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丁苯酞联合尤瑞克林对急性脑梗死患者神经功能及血浆内皮素-1和血清超敏C反应蛋白的影响
引用本文:张明勤,吴涛. 丁苯酞联合尤瑞克林对急性脑梗死患者神经功能及血浆内皮素-1和血清超敏C反应蛋白的影响[J]. 江苏预防医学, 2020, 0(1): 44-47
作者姓名:张明勤  吴涛
作者单位:;1.河南中医药大学第一附属医院
摘    要:目的观察丁苯酞联合尤瑞克林对急性脑梗死(ACI)患者神经功能及血浆内皮素-1和血清超敏C反应蛋白的影响。方法选择2015年5月-2017年5月收治的急性脑梗死患者102例作为试验对象,随机分为对照组和试验组,在接受常规治疗基础上,对照组予以尤瑞克林治疗,试验组予以尤瑞克林联合丁苯酞治疗。比较两组患者的治疗前后神经功能缺损程度(NIHSS)评分和生活能力(mRS)评分、血浆内皮素-1(ET-1)、血清超敏C反应蛋白(hs-CRP)水平以及临床疗效,记录治疗后2年随访期内患者主要脑血管不良事件的发生情况。结果试验组治疗后总有效率为90.20%,明显高于对照组70.59%,差异具有统计学意义(χ^2=6.220,P<0.05)。对照组和试验组治疗后的NIHSS评分和mRS评分均较治疗前低,差异有统计学意义(t值分别为7.341、34.327、22.526、45.305,P值均<0.05);治疗后试验组NIHSS评分、mRS评分显著低于对照组,差异均有统计学意义(t值分别为7.251、20.561,P值均<0.05)。对照组和试验组治疗后血浆ET-1和血清hs-CRP水平均显著低于治疗前,差异有统计学意义(t值分别为12.949、98.357、25.026、111.887,P值均<0.05);治疗后血浆ET-1水平和血清hs-CRP水平,试验组显著低于对照组,差异均有统计学意义(t值分别为13.674、12.812,P值均<0.05)。ACI患者发生不良脑血管事件的Kaplan-Meier生存曲线显示,实验组平均发生时间明显长于对照组,差异存在统计学意义(χ^2=12.868,P<0.001)。结论丁苯酞联合尤瑞克林有助于降低急性脑梗死患者神经功能的缺损程度,更好抑制ET-1和hsCRP的生成,从而改善患者血管内皮功能,降低脑梗死损伤程度,临床疗效显著。

关 键 词:丁苯酞  尤瑞克林  急性脑梗死  神经功能  内皮素-1  C反应蛋白

Effects of butylphthalide combined with urinary kallidinogenase on neurological function,plasma endothelin-1 and serum hypersensitive C-reactive protein in patients with acute cerebral infarction
ZHANG Ming-qin,WU Tao. Effects of butylphthalide combined with urinary kallidinogenase on neurological function,plasma endothelin-1 and serum hypersensitive C-reactive protein in patients with acute cerebral infarction[J]. Jiangsu Journal of Preventive Medicine, 2020, 0(1): 44-47
Authors:ZHANG Ming-qin  WU Tao
Affiliation:(The First Affiliated Hospital of He′nan University of Traditional Chinese Medicine,Henan Zhengzhou 450000,China)
Abstract:Objective To observe the effects of butylphthalide combined with urinary kallidinogenase on neurological function,plasma endothelin-1(ET-1)and serum hypersensitive C-reactive protein(hs-CRP)in patients with acute cerebral infarction(ACI).Methods A total of 102 ACI cases admitted and treated from May 2015 to May 2017 were selected as study subjects,who were randomly divided into control group and study group.The control group was treated with routine therapy combined with urinary kallidinogenase,while the study group was treated with routine therapy and combination of butylphthalide and urinary kallidinogenase.The scores of NIHSS and mRS,plasma ET-1 and serum hs-CRP levels of two groups were compared before and after treatment,while major cerebrovascular adverse events were recorded during 2-year follow-up after treatment.Results The total curative rate after treatment of study group was 90.20%,which was significantly higher than that of the control group(70.59%),the difference was statistically significant(χ^2=6.220,P<0.05).The NIHSS score and mRS score after treatment were both lower than before treatment in both control group and study group,with statistically significant differences(t values were 7.341,34.327,22.526 and 45.305,respectively,all P<0.05).After treatment,the NIHSS score and mRS score in study group were significantly lower than those in control group,with statistically significant differences(t values were 7.251 and 20.561,all P<0.05);the plasma ET-1 and serum hs-CRP levels in control group and study group were significantly lower than before treatment,with statistically significant differences(t values were 12.949,98.357,25.026,111.887,respectively,all P<0.05);the plasma ET-1 level and serum hs-CRP level were significantly lower in study group than in control group,with statistically significant differences(t values were 13.674 and 12.812,respectively,all P<0.05).The kaplan-meier survival curve of ACI patients showed that the mean duration of adverse cerebrovascular events was significantly longer in study group than in control group(χ^2=12.868,P<0.001).Conclusions Butylphthalide combined with urinary kallidinogenase in treatment of acute cerebral infarction can reduce the degree of neurological deficit,decrease the levels of ET-1 and hs-CRP,improve vascular endothelial function,reduce the degree of cerebral infarction,and has significant clinical efficacy.
Keywords:Butylphthalide  Urinary kallidinogenase  Acute cerebral infarction  Neurological function  Endothelin-1  C-reactive protein
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