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骨质疏松症的发病机制。

The pathogenesis of osteoporosis.

作者信息

Gallagher J C

机构信息

Creighton University, Department of Medicine, Omaha, NE 68105.

出版信息

Bone Miner. 1990 Jun;9(3):215-27. doi: 10.1016/0169-6009(90)90039-i.

DOI:10.1016/0169-6009(90)90039-i
PMID:2194602
Abstract

Changes in the calciotropic hormones with age contribute significantly to the pathogenesis of osteoporosis. In both postmenopausal (Type I) and senile osteoporosis (Type II) it is common to find reduced levels of serum 1,25-dihydroxyvitamin D and malabsorption of calcium. In Type I patients a reduced level of serum parathyroid hormone causes a real decrease in serum 1,25-dihydroxyvitamin D production and malabsorption of calcium, whereas in Type II patients the decline in 1 alpha-hydroxylase activity in the kidney causes a decline in serum 1,25-dihydroxyvitamin D which leads to malabsorption of calcium and secondary hyperparathyroidism. In the final analysis both pathways lead to bone loss. In some Type II patients there may be a decline also in the function or number of the vitamin D-binding receptors in the gut. Treatment of patients with vitamin D analogues, however, normalizes calcium absorption and improves calcium balance. The improvement in calcium balance reduces bone resorption and prevents further bone loss; in addition recent studies have shown that therapy with vitamin D analogues leads to a reduction in fracture incidence.

摘要

随着年龄增长,钙调节激素的变化在骨质疏松症的发病机制中起着重要作用。在绝经后(I型)和老年性骨质疏松症(II型)中,血清1,25-二羟维生素D水平降低和钙吸收不良都很常见。在I型患者中,血清甲状旁腺激素水平降低导致血清1,25-二羟维生素D生成实际减少和钙吸收不良,而在II型患者中,肾脏中1α-羟化酶活性下降导致血清1,25-二羟维生素D下降,进而导致钙吸收不良和继发性甲状旁腺功能亢进。归根结底,这两种途径都会导致骨质流失。在一些II型患者中,肠道中维生素D结合受体的功能或数量也可能下降。然而,用维生素D类似物治疗患者可使钙吸收正常化并改善钙平衡。钙平衡的改善减少了骨吸收并防止进一步的骨质流失;此外,最近的研究表明,维生素D类似物治疗可降低骨折发生率。

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