Olgaard Klaus, Lewin Ewa
University of Copenhagen, Department of Nephrology, P2132, Rigshospitalet, 9 Blegdamsvej, DK-2100 Copenhagen, Denmark.
Clin J Am Soc Nephrol. 2006 May;1(3):367-73. doi: 10.2215/CJN.01961205. Epub 2006 Mar 29.
Parathyroid hyperplasia, oversecretion of parathyroid hormone (PTH), and hyperparathyroid bone disease are characteristic features of chronic uremia; they develop early in the course of uremia and often in a progressive way. This review focuses on the potential for arrest or regression of hyperparathyroid-induced bone disease. For this purpose, the review addresses investigations that have used bone histology and not investigations that indirectly attempted to demonstrate changes in the skeleton by measurements of bone mineral density or laboratory indices of bone turnover, other than PTH. A prerequisite for inducing regression of the hyperparathyroid bone disease is a significant suppression of PTH secretion or reversal of hyperparathyroidism and uremia. It is concluded, on the basis of paired bone biopsy studies in patients with established hyperparathyroid bone disease, that bone histology can be improved or normalized after treatment that diminishes PTH levels. Oversuppression of PTH levels, however, might lead to adynamic bone disease.
甲状旁腺增生、甲状旁腺激素（PTH）分泌过多以及甲状旁腺功能亢进性骨病是慢性尿毒症的特征性表现；它们在尿毒症病程早期出现，且往往呈进行性发展。本综述聚焦于甲状旁腺功能亢进性骨病停止发展或逆转的可能性。为此，本综述探讨了使用骨组织学的研究，而非那些试图通过测量骨密度或除PTH之外的骨转换实验室指标来间接证明骨骼变化的研究。诱导甲状旁腺功能亢进性骨病逆转的一个先决条件是显著抑制PTH分泌或逆转甲状旁腺功能亢进和尿毒症。基于对已确诊甲状旁腺功能亢进性骨病患者的配对骨活检研究得出结论，降低PTH水平的治疗后，骨组织学可得到改善或恢复正常。然而，PTH水平过度抑制可能导致骨再生障碍性骨病。
