Parathyroid hormone deficiency and excess: Similar effects on trabecular bone but differing effects on cortical bone
Parathyroid hormone deficiency and excess: Similar effects on trabecular bone but differing effects on cortical bone
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DOI：
10.1210/jc.84.2.718
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发表时间：
1999-02-01
影响因子：
5.8
通讯作者：
Seeman, E
中科院分区：
文献类型：
--
作者：
Duan, YB;De Luca, V;Seeman, E
甲状旁腺激素(PTH)在松质骨中可能是合成代谢的，在皮质骨中可能是分解代谢的。由于骨骼的许多区域包含两种类型的骨，PTH缺乏或过剩的影响可能很难使用骨密度测量来评估，骨密度测量是一种整合了骨皮质和骨小梁间隔的技术。我们问了以下问题：1)术后甲状旁腺功能减退症患者的高骨密度是否是由于皮质骨而不是骨小梁的增加？2)术后甲状旁腺功能减退症患者的年龄相关性骨丢失是否减缓？3)原发性甲状旁腺功能亢进症患者的骨密度降低是否是由于腰椎皮质骨而不是小梁骨的缺陷？腰椎、股骨近端、桡骨远端和股骨中段的骨密度通过前后向扫描(PA)测量，而腰椎第三腰椎的骨矿含量(BMC)是用双x射线吸收仪侧向扫描测量的，年龄64.6±3.2岁。术后甲状旁腺功能减退症，25例女性，年龄68.7+/-1.6岁，为原发性甲状旁腺功能亢进症。8例甲状旁腺功能减退症患者在4.7+/-0.6年后重复测量，20名年龄匹配的对照组在4.0+/-0.4年后重复测量。在甲状旁腺功能减退症患者中，PA扫描第三腰椎(椎体加后突)的骨量z评分高于零(1.26+/-0.58so，P<；0.05)和侧扫(1.04+/-0.60So，P=0.1)，在小梁丰富的椎体(1.02+/-0.47SD，P=0.07)和以皮质为主的后突(0.98+/-0.66So，P=0.1)。股骨颈(0.89+/-0.48so，P=0.09)、股骨干(0.45+/-0.60，NS)和桡骨远端(0.04+/-0.51，NS)的BMDz评分均高于零。在随访期间，对照组的股骨颈骨密度下降，但甲状旁腺功能减退症患者的股骨颈骨密度没有下降(斜率，-0.00818+/-0.00496 g/cm(2)/年us。0.00907+/-0.00583 g/cm(2)/年，P=0.06)。两组腰椎骨密度均无明显变化。在25例原发性甲状旁腺功能亢进症患者中，PA或侧位扫描均未发现第三腰椎(椎体加后突)骨密度降低。侧位扫描显示椎体BMC增加(0.64±0.31 SD，P<；0.01)，后路BMC降低(-0.65±0.26 SD，P<；0.05)。骨密度在股骨中段较低(-0.82+/-0.37sn，P<；0.05)，在桡骨远端(-0.68+/-0.20sn，P<；0.01)，但不在股骨颈。(-0.08+/-0.20SO，NS)。甲状旁腺功能亢进症患者无法获得纵向数据。综上所述，甲状旁腺激素缺乏和过剩都会增加骨小梁。PTH缺乏会减缓皮质骨丢失，而PTH过量则会加速皮质骨丢失，因此抑制PTH可能会减少与年龄相关的骨丢失和骨折的风险。评估甲状旁腺激素缺乏和过剩的骨密度需要对皮质骨和松质骨进行单独研究。
Parathyroid hormone (PTH) may be anabolic at trabecular bone and catabolic in cortical bone. As many regions of the skeleton contain both types of bone, the effects of PTH deficiency or excess may be difficult to evaluate using bone densitometry, a technique that integrates the cortical and trabecular compartments of bone. We asked the following questions: 1) Is the higher bone mineral density (BMD) in postsurgical hypoparathyroidism due to higher cortical, not trabecular, bone? 2) Is age-related bone loss slowed in patients with postsurgical hypoparathyroidism? 3) Is lower BMD in primary hyperparathyroidism the result of deficits in cortical, not trabecular, bone?BMD of the lumbar spine, proximal femur, distal radius, and femoral midshaft was measured by postero-anterior (PA) scanning, while bone mineral content (BMC) of the third lumbar vertebra was measured by lateral scanning using dual x-ray absorptiometry in 10 women, ages 64.6 +/- 3.2 yr, with postsurgical hypoparathyroidism and in 25 women, ages 68.7 +/- 1.6 yr, with primary hyperparathyroidism. Measurements were repeated 4.7 +/- 0.6 yr later in 8 patients with hypoparathyroidism and 4.0 +/- 0.4 yr later in 20 age-matched controls. Data were expressed as z scores (SD, mean +/- sem) derived from 405 postmenopausal women.In patients with hypoparathyroidism, bone mass z score of the third lumbar vertebra (vertebral body plus posterior processes) was higher than zero by PA scanning (1.26 +/- 0.58 so, P < 0.05) and lateral scanning (1.04 +/- 0.60 so, P = 0.1), and higher at the trabecular-rich vertebral body(1.02 +/- 0.47 SD, P = 0.07) and predominantly cortical posterior processes (0.98 +/- 0.66 so, P = 0.1) determined by lateral scanning. The BMD z scores were higher than zero at the femoral neck (0.89 +/- 0.48 so, P = 0.09), but not at the femoral midshaft(0.45 +/- 0.60, NS) and distal radius (0.04 +/- 0.51, NS). During follow-up, femoral neck BMD decreased in controls but not in patients with hypoparathyroidism (slope, -0.00818 +/- 0.00496 g/cm(2)/year us. 0.00907 +/- 0.00583 g/cm(2)/year, respectively, P = 0.06). There was no change in lumbar spine BMD in either group. In 25 women with primary hyperparathyroidism, there were no deficits in BMD at the third lumbar vertebra (vertebral body plus posterior processes) by PA or lateral scanning. By lateral scanning, BMC was increased at the vertebral body (0.64 +/- 0.31 SD, P < 0.01) and reduced at the posterior processes (- 0.65 +/- 0.26 SD, P < 0.05). BMD was lower at the midshaft of the femur (- 0.82 +/- 0.37 sn, P < 0.05) and at the distal radius (-0.68 +/- 0.20 sn, P < 0.01), but not at the femoral neck. (- 0.08 +/- 0.20 so, NS). Longitudinal data were unavailable in hyperparathyroid patients.In summary, trabecular bone is increased by both PTH deficiency and excess. Cortical bone loss is slowed by PTH deficiency and accelerated by PTH excess so that suppression of PTH may reduce age-related bone loss and the risk of fracture. Assessment of BMD in PTH deficiency and excess requires the separate study of cortical and trabecular bone.