肺炎衣原体与不稳定性心绞痛相关性的临床研究

The clinical study of relationship between Chlamydia pneumoniae infection and unstable angina pectoris

目的 探讨肺炎衣原体感染与不稳定性心绞痛 (UAP)发病的关系。方法 UAP、稳定性心绞痛 (SAP)各 30例及正常对照组 2 0名。检测肺炎衣原体特异性抗体IgG、IgM滴度 ,肿瘤坏死因子α(TNFα)、C反应蛋白 (CRP)水平 ,组织型纤溶酶原激活剂 (tPA )及其抑制物 1(PAI 1)活性。结果 (1)UAP组TNFα、CRP和PAI 1较SAP组和对照组升高 ;(2 ) 3组肺炎衣原体 IgG阳性率分别为 83.3%、6 0 %和 35 %,UAP组高于SAP组和对照组。IgM阳性率组间比较差异无显著性意义 ;(3)IgG阳性组TNFα、CRP、PAI 1及TG、TC、LDL C均显著高于阴性组 ,tPA低于阴性组。IgM阳性组和阴性组各参数比较差异无显著性意义。结论 肺炎衣原体慢性感染与UAP发生有关 ,其参与UAP的机制可能是 :肺炎衣原体感染诱导TNFα和CRP产生 ,促进PAI 1活性表达、降低tPA活性 ,并干扰血浆脂质代谢 ,从而促进UAP发生。

Objective To investigate the relationship between chronic infection with Chlamydia pneumoniae(Cpn) and unstable angina pectoris (UAP).Methods Blood samples were collected from 30 UAP,30 stable angina pectoris (SAP) and 20 healthy controls.The serum specific antibodies to Cpn were measured by the microimmunofluorescence test.Serum tumor necrosis factor α (TNFα) was determined by ELISA,and C-reactive protein (CRP) was examined by immunonephelometry.Tissue-type plasminogen activator (tPA) and the inhibitor 1 (PAI-1) were analyzed by chromogenic substrate s-2251 assay.Results (1)The levels of TNFα,CRP and PAI-1 in UAP patients were higher than those in SAP patients and control group.There was no difference in tPA between the three groups.(2)The positive rate of Cpn-specific IgG antibody was 83.3% in UAP cases,60% in SAP patients and 35% in controls;IgM antibody was 23.3%,26.7% and 25% respectively.The difference of positive rates of IgG antibody was significant,while that of IgM antibody was insignificant.(3)The levels of TC,TG,LDL-C,and TNFα,CRP concentrations,along with the activity of PAI-1 in seropositive individuals were higher whereas the activity of tPA was lower than in seronegative cases.Conclusion Chronic infection with Cpn is significantly associated with UAP and may contribute to the initiation and progression of atherosclerosis by inducing the proinflammatory cytokine TNFα and inflammatory acute phase protein CRP,increasing the expression of PAI-1 activity and decreasing tPA activity,as well as interfering the metabolism of plasma lipid.