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目的探讨幽门螺杆菌 (HP)感染、HP的细胞毒素相关蛋白A(CagA)阳性菌株感染和血清HP特异性抗体IgG(HP IgG)的浓度与初发脑梗死的关系。 方法采用病例对照 1∶1配对研究方式 ,对 5 0例患者 (观察组 )和对照组的血清标本行HP IgG定性和定量检查及HPCagA抗体IgG(HPCagA IgG)的定性检查 ,同时检测C 反应蛋白浓度等。结果观察组与对照组之间HP IgG和HPCagA IgG的阳性率差别无显著性意义 (P =0 .82 7和P =0 .6 70 )。观察组HP IgG浓度高于对照组 (P =0 .0 18)。动脉粥样硬化性血栓性、单发病灶、单侧脑组织病灶、中型和重型临床神经功能缺损脑梗死患者的HP IgG浓度均高于对照组 (依次为P =0 .0 34、P =0 .0 2 0、P =0 .0 0 1、P =0 .0 0 1) ;观察组 4 8% ,对照组 2 6 %HP IgG浓度 >10 0U/ml,两者之间的差别有显著性意义 (χ2 =4 .4 81,P =0 .0 34,OR =2 .375 ,95 %CI 1.0 6 6～5 .2 91) ;HP IgG浓度与C 反应蛋白浓度正相关 (r =0 .334,P =0 .0 18) ,与脑梗死发病后临床神经功能缺损程度正相关 (r=0 .4 2 7,P =0 .0 0 2 )。结论HP感染率、HPCagA阳性菌株感染率与脑梗死发病无相关性。HP IgG浓度 >10 0U/ml时与脑梗死发病相关。HP IgG浓度与C 反应蛋白浓度正相关 ,与脑梗死发病后临床神经功能缺损程度正相关。
Objective To investigate the relationship between Helicobacter pylori (HP) infection, HP infection of CagA-positive strains and serum HP-specific IgG (HP IgG) concentration in primary cerebral infarction. Methods Serum samples of 50 patients (observation group) and control group were qualitatively and quantitatively detected by HP IgG and HPCagA IgG (HPCagA IgG) by case-control 1: 1 paired study. Meanwhile, C-reactive protein Concentration and so on. Results There was no significant difference in the positive rates of HP IgG and HPCagA IgG between the observation group and the control group (P = .82 7 and P = .6 70). The concentration of HP IgG in observation group was higher than that in control group (P = 0.018). HP IgG concentrations in atherosclerotic thrombosis, single lesion, unilateral brain lesion, moderate and severe clinical neurological deficit cerebral infarction patients were higher than those in control group (P = 0.34, P = 0 .0 2 0, P = 0. 0 0 1, P = 0. 0 0 1); 48% in the observation group and 26% HP IgG in the control group> 10 0U / ml, the difference between the two groups was significant (Χ2 = 4.481, P = 0.034, OR = 2.375, 95% CI 1.06 6-5.291). There was a positive correlation between HP IgG concentration and C-reactive protein (r = 0 .334, P = 0.018), which was positively correlated with the degree of clinical neurological deficit after the onset of cerebral infarction (r = 0.42 7, P = .0 0 2). Conclusion The infection rates of HP and HPCagA positive strains have no correlation with the incidence of cerebral infarction. HP IgG concentration> 10 0U / ml with the incidence of cerebral infarction. HP IgG concentration and C-reactive protein concentration is positively correlated with the degree of clinical neurological deficits after the onset of cerebral infarction is positively correlated.