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.

中文翻译：

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通过连续四年的甲状腺功能减退症的rhPTH（1-84）治疗，骨骼微结构的变化。

甲状旁腺功能减退症的骨重塑减少，通过双能X线骨密度仪（DXA）进行的区域骨矿物质密度（BMD）的增加和通过trans骨活检的骨骼异常指标的增加。现在，我们通过重组人PTH（1-84）（rhPTH [1-84]）治疗4年的33例甲状旁腺功能减退症患者（19例外科手术后），通过高分辨率外周定量CT（HR-pQCT）研究了骨骼的微观结构疾病，14种特发性）。我们计算了Z与先前发布的规范值相比，我们的同类群组的得分。我们报告了在基线以及rhPTH（1-84）连续治疗1、2和4年的结果。在4年的大部分时间里，大多数患者（62％）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％）的面骨密度增加，全髋关节（-2.3％±0.8％）和超dist半径的骨密度降低（ -2.1％±0.7％）（全部p  <.05）。通过HR-pQCT，在site骨部位，与超远端DXA部位非常相似，总体积BMD从基线开始下降，但在48个月时仍高于标准值（Z评分+ 0.56）。基线时the骨和胫骨的皮质体积BMD低于正常对照（Z得分分别为−1.28和− 1.69），并在48个月时进一步下降（分别为−2.13和− 2.56）。在胫骨基线，皮质孔隙率高于正常对照组（Z分数+ 0.72），并且在两个部位治疗48个月后均增加（Z分数分别为+1.80和+ 1.40）。48骨和胫骨的失败负荷均从基线下降，尽管在48个月时仍高于规范对照组（Z得分分别为+1.71和+ 1.17）。这是在这段时间内使用任何PTH疗法治疗的甲状旁腺功能减退患者的无创高分辨率成像的首次报道。结果为长期rhPTH（1-84）在甲状旁腺功能减退中的作用提供了见识。©2020美国骨骼和矿物质研究学会。