期刊文献+

基于“血瘀”理论探讨绝经后骨质疏松症的“铁过载”相关机制 被引量:11

Exploration of the mechanism of iron overload in postmenopausal osteoporosis based on the theory of blood stasis
下载PDF
导出
摘要 绝经后骨质疏松症(postmenopausal osteoporosis,PMOP)是涉及雌激素水平、钙离子代谢、环境因素等多种复杂诱因的常见代谢性骨疾病,严重危害中老年女性的身体健康及生活质量。伴随PMOP病因学研究的不断深入,越来越多的学者认为"铁过载"与绝经后女性的骨量变化存在相关性,并作用于PMOP发病始末。该机制与祖国医学中"血瘀"理论密切联系,在指导PMOP的临床防治上意义深远,有形实邪易于结聚,结而不散致机体营养缺乏,累于筋骨日久则致髓减骨枯,进一步诱发骨质疏松。笔者基于中医"血瘀"理论,就"铁过载"影响机体骨量变化及诱发PMOP的作用机制展开综述,旨在为从事相关工作的临床工作者提供新思路,以期更好地指导临床。 Postmenopausal osteoporosis(PMOP)is a common metabolic bone disease relating to estrogen levels,calcium metabolism,environmental factors,and a variety of complex causes,serious harming the health and quality of life of middle-aged and old women.With the study of the development of PMOP etiology,more and more scholars believe that iron overload has a certain correlation with the change of bone mass in postmenopausal women and is related to the onset and end of PMOP.This mechanism is closely related to the theory of blood stasis in Chinese medicine.Blood stasis makes it easy for physical and solid pathogens to gather,deficiency of the nourishment,and bone marrow reduction and bone wasting,leading to the onset of osteoporosis.Based on the theory of blood stasis,the authors summarize the effect of iron overload on bone mass change and the mechanism of inducing PMOP,in order to provide a new way of thinking for clinical workers and a better guide the clinical practice.
作者 李红专 史恒蔚 张敏 马同 李彦强 张永健 LI Hongzhuan;SHI Hengwei;ZHANG Min;MA Tong;LI Yanqiang;ZHANG Yongjian(Gansu Provincial Hospital of Traditional Chinese Medicine,Lanzhou 730050;Gansu University of Traditional Chinese Medicine,Lanzhou 730030,China)
出处 《中国骨质疏松杂志》 CAS CSCD 北大核心 2021年第7期1071-1074,共4页 Chinese Journal of Osteoporosis
基金 国家自然科学基金(81760877) 卫生部医药卫生科技发展研究中心科研基金(W2014ZT210) 甘肃省卫生行业项目(GWGL2014-11) 甘肃中医药大学研究生创新基金项目(CX2018-10)。
关键词 “血瘀”理论 绝经后骨质疏松症 铁过载 相关机制 中医中药 blood stasis theory postmenopausal osteoporosis iron overload relevant mechanism traditional Chinese medicine
  • 相关文献

参考文献25

二级参考文献244

共引文献654

同被引文献199

引证文献11

二级引证文献14

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部