甲状腺功能减退致骨质疏松症的机制及治疗进展

Mechanism and treatment progress of osteoporosis induced by hypothyroidism

骨质疏松症是一种以低骨量和骨组织微结构破坏为特征,骨质脆性增加和易于骨折为特点的系统性骨病,其发病与甲状腺激素水平密切相关。甲状腺激素可以通过生长激素/胰岛素样生长因子-1(Growth Hormone/Insulin-like Growth Factor-1,GH/IGF-1)、成纤维细胞生长因子(Fibroblast Growth Factor,FGF)、甲状旁腺激素相关肽(Parathyroid Hormone related Peptide,PTHr P)反馈回路和激活白细胞介素-6核因子(Interleukin-6 Nuclear Factor,NF-IL-6),诱导破骨细胞分化因子(Osteoclast Differentiation Factor,ODF)表达等多种通路,分别刺激成骨细胞和破骨细胞活性,调节骨吸收与骨形成平衡。此外,甲状腺激素还可协同甲状旁腺素、降钙素、泌乳素、生长激素、性激素(雌激素、雄激素)等多种内分泌因素共同参与全身骨代谢过程(如骨骼的生长、发育和成熟,骨重建,骨吸收,钙、磷的代谢)。目前关于甲状腺疾病与骨质疏松症的研究多着重于甲状腺功能亢进与骨质疏松症的相关性,鲜有对甲状腺功能减退与骨质疏松症的相关性进行明确分析。本文在该方面研究进展作一综述,深入探讨甲状腺激素减退对骨吸收及骨矿化的作用原理,旨在为甲状腺功能减退致骨质疏松症的治疗提供新的思路与方向。

Osteoporosis is a systematic disease characterized by low bone mass,bone microstructure damage,increased bone fragility and increased risk for fractures. The pathogenesis of osteoporosis is closely related to thyroid hormone levels. Thyroid hormone stimulates the activity of osteoblast and osteoclast and regulates bone turnover via the pathways of Growth Hormone/Insulin-like Growth Factor-1（GH/IGF-1）,Fibroblast Growth Factor（FGF）,Parathyroid Hormone related Peptide（PTHrP）,activation of Interleukin-6 Nuclear Factor（NF-IL-6）,and inducing the expression of Osteoclast Differentiation Factor（ODF）. In addition,thyroid hormone acts synergistically with parathyroid hormone,calcitonin,prolactin,growth hormone and sex hormone（estrogen,androgen） in regulating the progress of bone metabolism including bone growth,development,remodeling and absorption,and the metabolism of calcium and phosphorus. Current researches on thyroid disease and osteoporosis have been mainly focused on the correlation between hyperthyroidism and osteoporosis, with limited research on the correlation between hypothyroidism and osteoporosis. In this review,research progress on hypothyroidism and osteoporosis was summarized,and the mechanism of action that hypothyroidism influences bone absorption and mineralization was discussed in detail,with the aim of providing new ideas and directions for the treatment of osteoporosis induced by hypothyroidism.