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幽门螺杆菌感染与缺血性卒中的相关性研究
引用本文:郑兢,陈力宇,吴赛珍,蔡亦强,沈媛媛,王乐微,陈晓军,李未今. 幽门螺杆菌感染与缺血性卒中的相关性研究[J]. 北京医学, 2014, 0(5): 340-343
作者姓名:郑兢  陈力宇  吴赛珍  蔡亦强  沈媛媛  王乐微  陈晓军  李未今
作者单位:郑兢(325600,温州医科大学附属乐清医院神经内科);陈力宇(325600,温州医科大学附属乐清医院神经内科);吴赛珍(325600,温州医科大学附属乐清医院神经内科);蔡亦强(325600,温州医科大学附属乐清医院神经内科);沈媛媛(325600,温州医科大学附属乐清医院神经内科);王乐微(325600,温州医科大学附属乐清医院神经内科);陈晓军(325600,温州医科大学附属乐清医院神经内科);李未今(325600,温州医科大学附属乐清医院神经内科);
基金项目:温州市医药卫生科研项目(项目编号:2012A016)
摘    要:目的探讨幽门螺杆菌(Helicobacter pylori, Hp)感染与缺血性卒中的相关性。方法按照改良TOAST分型标准对纳入的93例缺血性脑卒中患者(病例组)进行病因学分型,其中动脉粥样硬化血栓形成69例,心源性栓塞10例,小动脉卒中11例,其他3例;同时从体检人群中随机选取101例无感染史、卒中病史及其他血管病史者作为对照组。采用酶联免疫吸附法测定血清Hp特异性抗体IgG。采用Logistic回归对缺血性卒中危险因素进行分析,判定Hp感染与缺血性卒中发病相关性。结果病例组Hp—IgG阳性率高于对照组,但差异无统计学意义(69.9%vs.66-3%,OR=1.178,95%CI:0.643—2.158,P=0.645);校正Hp感染的潜在危险因素及卒中相关危险因素后,两者间差异仍无统计学意义(OR=1.010,95%CI:0.499~2.043,P=0.979)。在亚型研究中得出相似结果(动脉粥样硬化血栓形成:OR=1.243,95%CI:0.640~2.415,P=0.615;心源性栓塞:OR=0.761,95%CI:0.201~2.880,P=0.733;小动脉卒中:OR=1.353,95%CI:0.337~5.431,P=0.988),校正相关因素后差异仍无统计学意义。结论HD感染与缺血性卒中无明确相关性,有待于研究Hp在缺血性卒中发病作用机制。

关 键 词:幽门螺杆菌  缺血性卒中  危险因素

Study on the correlation between Helicobacter pylori infection and ischemic stroke
Zheng Jing,Chen Liyu,Wu Saizhen,Cai Yiqiang,Shen Yuanyuan,Wang Lewei,Chen Xiaojun,Li Weijin. Study on the correlation between Helicobacter pylori infection and ischemic stroke[J]. Beijing Medical Journal, 2014, 0(5): 340-343
Authors:Zheng Jing  Chen Liyu  Wu Saizhen  Cai Yiqiang  Shen Yuanyuan  Wang Lewei  Chen Xiaojun  Li Weijin
Affiliation:.( Department of Neurology, The People 's Hospital of Yueqing, Yueqing 325600, China)
Abstract:Objective To investigate the association between helicobacter pylori (Hp) infection and ischemic stroke (IS). Methods Totally 93 patients with IS were enrolled. Analyses were stratified for etiologic IS according to the modified TOAST criteria: 69 patients with atherothrombosis(AT), 10 patients with cardioembolism(CE), 11 patients with small artery disease(SAD) and 3 patients with other diseases. 101 control subjects without infection history, history of stroke and vascular disease were randomly selected from clinic. The serumal specific antibody IgG of Hp was detected by enzyme linked immunosorbent assay(ELISA). Conditional logistic regression was used for statistical analysis. Results The positive rate of Hp-IgG was higher in patients than that of the control group, but the difference was not statistically significant (69.9% vs. 66.3%, OR=1.178, 95%CI:0.643-2.158, P = 0.645). This difference was not significant after adjusted for potential risk fac- tors for Hp infection and known risk factors for IS (OR=1.010, 95%CI:0.499-2.043, P = 0.979). Subgroup analyses yielded similar results in all etiological stroke subtypes (univariate analysis AT:OR=1.243, 95%CI:0.640-2.415, P = 0.615; CE: OR=0.761, 95%CI:0.201-2.880, P = 0.733; SAD: OR=1.353, 95%CI:0.337-5.431, P = 0.988. Multivariate analysis AT: OR=1.291, 95%CI:0.588-2.836, P = 0.524; CE: OR=0.468, 95%CI:0.096-2.284, P = 0.348; SAD: OR=1.349, 95%CI: 0.282-6.446, P = 0.708). Conclusion Our case-control study does not shown the association between Hp chronic infection and IS. Large case-control and prospective studies are needed to investigate the contribution of infection to IS risk in some particularly subgroups.
Keywords:Helicobacter pylorl (HP) Ischemic stroke (IS) Risk factor
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