 名甲状旁腺功能减退症患者(19 名手术后疾病,14 名特发性)进行了 4 年的重组人 PTH(1-84)(rhPTH[1-84])治疗。我们将我们的队列与以前发表的正常参考值进行了 Z 评分比较。我们报告了基线以及 rhPTH(1-84)连续治疗 1、2 和 4 年后的结果。大多数患者(62%)在 4 年内的大部分时间里每隔一天服用 rhPTH(1-84)100μg。在 48 个月时,腰椎(+4.9%±0.9%)和股骨颈(+2.4%±0.9%)的面积骨密度增加,而全髋(-2.3%±0.8%)和桡骨远端(-2.1%±0.7%)的骨密度下降(所有 p<0.05)。通过 HR-pQCT,在桡骨部位,与桡骨远端 DXA 部位非常相似,总容积 BMD 从基线下降,但在 48 个月时仍保持在正常值以上(Z 评分+0.56)。桡骨和胫骨的皮质容积 BMD 低于基线时的正常对照值(Z 评分分别为-1.28 和-1.69),并且在 48 个月时进一步下降(分别为-2.13 和-2.56)。与基线相比,胫骨的皮质孔隙率高于正常对照组(Z 评分+0.72),并且在治疗的 48 个月期间在两个部位均增加(Z 评分分别为+1.80 和+1.40)。桡骨和胫骨的破坏负荷均从基线下降,但在 48 个月时仍高于正常对照组(Z 评分分别为+1.71 和+1.17)。这是首次报道在接受任何 PTH 治疗的甲状旁腺功能减退症患者队列中进行非侵入性高分辨率成像。这些结果深入了解了长期 rhPTH(1-84)在甲状旁腺功能减退症中的作用。©2020 美国骨矿研究协会。