| Objective: Acute cerebral infarction(ACI) is a common disease which has many risk factors. Up to now same studies reuealed that several factors incuding aged, hereditary factors, hypertension, diabetes mellitus, cardiac diseases, history of transient ischemic attack, smoking, high intaking of alcohol and hyperlipidaemia are risk fectors of brain infarction.Ho wever, these risk factors is persistently existed and relatively stable yet the incidence of cerebral infarction are in sudden and are not associated with the state and time of an illness. So there must be same other factors to trigger the out-break of cerebral infarctions. Many studies showed the infection within the one preceding week cerebral infarction in patients was approximately 30%-35%, significantly higher than those in the control subjects. More recent studies indicated that preceding infection maybe is a "physiological trigger" or direct cause for cerebral infarction in part of the cases. The pathogenetic mechanisms possibly Unking infection and cerebral infarction remain to clarify. A further aim of this study was to investigate thepathogenetic pathways linking infection and cerebral infarction, on the basis of circulating immune complex and immune reaction. In the light of the theory that infection lead to immune damages, we investigated the role of circulating immune complex in infection-associated cerebral infarction and confirm the relation between infection and cerebral infarction .Methods: A case -control study was camied out in which 97 ACI cases were in volved . For the ACI case CT or MRI tests were used to confirm their diagnosis while the control groups were confirmed nonliver or kidney illness involved. Control subjects were individually matched to patients by sex, age, and season of admission, and other risk factors. According to recent infection the 95 patients were divided into two groups: 26 with and 69 without infection within 2 week before infarction. We test CIC, complement C3, C4, Clq and c-reaction protein (CRP) level at the onset for cerebral infarction.SAS(V8) software was used for the statisticed analyses. In the statistical analysis for risk factors, we used univariate and multiple logistic regression analysis. The chi-square test was applied to compare infection proportions in patients and control groups. For the comparison of immunohematologic characteristics, we applied the analysis of variation. For the association of risk factors, we used the spearman's correlation analysis.Results: the results of univariate logistic regression analysis showed that preceding infection(OR,2.67; 95%CI, 1.2 to 5.9), CIC(OR,1.08; 95%CI, 1.03 to 1.12) and CRP (OR,1.27; 95%CI, 1.16 to 1.39) level rising, Clq (OR,0.88; 95%CI, 0.83 to 0.93), C3(OR,0.98; 95%CI, 0.96 to 0.99), C4 (OR,0.93; 95%CI, 0.89 to 0.97) level reducing were risk factors of cerebral infarction. The results of multiple logistic regression analysis showed that CRP (OR, 1.26; 95%CI, 1.12 to 1.43) level rising, C3 (OR,0.98; 95%CI, 0.96 to 0.99), Clq (OR,0.88; 95%CI 0.82 to 0.94) level reducing were risk factors of cerebral infarction ( x2=6.07,p<0.05) .Infection within the two preceding weeks in patients (26.8%) was significantly more often than that in the control (12.1%) by chi-square test.CIC level in initial stage in both CI cases with and without preceding infection were higher than that in the control group [(4.26+3.31)mg/dl]. CIC level in initial stage in cases with preceding infection [(12.88+2.4)mg/dl] was higher than that without infection [(7.19+2.69)mg/dl]. CRP level in both CI cases with infection [(10.23+ 1.82)mg/dl] and without infection [(8.91+2.04)mg/dl] were higher than that in control group [(5.62+1.78)mg/dl], but the two case groups had no significantly difference. Clq, C3, C4 level in cases with infection [(7.24 +1.55)mg/dl], [(75.86+1.26)mg/dl], [(18.2 +1.48)mg/dl], and without infection [(7.41+ 1.66)mg/dl], [(79.43+1.35)mg/dl], [(20.42 +1.55)mg/dl]were lower than control group [(11.22+1.82)mg/dl], [(95.5+...
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