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从虚瘀论治对骨质疏松骨代谢指标PINP CTX影响的研究 被引量:5

Study on the effect of treatment of deficiency and stasis on PINP and CTX of bone metabolism indexes of osteoporosis
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摘要 目的观察中医从虚、瘀论治对骨质疏松患者骨代谢标志物PINP、CTX的影响。方法研究病例72例分为3组,各24例,均采用碳酸钙D3基础治疗。补肾组在对照组基础上配合补肾中药应用,祛瘀组配合活血化瘀中药。观察6周后PINP、CTX的变化以及症状改善情况。结果与对照组相比,补肾组及祛瘀组在治疗前后PINP均有明显改善(P<0.01),补肾组CTX改善程度优于其他组(P<0.05);祛瘀组症状缓解有效率79.2%,高于其他组(P<0.05)。结论补肾中药能够促进成骨细胞活性,抑制破骨细胞活性,从而起到抗骨质疏松作用;活血化瘀中药能够抑制破骨细胞活性,改善临床症状;在改善骨代谢上补肾法优于祛瘀法,在临床症状缓解上祛瘀法优于补肾法。 Objective To observe the treatment effect from deficiency and stasis on PINP and CTX in osteoporosis patients. Methods 72 cases of study cases were divided into three groups of 24 cases and treated with Calcium Carbornate D3. Kidney-invigorating group in the control group based on the application with kidney-reinforcing drugs, removing-stasis group with promoting-circulation drugs. To observe the changes of PINP and CTX after 6 weeks, and the improvement of symptoms. Results Compared with the control group, kidney-invigorating and removing-stasis groups of PINP before and after treatment were significantly improved(P〈0.01), CTX improved in kidney-invigorating group was better than other groups,the response rate of group removing-stasis was 79.2% higher than that of other groups(P〈0.05). Conclusion Kidney-reinforcing drugs can promote osteoblast activity, inhibition of osteoclast activity, which play anti-osteoporosis. Promoting-circulation drugs can inhibit osteoclast activity, improve clinical symptoms. Improved bone metabolism kidney-invigorating is better than removing-stasis, clinical symptom relief removing-stasis is better than kidney-invigorating.
作者 张鹏 罗伟 ZHANG Peng;LUO Wei(Department of TCM,Affiliated Xuzhou Central Hospital of Nanjing University of Traditional Chinese Medicine,Xuzhou 221009,Jiangsu Province,China)
出处 《吉林中医药》 2018年第9期1024-1026,共3页 Jilin Journal of Chinese Medicine
基金 江苏省中医药局科技项目(YB2015088)
关键词 骨质疏松 Ⅰ型胶原羧基末端肽 Ⅰ型前胶原氨基末端肽 deficiency stasis osteoporosis type I procollagen amino-terminal peptide type I collagen carboxy- terminal peptide
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