The Relationship Between The Effect Of Atorvastatin Treatment And Plasma C-reactive Protein Level And The1059G/C Gene Polymorphism

Objective To explore the relationship between the serum C-reactive proteinlevels and the CRP1059G/C (rs1800947) gene polymorphism with the effective ofatorvastatin.And their influences for cerebral infarction of the Han populationneurological function. Whether relationship on serum concentration of CRP andLDL-C down with atorvastatin.Methods A case-control with retrospective analysis on97healthy controls and123stroke patients.Lipid levels was determined by Enzymatic (GPO-PAP).Andimmune transmission measured serum CRP levels.The genotype and allelefrequencies of CRP1059G/C gene polymorphism were analyzed by polymerase chainreaction and restriction fragment length polymorphism. Atorvastatin the conventionaldose20mg everyday.Follow-up3months,reviewed the serum CRP levels and LDL-C.Differences of measurement data were compared with the t test,ANOVA method orrank sum test.The enumeration data were compared with the chi-square test. The riskfactors were analyzed using logistic regression analysis.All data were analyzed usingSPSS for windows13.0.Results There were significant differences for CRP1059G/C genotypefrequencies between the health controls and the patients(P <0.05). On the patients,theallele frequency of CRP1059G/C was G92.68%, C7.32%. On the controls,the allelefrequency was G78.35%,C21.65%(P <0.05). All the people on case group andcontrol group, the Log CRP level among CRP1059G/C genotype were G/G(-1.45±1.51), G/C(-1.32±1.57), C/C(-2.72±1.08) log mg/L, the differences was significant.There was no signficant correlation of the decline on serum levels of CRP between CRP1059G/G and G/C genotype with atorvastatin (P＞0.05). Atorvastatinsignificantly reduced the serum Log CRP levels（before-0.75±1.26,after-1.53±1.28）Log mg/L and LDL-C levels（before3.32±1.26,after1.81±0.78）mmol/L,in patientswith cerebral infarction(P <0.05). There were no significant correlation of the declinein serum levels of CRP and LDL-C with atorvastatin(P＞0.05). NIHSS score wasassociated with serum CRP levels in patients with cerebral infarction. There weresignificant differences that the CRP levels with stroke rating for NIHSS was higherthan the others(P <0.05). Even through,there were no statistical differences thatneither CRP genotype or alleles showed an association with patient’s condition (P>0.05).Logistic regression analysis displayed that the major risk factors for cerebralinfarction including:history of smoking or alcohol consumption, hypertension,CRPlever,also hyperglycemia associated with CI,CRP1059G/C+C/C genotype andHDL-C were protective factors for CI.Conclusion There were significant differences for CRP1059G/C genotypefrequencies between the health controls and the patients.The C allele is a protectivefactor of the Han population cerebral infarction.There was no connection between thealleles of CRP1059G/C and serum CRP levels with atorvastatin. Within atorvastatintreatment,serum CRP and LDL-C levels of the Han population CI were significantlydecreased,but the decline has no significant correlation.