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原发性甲状旁腺功能亢进症中的骨骼疾病。

Bone disease in primary hyperparathyrodism.

机构信息

Section of Endocrinology and Bone Metabolism, Department of Endocrinology and Metabolism, University of Pisa, Via Paradisa 2, 56124 Pisa, Italy.

出版信息

Ther Adv Musculoskelet Dis. 2012 Oct;4(5):357-68. doi: 10.1177/1759720X12441869.

Abstract

Nowadays, primary hyperparathyroidism (PHPT) is mostly a mild disease. Overt skeletal manifestations are rare but decreased bone mineral density (BMD) can still be demonstrated. Even in mild cases, excess parathyroid hormone (PTH) increases bone turnover leading to bone loss particularly at cortical sites. Conversely, a relative preservation of cancellous bone has been shown by histomorphometric analyses and advanced imaging techniques. An increased fracture rate has been demonstrated in untreated patients with PHPT at peripheral sites and in the spine. Parathyroidectomy (PTx) is the definitive cure for PHPT. With the restoration of normal PTH, bone resorption is quickly tapered down, while bone formation proceeds at the level of bone multicellular units, which were activated prior to PTx. The rapid refilling of the enlarged remodeling space and the subsequent matrix mineralization will result in an increase in BMD at sites rich in trabecular bone, such as lumbar spine and hip, which mainly occurs during the first 6-12 months after PTx. Cortical bone is less responsive to PTX because of the low rate of bone turnover, but sensible increases in BMD at the distal third of the radius can be observed in the long term. PTx seems to decrease the risk of fractures but more data are needed before a definitive conclusion on this important matter can be reached. Treatment with bisphosphonates can be considered for patients with low BMD who do not undergo PTx. Two-year treatment with alendronate has been shown to decrease bone turnover markers and increase BMD at the lumbar spine and hip, but not at the distal radius. Cinacalcet stably decreased serum calcium levels across a broad range of PHPT severity, but no change in BMD occurred in patients treated for up to 5.5 years.

摘要

如今,原发性甲状旁腺功能亢进症(PHPT)大多是一种轻度疾病。明显的骨骼表现很少见,但仍可显示骨密度降低(BMD)。即使在轻度病例中,过量的甲状旁腺激素(PTH)也会增加骨转换,导致皮质部位的骨丢失。相反,组织形态计量学分析和先进的成像技术显示松质骨有相对保留。未经治疗的 PHPT 患者在周围部位和脊柱的骨折发生率增加。甲状旁腺切除术(PTx)是 PHPT 的明确治疗方法。随着正常 PTH 的恢复,骨吸收迅速减少,而骨形成则在骨多细胞单位的水平上进行,这些单位在 PTx 之前就已经被激活。扩大的重塑空间的快速填充以及随后的基质矿化将导致富含小梁骨的部位(如腰椎和髋部)的 BMD 增加,这主要发生在 PTx 后 6-12 个月内。由于骨转换率低,皮质骨对 PTX 的反应性较低,但在桡骨远端可以观察到 BMD 的长期敏感增加。PTx 似乎降低了骨折的风险,但在得出关于这一重要问题的明确结论之前,还需要更多的数据。对于未接受 PTx 的低 BMD 患者,可以考虑使用双膦酸盐治疗。为期 2 年的阿伦膦酸盐治疗已被证明可以降低腰椎和髋部的骨转换标志物和 BMD,但对桡骨远端没有影响。西那卡塞可稳定降低各种严重程度 PHPT 患者的血清钙水平,但在接受治疗长达 5.5 年的患者中,BMD 没有变化。

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