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作 者:徐瑞雪 黄高忠[1] XU Rui-Xue;HUANG Gao-Zhong(Department of Priority, Sixth People′s Hospital Affiliated to Shanghai Jiaotong University, Shanghai 200233,China)
出 处:《中华老年多器官疾病杂志》2019年第8期632-636,共5页Chinese Journal of Multiple Organ Diseases in the Elderly
摘 要:阻塞性睡眠呼吸暂停综合征(OSAS)是临床上常见的睡眠障碍表现,同时也是患骨质疏松症的危险因素。OSAS患者的骨密度倾向于降低,但持不同观点的学者认为OSAS患者骨密度增加或不变。骨转换标志物包括骨吸收标志物和骨形成标志物,与骨密度相比,可快速反映骨代谢变化。OSAS患者存在长期慢性间歇性缺氧的病理生理基础,该过程可诱导骨代谢相关基因的表达发生改变,通过核转录因子-κB信号通路等机制影响骨代谢,但在临床上并未得到确切证实,目前相关机制尚不明确。Obstructive sleep apnea syndrome(OSAS) is a common sleep disorder and a risk factor for osteoporosis. Bone mineral density tends to decrease in OSAS patients, but studies by different scholars have shown that bone density increases or remains unchanged . Bone turnover markers, including bone resorption markers and bone formation markers, reflect quickly changes in bone metabolism as compared with bone density. Long-term chronic intermittent hypoxia in OSAS patients induces alterations in the genes related to bone metabolism, affecting bone metabolism through signaling pathways such as changes in nuclear factor-κB. However, this has not been confirmed clinically and the related mechanism remains unknown.
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