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特发性高钙尿症中的骨病与细胞因子:综述

Bone disease and cytokines in idiopathic hypercalciuria: a review.

作者信息

Santos Augusto C S, Lima Eleonora M, Oliveira Eduardo Araújo, Simões e Silva Ana Cristina

机构信息

Department of Pediatrics, Pediatric Nephrology Unit, Hospital das Clínicas, Federal University of Minas Gerais, Belo Horizonte, Brazil.

出版信息

J Pediatr Endocrinol Metab. 2011;24(7-8):405-10. doi: 10.1515/jpem.2011.243.

Abstract

Bone remodeling is a continuous and dynamic process of skeletal destruction and renewal. A complex regulatory mechanism with the participation of several cytokines precisely defines the role of osteoclasts in the chain of events leading to bone resorption. There are multiple mechanisms underlying the regulation of bone resorption, which can involve increased calcium excretion and decreased bone density in patients with idiopathic hypercalciuria (IH). However, the pathogenesis of bone mass reduction in IH remains uncertain. The purpose of this review is to summarize the recent published evidence on the possible mechanisms by which cytokines could be associated with the pathogenesis of IH.

摘要

骨重塑是骨骼破坏与更新的一个持续且动态的过程。一个由多种细胞因子参与的复杂调控机制精确地界定了破骨细胞在导致骨吸收的一系列事件中的作用。骨吸收的调控存在多种机制,这可能涉及特发性高钙尿症(IH)患者钙排泄增加和骨密度降低。然而,IH中骨量减少的发病机制仍不明确。本综述的目的是总结最近发表的关于细胞因子可能与IH发病机制相关的证据。

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