甲状腺功能亢进性骨质疏松症发病机制及临床特点的研究进展

Research progress on pathogenesis and clinical characteristics of osteoporosis induced by hyperthyroidism

甲状腺功能亢进症(甲亢)是导致继发性骨质疏松症(OP)的原因之一。甲状腺激素(TH)和促甲状腺激素(TSH)可通过多种信号通路及调节因子作用于软骨细胞、成骨细胞及破骨细胞调节骨代谢,毒性弥漫性甲状腺肿(GD)中免疫因素对骨的影响随着骨免疫学说的提出逐渐成为研究热点,但其机制尚不明确。甲亢时钙磷代谢紊乱、骨吸收和骨形成增加且骨吸收大于骨形成,骨密度(BMD)降低及骨折风险增加,老年及绝经后女性更为显著。甲亢程度及持续时间与骨丢失程度相关,甲亢时全身BMD降低,以前臂降低最为明显。积极抗甲状腺治疗或联合抗OP治疗可有效改善BMD和降低骨折风险,但目前尚无统一规范的治疗方案。本文对甲亢性OP的发病机制及临床特点做一综述,旨在为其提供科学诊疗依据。

Hyperthyroidism is one of the causes of secondary osteoporosis(OP).Thyroid hormone(TH)and thyroid stimulating hormone(TSH)can act on chondrocytes,osteoblasts and osteoclasis to regulate bone metabolism through a variety of signaling pathways and regulatory factors.The effect of immune factors on bone in Graves'disease(GD)has gradually become a research hotspot with the development of bone immunity theory,but its mechanism remains unclear.In hyperthyroidism,calcium and phosphorus metabolism are disturbed,bone resorption and bone formation are increased,and bone resorption is greater than bone formation,and bone mineral density(BMD)is decreased and fracture risk is increased,especially in elderly and postmenopausal women.The degree and duration of hyperthyroidism were correlated with the degree of bone loss.BMD decreased in the whole body,especially in the forearm.Active anti-thyroid therapy or combined anti-osteoporosis therapy can effectively improve BMD and reduce fracture risk,but there is no standardized treatment plan.This article reviews the pathogenesis and clinical characteristics of OP induced by hyperthyroidism,in order to provide scientific diagnosis and treatment basis for this disease.