心肌梗死患者对氧磷酶-1 Q/R192基因多态性及活性检测的临床意义

目的探讨心肌梗死(AMI)患者对氧磷酶-1(PON1)Q/R192基因多态性及其活性检测的临床意义。方法分别采用紫外线分光光度法和聚合酶链式反应-限制性片段长度多态性(PCR-RELP)法检测65例AMI患者和70名健康体检者PON1活性及PON1Q/R192基因多态性。结果 AMI组血清PON1活性[(78.56±16.69)U/mL]明显低于健康对照组[(118.65±30.25)U/mL](P<0.01)。AMI组与健康对照组3种基因型及2种等位基因频率分布差异无统计学意义(P>0.05);AMI组与健康对照组间不同PON1 Q/R192基因型间血清PON1活性相比差异有统计学意义(P<0.01);AMI组内及健康对照组内PON1 Q/R192不同基因型间血清PON1活性相比差异无统计学意义(P>0.05)。结论血清PON1活性降低是AMI的危险因素之一;PON1Q/R192基因多态性与AMI的发生无相关性。     

郑州地区2型糖尿病肾功能衰竭患者芳香酯酶与基因Q192R多态性的关系

目的 探讨郑州地区汉族人群2型糖尿病慢性肾功能衰竭(DN-CRF)与血清芳香酯酶(ArE／PON1)活性及其192位基因多态性的关系。方法 通过检测2型糖尿病组(DM，121例)、DN-CRF组(123例)、健康对照组(127例)等观察对象的血清ArE／PONl活性及其192位基因多态性、血脂和脂蛋白等，进行分析研究。结果 郑州地区汉族人群中存在有ArE／PON1 192位等位基因Q与R，DN-CRF组Q、R基因频率为0．45和0．55，与DM、对照组比较，差异无统计学意义；两病例组患者血清酶活性均低于对照组，DN-CFR组降低幅度最大；DN-CFR组内RR基因型患者高密度脂蛋白胆固醇(HDL-C)、高密度脂蛋白2胆固醇(HDL2-C)水平低于QQ基因型，总胆固醇(TC)、甘油三酯(TG)和氧化型低密度脂蛋白(oxLDL)高于QQ基因型。结论 DN-CRF组ArE／PONl192位基因多态性与DM、健康对照组间虽差异无统计学意义，但不能排除DM合并DN-CRF与ArE／PON1的192位基因多态性有关；DN-CRF患者血清ArE／PON1活性降低，可能是DM合并DN的危险因素。     

对氧磷酶1基因Q192R和L55M位点多态性与川崎病冠状动脉损伤的相关性

目的探讨对氧磷酶1(paraoxonase 1, PON1)基因Q192R和L55M位点基因多态性与川崎病患儿冠状动脉损伤的关系。方法川崎病患儿73例(川崎病组),其中有冠状动脉损伤34例为损伤组,无冠状动脉损伤39例为未损伤组;同期50例健康儿童为对照组。3组采集空腹静脉血提取全血DNA,采用限制性片段长度多态性PCR技术检测PON1基因Q192R和L55M位点多态性,并进行比较。结果川崎病组Q192R位点RR、QR基因型分布频率(40.0%、44.0%)及Q等位基因频率(38.0%)与对照组(39.7%、45.2%、37.7%)比较差异无统计学意义(P0.05),L55M位点LL基因型分布频率及L等位基因频率(90.0%、95.0%)与对照组(86.3%、92.5%)比较差异无统计学意义(P0.05)。损伤组PON1基因Q192R位点RR基因型分布频率(52.9%)及R等位基因频率(72.1%)均高于未损伤组(28.2%、53.8%)(P0.05)。损伤组PON1基因L55M位点LM+MM基因型分布频率(23.5%)及M等位基因频率(13.2%)均高于未损伤组(5.1%、2.6%)(P0.05)。结论 PON1基因Q192R和L55M位点基因多态性与川崎病发生无明显相关性,与川崎病患儿冠状动脉损伤关系密切。     

糖尿病合并冠心病与芳香酯酶基因Q192R多态性分析

目的 :探讨糖尿病 (DM)芳香酯酶 (ArE/PON1)基因Q192R多态性与糖尿病合并冠心病 (DM -CAD)的关系 ,为防治DM -CAD提供理论依据。方法 :调查对象为郑州地区汉族健康人群 6 4例 (对照组 )、2型糖尿病 6 0例 (DM组 )与DM -CAD6 7例 (DM -CAD组 )。测定其血清ArE/PON1活性 ,并用聚合酶链式反应 -单链构型多态性 (PCR -SSCP)分析技术检测ArE/PON1基因Q192R的多态性 ,进行分析研究。结果 :发现对照组、DM组和DM -CAD组均存在ArE/PON1基因 192位点 (Q/R)多态性。对照组基因频率Q为 0 .5 5、R为 0 .4 5 ;DM组为 0 .5 3与 0 .4 7;DM -CAD组为 0 .38与 0 .6 2。DM -CAD组R基因频率明显高于DM组和对照组 (P <0 .0 5 ) ,DM组与对照无显著差异 (P >0 .0 5 ) ,DM与DM -CAD组血清ArE/PON1活性 (分别为 0 .2 2 5± 0 .0 18μ/ml与 0 .2 0 0± 0 .0 19μ/ml)均低于对照组 (0 .2 5 9± 0 .0 18μ/ml) ,DM -CAD组低于DM组 (P <0 .0 5 )。 3组中每组内每种基因型组间酶活性无显著差异。结论 :郑州汉族人群存在ArE/PON1Q192R(GIn/Arg)多态性 ,基因频率分布不同于白种人 ,提示R基因可能是DM合并CAD的危险因素。     

脑梗死与对氧磷酶1基因192G/A位点多态性的关系

目的:评估脑梗死患者对氧磷酶1(paraoxonase 1,PON1)的基因192G/A多态性与脑梗死间的关系。方法:采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)方法分析295例脑梗死患者(脑梗死组)及117名正常对照者(对照组)的PON1基因192G/A多态性。结果:PON1基因192G/A多态性在对照组和脑梗死组中的GG型、GA型和AA型基因型分布分别为36.75%、50.43%、12.82%和28.14%、50.85%、21.02%。G、A等位基因分布在对照组和脑梗死组中分别为61.97%、38.03%和53.56%、46.44%。经检验,PON1基因192G/A位点基因型频率在2组人群中的分布差异无统计学意义(P>0.05),而等位基因频率在2组人群中的分布差异有统计学意义(P     

C反应蛋白基因＋1444C／T多态性与缺血性脑卒中的相关分析

目的探讨C反应蛋白（CRP）基因＋1444C／T多态性与缺血性脑卒中的关系。方法选择286例缺血性脑卒中患者,根据脑动脉狭窄情况分为狭窄（136例）和无狭窄（150例）两组。同期健康体检者140例为对照组,应用PCR-RFLP方法检测受试者的CRP基因型,同时测定血清高敏C反应蛋白（ks．CRP）浓度。结果狭窄、无狭窄脑卒中组血清CRP浓度均显著高于对照组（P均〈0．01）,而这两组间CRP浓度差异无统计学意义。CRP基因＋1444C／T多态性在各组人群中的分布无统计学差异（P〉0．05）。对照组CT基因型患者血清CRP浓度显著高于CC基因型患者[1．59（0．73—4．62）mg／Lvs0．67（0．10—1．81）mg／L,P〈0．01],但卒中组不同基因型个体间hs-CRP浓度无统计学差异。结论血清hs-CRP浓度与缺血性脑卒中相关,而与卒中患者狭窄与否无关。CRP基因＋1444C／T多态性与缺血性脑卒中无相关性,但其与健康人群血清CRP浓度有关。     

缺血性脑卒中患者半胱氨酸与PON-1 Q192R基因多态性的研究

目的探讨缺血性脑卒中患者同型半胱氨酸(Hcy)与PON-1 Q192R基因多态性的相关性。方法采用循环酶联免疫法检测血浆Hcy浓度以及使用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)方法检测140例缺血性脑卒中患者(病例组)和117名健康者(对照组)PON-1 Q192R基因多态性。结果病例组和对照组平均空腹血浆Hcy浓度分别为(14.02±4.94)μmol/L和(11.64±4.18)μmol/L,两组差异有统计学意义(t=4.09,P<0.001);将病例组和对照组作为一个研究整体发现:PON-1QQ型、QR型、RR型的平均空腹血浆Hcy浓度分别是(13.34±3.91)μmol/L、(13.14±4.98)μmol/L、(13.30±4.31)μmol/L,经方差分析,PON-1各基因型间血浆Hcy浓度差异无统计学意义(F=0.033,P=0.967)。结论血浆Hcy浓度升高与缺血性卒中有关,并且缺血性脑卒中患者Hcy与PON-1 Q192R基因多态性无关。     

血清对氧磷酯酶-1活性与肝硬化Child-Pugh分级的关系

目的 探讨血清对氧磷酯酶-1(PON1)酶活性与肝硬化Child-Pugh分级的关系.方法 以对氧磷(paraoxon)为底物测定76例正常、26例急性肝炎、45例慢性肝炎和72例肝硬化患者血清基础PON-1活性和1 mol/L NaC1刺激后PON1活性;PCR扩增PON1基因,Alw I酶切PCR产物,对PON1基因192位多态性进行分型.结果 正常对照组、急性肝炎、慢性肝炎和肝硬化患者血清PON-1基础活性水平分别为403z±145,312±83,201±114,137±99 U/ml;1 m01/L NaC1刺激后PON-1活性分别为673±232,509±139,335±151,233±162 U/ml.与正常对熙比较,急性肝炎、慢性肝炎和肝硬化患者血清PON-1活性基础水平和1 mol/L NaC1刺激后PON1活性均显著下降(P<0.01),肝硬化组下降最明显.肝硬化Child A,Child B和Child C组患者血清PON-1活性基础水平分别为185.5±98.6,141.6±93.6,86.7±51.2 U/ml;1mol/L NaC1刺激后PON-1活性分别为308.9±161.3,227.1±116.3,124.9±78.1 U/ml.Child B组比A组PON1酶活性显著下降(P<0.05),而Child C组又比B组PON1酶活性显著下降(P<0.01).在肝硬化Child A,Child B和Child C组患者PON1的192位R-Q多态性分布频率无显著性差异(P>0.05).结论 血清PONl活性下降与肝硬化Child-Pugh分级相关,可反应肝硬化的严重程度,且PON1基因192位多态性不影响肝硬化各组的PONl酶活性.     

凝血因子Ⅶ基因R353Q多态性与脑梗死的相关性研究

目的 探讨我国汉族人凝血因子Ⅶ(FⅫ)基因第八外显子R353Q基因多态性分布及其与脑梗死的相关性.方法 应用聚合酶链反应-限制性片断长度多态性的方法 (PCR-RFLP),检测100例脑梗死患者及106例正常健康人FⅦ第八外显子R353Q各基因型及R、Q等位基因分布频率.结果 脑梗死人群中及正常健康人群中存在FⅦR353Q基因多态性分布,RR及RQ基因型在脑梗死组和正常对照组分布均符合Hardy-Weinberg平衡.脑梗死组中RR基因型91例,RQ基因型9例,QQ基因型0例,各基因型分布频率分别为91.00%(91/100)、9.00%(9/100)、0;R、Q等位基因频率分别为95.50%(191/200)和4.50%(9/200).健康对照组中RR基因型94例,RQ基因型12例,QQ基因型0例,基因型分布频率分别为88.70%(94/106)、11.30%(12/106)、0;R、Q等位基因频率分别为94.33%(200/212)和5.67%(12/212).脑梗死组与对照组之间整体基因型分布差异无统计学意义(χ20.3027,P=0.5822).R、Q等位基因在2组间的分布无统计学意义(χ20.2865,P=0.5925);Q等位基因携带者的频率在病例组与正常对照组的差异无统计学意义(χ20.2865,P=0.5925).结论我国汉族人群中存在凝血因子Ⅶ基因的R353Q多态性,不支持Q基因型是脑梗死的保护因子这一观点.     

E-选择素基因SER128ARG多态性与急性心肌梗死易感的相关性研究

目的 探讨E-选择素基因SER128ARG(S128R)多态性在急性心肌梗死(AMI)患者和正常人群中的分布特点及与AMI的易感相关性,以及对血清E-选择素水平的影响.方法 采用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)技术,检测168例AMI患者和200例健康对照者E-选择素基因多态性,同时采用酶联免疫吸附试验(ELISA)法检测所有参与者血清E-选择素水平.结果 E-选择素基因S128R基因型频率和等位基因频率,在AMI组和对照组的分布差异有统计学意义(P＜0.05);基因型频率的相对风险分析发现,SR杂合子基因型携带者患AMI的风险是SS纯合子基因型的2.234倍(OR=2.234,95%CI:1.112～4.437);AMI组血清E-选择素水平明显高于对照组(P＜0.05);SR杂合子基因型携带者血清E-选择素水平显著高于SS纯合子基因型(41.65±8.87)μg/L和(34.23±6.72)μg/L,P＜0.05.结论 E-选择素S128R基因多态性与AMI的发病有关联,并影响血清E-选择素水平;提示R基因可能是AMI发病的遗传易感基因.     

Hyperhomocysteinemia, paraoxonase activity and risk of coronary artery disease

OBJECTIVES: Paraoxonase-1 (PON1) detoxifies homocysteine thiolactone (HcyT) in human blood and could thus delay the development of atherosclerosis. We investigated (a) PON1 activity and polymorphisms, and (b) the relationship between PON1 activity, homocysteine (Hcy) and the severity of CAD patients in Tunisian population. DESIGN AND METHODS: We used PCR-RFLP analysis to detect the Q192R and L55M variants of the PON1 gene in 100 patients with CAD and in 120 healthy controls. Paraoxonase activity was measured spectrophotometrically using phenylacetate as a substrate. Total plasma homocysteine concentrations were determined by direct chemiluminescence assay. RESULTS: We found an increased Hcy level in CAD patients compared to the control group (15.86+/-8.63 vs. 11.9+/-3.25 micromol/L respectively, P<0.001), and a decrease in PON1 activity in CAD patients as compared to the control group (117+/-56 vs. 181+/-73 U/mL respectively, P<0.001). PON1 Q192R and L55M polymorphisms were not associated with the presence of CAD (P=0.592, P=0.294, respectively). However, we found that PON1 activity is lower with the PON1 192RR than with PON1 192QQ genotypes in the study population. Furthermore, there were no association between PON1 L55M polymorphism and PON1 activity. We showed a significant decrease in PON1 activity in CAD patients presenting 0- to 3-vessel stenosis (155+/-39; 135+/-36; 103+/-22; 77+/-24 U/mL, respectively; P<0.001). CONCLUSION: In this study, we showed that low PON1 activity is associated with the PON1 192RR genotypes and associated with the severity of CAD in the Tunisian population. We hypothesize that high level of Hcy together with low PON1 activity results in an increased plasma HcyT plasma concentration leading to protein N-homocysteinylation and the development and progression of atherosclerosis.     

The paraoxonase-1 codon 192 polymorphism is associated with fasting total cholesterol and LDL-cholesterol concentrations only in postmenopausal women. The REGICOR study.

Paraoxonase-1 (PON1) is a high-density lipoprotein (HDL)-linked enzyme which appears to protect low-density lipoproteins (LDL) from oxidation. PON1 activity is associated with variation at the PON1 gene locus, specifically the common amino acid polymorphism at codon 192, for which the Q192 allele specifies low activity and the R192 allele specifies high activity. We investigated the association between the PON1 codon 192 polymorphism and fasting concentrations of glucose, lipids, lipoproteins and PON1 activity in 1380 subjects (724 men and 656 women). Several anthropometric and environmental factors were assessed in the present study. The PON1 Q192 allele frequency was 0.70 and 0.68 in men and women, respectively. In women, but not in men, significant associations were found between the PON1 codon 192 genotype and both total and LDL-cholesterol (p=0.004 and p=0.008, respectively), and subgroup analysis indicated that this relationship was predominant in postmenopausal women. Specifically, the Q192 allele was associated with increased total and LDL-cholesterol concentrations. Furthermore, these lipoprotein variables were higher among postmenopausal women with Q192/Q192 and Q192/R192 genotypes than in premenopausal women with the same genotypes (p<0.001). The findings suggest a gender-specific lipoprotein-genotype association with PON1 codon 192 genotypes in this study sample.     

高同型半胱氨酸血症患者氧化应激指标的研究

目的观察高同型半胱氨酸血症(HHcy)患者氧化应激指标的水平,并对其临床价值做初步评价。方法检测108例HHcy患者、106名健康体检者(正常对照组)循环谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)、对氧磷酯酶1(PON1)、一氧化氮合酶(NOS)活性及同型半胱氨酸(Hcy)、一氧化氮(NO)和丙二醛(MDA)水平。分析Hcy与GSH-Px、SOD、PON1、NOS、NO、MDA之间的相关性。结果 HHcy患者血浆MDA水平[(6.23±1.55)μmol/L]明显高于正常对照组[(4.14±1.13)μmol/L](P0.01),而GSH-Px[(189.3±25.1)U/L]、SOD[(77.3±20.5)NU/mL]、PON1[(133.6±23.9)kU/L]、NOS活性[(25.3±2.9)U/mL]及NO[(68.3±10.1)μmol/L]水平低于正常对照组[(240.3±78.1)U/L、(89.2±24.8)NU/mL、(168.2±26.0)kU/L、(30.0±3.3)U/mL、(92.1±12.1)μmol/L](P均0.01)。HHcy患者血浆Hcy与MDA呈正相关(r=0.72,P0.01),与GSH-Px、SOD、PON1、NOS、NO呈明显负相关(r值分别为-0.60、-0.49、-0.51、-0.43、-0.50,P均0.01)。结论 HHcy患者氧化应激增强可能与Hcy氧化过程中产生过多的过氧化物及活性氧、Hcy损伤NO/L-精氨酸系统及直接抵制抗氧化酶活性有关。Hcy可能通过增加氧化应激和降低抗氧化能力在动脉粥样硬化发生、发展中起重要的作用。     

Low paraoxonase activity in type II diabetes mellitus complicated by retinopathy

Human serum paraoxonase 1 (PON1) is located on high-density lipoprotein and has been implicated in the detoxification of organophosphates, and possibly in the prevention of lipid peroxidation of low-density lipoprotein. PON1 has two genetic polymorphisms, both due to amino acid substitutions: one involving glutamine (Q genotype) and arginine (R genotype) at position 192, and the other involving leucine (L genotype) and methionine (M genotype) at position 55. We investigated the effects of these polymorphisms, and of a polymorphism of the PON2 gene at position 310 (Cys/Ser; C and S genotypes respectively), on serum PON1 activity and concentration, plasma lipids and lipoproteins and glycaemic control in 93 individuals with type II diabetes with no complications and in 101 individuals with type II diabetes with retinopathy. Serum PON1 activity in the group with no complications [median 164.1 nmol.min(-1).ml(-1) (range 8.0-467.8)] was significantly higher than in the group with retinopathy [113.4 nmol. min(-1).ml(-1) (3.0-414.6)] (P<0.001), but the serum PON1 concentration was not different between the groups. The gene frequencies of the PON1-55 and PON1-192 polymorphisms and of the PON2-310 polymorphism were not different between the study populations. The PON1-55 and PON1-192 polymorphisms affected PON1 activity in the way described in a previous study of a control group and subjects with type II diabetes. The PON2-310 polymorphism also significantly affected serum PON1. PON1 activity was significantly higher in individuals with the PON2-310 CC genotype in both groups with type II diabetes, and the PON1 concentration was significantly higher in PON2-310 CC homozygotes with no complications than in the group with retinopathy. Neither the PON1-55 nor the PON1-192 polymorphism was correlated with the serum lipid or lipoprotein concentration in either group. In the group with retinopathy (but not the group with no complications), all three PON polymorphisms were correlated with glycaemic control, which was worse for the PON1-55 genotypes in the order MM>LM>LL (P=0.0032), for the PON1-192 genotypes in the order RR>QR>QQ (P=0.011) and for the PON2-310 genotypes in the order CC>CS>SS (P=0.010). Low serum PON1 activity in retinopathy may be related to an increased tendency for lipid peroxidation. Our findings thus raise the possibility that, in retinopathy, the PON2 gene may influence PON1, and that an inter-relationship between the PON1 and PON2 genes may influence glycaemic control in subjects with type II diabetes complicated by retinopathy.     

甲状腺功能亢进症患者血浆对氧磷酯酶1活性的测定

目的：探讨甲状腺功能亢进症（甲亢）患者血浆对氧磷酯酶1（PON1）活性变化以及与其它氧化应激指标的关系。方法：分别测定50名对照组和78例甲亢组空腹血浆中游离三碘甲状腺原氨酸（FT3）、游离甲状腺素（FT4）、促甲状腺激素（TSH）、PON1活性、超氧化物歧化酶（SOD）、丙二醛（MAD）、氧化低密度脂蛋白（ox-LDL）及血脂含量,并进行相关性分析。结果：甲亢患者血浆PON1活性（139±64）kU/L,ox-LDL（598.3±58.6）μg/L,MDA（15.11±3.26）μmol/L及SOD（80.2±25.3）NU/mL。对照组上述指标分别为：PON1（168±70）kU/L,ox-LDL（446.2±62.2）μg/L,MDA（10.02±3.00）μmol/L,SOD（92.9±26.9）NU/mL。血浆PON1和SOD活性显著低于对照组（P〈0.01）,ox-LDL和MDA水平显著高于对照组（P〈0.01）。甲亢患者血浆PON1活性与SOD呈正相关（r=0.381,P〈0.05）,与ox-LDL、MDA呈负相关（r=-0.411,r=-0.445,P〈0.01）。结论：甲亢患者血浆PON1活性显著降低,可能与氧化应激增强有关。     

Paraoxonase 1-192Q allele is a risk factor for idiopathic chronic pancreatitis.

BACKGROUND: The cause of chronic pancreatitis (CP) remains unknown. However, oxidative stress might play a role since recent animal studies have demonstrated that oxygen-free radicals contribute to the pathogenesis of experimental pancreatitis. Human serum paraoxonase (PON1) is an antioxidant enzyme that protects against cellular damage from oxidative stress. Genetic variations resulting in variable activity rates of this enzyme, are of toxicological and physiological importance. AIM: We investigated whether genetic polymorphisms of the PON1 gene modify the risk for CP. MATERIALS AND METHODS: DNA samples were obtained from 236 adult CP patients of hereditary (n = 23), alcoholic (n = 137), or idiopathic (n = 76) origin. DNA from 113 healthy controls and from 93 alcoholic controls were analyzed for comparison. Patients and controls were all of Caucasian origin. Genetic polymorphisms (L55M and Q192R) in PON1 were determined by PCR, followed by restriction fragment length polymorphism analyses in all subjects. RESULTS: The frequencies of the PON1-55 alleles did not differ between CP patients and healthy controls. However, the PON1-192Q allele was significantly more common in idiopathic CP patients (OR : 1.5, 95% CI 1.02, 2.5) compared with healthy controls. CONCLUSIONS: These data suggest that the PON1-192Q allele, resulting in partly deficient antioxidant and detoxification activity of this enzyme, might be a risk factor for idiopathic CP in Caucasians.     

Are PON1 Q/R 192 and M/L 55 polymorphisms risk factors for diabetes complications in Turkish population?

ObjectivesWe investigated whether the human serum paraoxonase (PON1) Q/R 192 and M/L 55 polymorphisms are associated with the complications of the type 2 diabetes (T2D).Design and methodsStudy group was consisted of 50 healthy subjects and 100 type 2 diabetes mellitus (DM) patients. Following measuring of serum PON1 activity, isolation of DNA and genotyping analyses were performed.ResultsPON1 activity of the patients with complications was significantly reduced by 23.5% compared to the group of diabetic patients and by 26.3% than the controls. According to multivariate analysis, we observed a three times significant effect of Q/R 192 polymorphism on the susceptibility to the occurrence of complications.ConclusionsProtective effects of paraoxonase against peroxidation of LDL particles are important in T2D complications. Although both of the two polymorphisms are associated, 192 polymorphism seems to be stronger predictor of the risk of diabetic complications.     

血管紧张素II1型受体基因多态性与原发性高血压的关系

目的探讨血管紧张素Ⅱ1型受体（AT1R）基因多态性与原发性高血压（EH）之间的关系。方法应用聚合酶链反应-限制性片段长度多态性（PCR—RFLP）对200例汉族EH患者（EH组）和192例正常血压者（对照组）的ATlR基因1166A／C及-810A／T多态性进行检测,测定空腹血糖、甘油三酯（TG）、总胆固醇（TC）、低密度脂蛋白胆固醇（LDL—C）及高密度脂蛋白胆固醇（HDL—C）等生物化学指标,分析各基因型和等位基因频率与EH的关系。结果1166A／C等位基因和基因型频率在EH组和对照组的分布无统计学差异（P均〉0．05）,-810A／T各基因型在EH组和对照组间差异有统计学意义（χ^2=10．862,P=0．004）,-810T等位基因频率在EH组显著增高[22．5％（102／400）与11．5％（44／384）,χ^2=12．745,P=0．000],用Logistic回归模型校正了传统危险因素的影响后,-810AT和TT基因型的携带者患高血压的危险性显著增加（P=0．003,OR值为2．57,95％CI：1．37～4．84）。结论AT1R-810A／T多态性与EH发病相关,-810T等位基因可能是EH发病的风险因子。