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目的调查山西地区血管紧张素原(angiotensinogen,AGT)和α-内收蛋白(alpha-aduction,ADD1)基因多态性与原发性高血压(essential hypertension,EH)的关系。方法采用病例对照研究,用诱变分离聚合酶链反应(mutagenically separated polymerase chain reactions,MS-PCR)检测山西地区EH患者299例(病例组)和血压正常者218例(对照组)的AGT基因M235T多态性和ADD1基因Gly460Trp多态性。结果病例组AGT基因的TT基因型分布与对照组差异有统计学意义(P<0.001),但病例组T等位基因频率(0.426)与对照组(0.378)相比,差异无统计学意义(P=0.121)。病例组ADD1基因型分布和等位基因频率与对照组相比,差异均无统计学意义(P分别为0.306和0.072)。TT+TT联合基因型患EH的危险度增加(MT+GG:OR=0.410,P=0.041;MT+GT:OR=0.364,P=0.020;MT+TT:OR=0.262,P=0.002)。Logistic回归分析提示,AGT基因的TT基因型较MM、MT基因型患EH的相对危险度增加(MM:OR=0.502,P=0.019;MT:OR=0.306,P<0.001)。结论 AGT M235T多态性与山西地区人群患EH相关,TT基因型可能与EH危险增加有关。AGT M235T多态性与ADD1基因Gly460Trp多态性间存在基因间的协同作用。
Objective To investigate the relationship between angiotensinogen (AGT) and alpha-adduct (ADD1) gene polymorphism and essential hypertension (EH) in Shanxi Province. Methods A case-control study was conducted to detect AGT gene M235T in 299 patients with EH and 218 patients with normal blood pressure in Shanxi Province using mutagenically separated polymerase chain reactions (MS-PCR) Polymorphism and ADD1 Gene Gly460Trp Polymorphism. Results The distribution of TT genotype of AGT gene in case group was significantly different from that in control group (P <0.001). However, there was no significant difference in T allele frequency (0.426) and control group (0.378) P = 0.121). ADD1 genotype distribution and allele frequency in the case group compared with the control group, the difference was not statistically significant (P = 0.306 and 0.072, respectively). TT + TT genotype increased the risk of EH (MT + GG: OR = 0.410, P = 0.041; MT + GT: OR = 0.364, P = 0.020; MT + TT: OR = 0.262, P = 0.002). Logistic regression analysis showed that the TT genotypes of AGT increased the relative risk of EH (MM: OR = 0.502, P = 0.019; MT: OR = 0.306, P <0.001) compared with MM and MT genotypes. Conclusion The AGT M235T polymorphism is associated with EH in Shanxi population. TT genotype may be related to the increased risk of EH. There is an inter-gene synergy between the AGT M235T polymorphism and ADD1 gene Gly460Trp polymorphism.