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摘要Hypertension is leading risk factor for cardiovascular disease and its contribution to the health burden is outstanding.The prevalence of this disease in china in adult population is 27％,and the morbidity and mortality due to CVD is projected to increase,both in absolute terms and as proportional of total disease burden over the next ten years.Definitive strategies for preventing and treatment should be in place to fight this disease.Recently it has been pointed out that inflammatory process and immune response abnormality play a role in pathogenesis of essential hypertension and contribute to end organ damage.The aim of this study to assess how the Th1,Th2,Th17 and MCP-1 mediated cytokines and chemokines associated with Autoantibodies against AT1 and α1 receptors in essential hypertensive patients and it correlates with clinical severity.<br>　　This is cross-sectional study in which serum cytokines and chemokines concentration were measured by Bio-plex and the presence or absence of GPCR autoantibody in patients'serum samples was detected and with other clinical parameters such as TC,HDL,LDL,MAP,LVDs and eCr was also measured.<br>　　We detected low concentration of Th2 mediated cytokine (IL-4,IL-13) and there is no significant difference of mean concentration of IL-4,IL-6,IL-10,IL-12,IL-13,IL-17 and MCP-1 between patients who are positive GPCR autoantibodies and those who are negative and there is no significant difference in clinical severity between autoantibodies positive and negative group.Also we found out IL-10 is significantly increased in patient serums whereas expression of Th1 mediated cytokines is high regardless that the patient is autoantibodies positive or negative.<br>　　There is high possibility that Th2 doesn't play a role in the generation of autoantibodies against AT1 and α1 receptors and large extensive and well controlled clinical research is required to clarify the role by which Th1 and GPCR autoantibodies contributes to the pathogenesis and progression of essential hypertension,and how they affect/interact with each other and their part in causing end organ damage.