ALOX5AP基因SG13S114A/T多态性与颈动脉粥样硬化斑块稳定性的相关性

Objective To investigate the relationship between the polymorphism of SG13S114 A/T in the 5-lipoxygenase-activating protein (ALOX5AP)gene and the stability of carotid atherosclerosis. Methods Polymorphism of SG13S114 A/T in the ALOX5AP gene was analyzed in 152 cases of acute infarction with stable plaque, and 132 cases of acute infarction with vulnerable plaques, by using polymerase chain reaction and restriction fragment length polymorphism. Carotid artery plaque was analyzed by carotid artery color ultrasound. Results The frequencies of SG13S114 AA genotype and the A allele in the vulnerable plaque group were higher than that in the stable plaque group (P＜0.01). Conclusion The polymorphism of SG13S114 A/T in the ALOX5AP gene may be associated with the instability of atherosclerosis. And the SG13S114 A allele may be a risk factor of vulnerable plaques.     

ALOX5AP基因SG13S114A/T多态性与颈动脉粥样硬化斑块稳定性的相关性

Objective To investigate the relationship between the polymorphism of SG13S114 A/T in the 5-lipoxygenase-activating protein (ALOX5AP)gene and the stability of carotid atherosclerosis. Methods Polymorphism of SG13S114 A/T in the ALOX5AP gene was analyzed in 152 cases of acute infarction with stable plaque, and 132 cases of acute infarction with vulnerable plaques, by using polymerase chain reaction and restriction fragment length polymorphism. Carotid artery plaque was analyzed by carotid artery color ultrasound. Results The frequencies of SG13S114 AA genotype and the A allele in the vulnerable plaque group were higher than that in the stable plaque group (P＜0.01). Conclusion The polymorphism of SG13S114 A/T in the ALOX5AP gene may be associated with the instability of atherosclerosis. And the SG13S114 A allele may be a risk factor of vulnerable plaques.     

基质金属蛋白酶8-799C/T基因多态性与颈动脉斑块易损性的关联分析

目的 探讨我国浙江地区汉族人群基质金属蛋白酶-8 (matrix metalloproteinase-8,MMP-8)启动子基因-799C/T多态与颈动脉斑块易损性的关系.方法 451例脑梗死患者根据颈动脉超声分为易损斑块组(共135例)和稳定斑块组(共316例).采用酶联免疫吸附法测定两组血清MMP-8水平,并采用聚合酶链反应-限制性片段长度多态性方法分析两组MMP-8启动子基因-799C/T多态的基因型.结果 易损斑块组发病48 h内血清MMP-8水平为(0.86±0.16)ng/μL,稳定斑块组为(0.80±0.13) ng/μL,两者差异有统计学意义(t=2.894,P=0.004).易损斑块组CT+ TT基因型频率为73.3％,稳定斑块组为54.7％,两者差异有统计学意义(x2=13.65,P=0.000);T等位基因频率在易损斑块组为48.1％,在稳定斑块组为33.5％,两者差异有统计学意义(x2=17.14,P=0.000).CC基因型组血清MMP-8水平为(0.79±0.13) ng/μL,TT基因型组血清MMP-8水平为(0.92±0.11) ng/μL,两者比较差异有统计学意义(t=3.141,P=0.001).结论 MMP-8启动子基因-799C/T多态可能与浙江地区汉族人颈动脉易损斑块发生的倾向有关,T等位基因可能是颈动脉斑块易损的遗传易患性标志之一.     

原发性高血压颈动脉内-中膜厚度与eNOS4a/b基因多态性的相关性研究

目的:探讨皖北地区汉族人群原发性高血压(EH)颈动脉内-中膜厚度(IMT)与内皮一氧化氮合酶(eNOS) 4a/b基因多态性的关系.方法:随机选取本院门诊与住院的EH患者79例(EH组),根据颈动脉IMT是否增厚及有无粥样斑块进一步分为两个亚组,不伴有IMT增厚和颈动脉粥样斑块者36例归入H1组 , 伴有IMT增厚和/或颈动脉粥样斑块者43例归入 H2组.选取同期在门诊体检的健康人68例作为对照组(N组).所有受试者进行eNOS 4a/b基因多态性检测,并进行组间比较.结果:H1组IMT高于N组(P＜0.01), H2组IMT高于H1组及N组(P＜0.01);H2组左房内径(LA)和左室重量指数(LVMI)高于N和H1组(P＜0.01),而EF值低于N和H1组(P＜0.01).aa+ab基因型在EH组比率为27.8%(22/79), N组为10.3%(7/68),两组比较差异有统计学意义(P＜0.01);H2组中aa+ab基因型比率为39.5%(17/43),高于N组10.3%(7/68)及H1组13.9%(5/36), 差异有统计学意义(P＜0.05);H2组a等位基因分布比率为20.9%(18/86),高于H1组6.9%(5/72), 差异有统计学意义(P＜0.05);N组等位基因比率为5.1%(7/136)与H组14.6%(23/158)比较,差异有统计学意义( P＜0.01).结论:皖北地区汉族EH患者与正常对照相比,其eNOS 4a/b基因多态性中各基因型分布存在差异,提示eNOS 4a/b基因多态性与EH的发病及并发动脉粥样硬化相关.     

TGF-β1基因启动子-800G/A、-509C/T多态性与食管癌的研究

目的研究转化生长因子β1(TGF-β1)基因启动子多态性各等位基因及基因型在食管癌患者中的分布频率,初步分析其基因型及血清水平与食管癌的相关性.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118例食管癌患者和130例正常对照组TGF-β1的基因多态性,包括TGF-β1基因启动子-800G/A、-509C/T位点,同时采用ELISA检测血清TGF-β1水平.结果食管癌患者血清TGF-β1水平显著高于对照组(P＜0.01),TGF-β1基因-800G/A位点多态性在食管癌组和正常人群中的分布差异无显著性(P＞0.05),而TGF-β1基因-509C/T多态性各等位基因及基因型频率在两组人群中的分布差异存在显著性(P＜0.05);等位基因频率的相对风险分析发现,T等位基因携带者患食管癌的风险是C等位基因的1.624倍(OR=1.624,95%CI1.134～2.324),携带T等位基因的食管癌患者血清TGF-β1水平显著高于不携带者(50.97±8.91μg/LVS44.23±8.54μg/L,P＜0.01).结论TGF-β1基因-509C/T多态性与食管癌的发病具有相关性,其中T等位基因可能是食管癌发病的遗传易感基因;携带T等位基因的个体可能通过促进TGF-β1的高度表达进而增加了食管癌的发病风险.     

IFN-γ基因多态性与小儿哮喘的相关性

目的探讨IFN-γ基因多态性、等位基因在儿童哮喘发病机理中的意义。方法采用PCR-SSP方法对30例小儿哮喘病儿及26例非哮喘呼吸道疾病患儿作IFN-γ基因多态性分析。结果30例哮喘组IFN-γ基因型中,T/T1例,T/A7例,A/A22例,26例非哮喘组IFN-γ基因型中,T/T7例,T/A11例,A/A8例。χ2=11.696,P<0.005,两组IFN-γ基因型有明显差异。哮喘组IFN-γ等位基因T和A的频率为15%和85%,非哮喘组IFN-γ等位基因T和A的频率为51.9%和48.1%,哮喘组IFN-γ等位基因A的频率比非哮喘组IFN-γ等位基因A高,相对危险度0.191,95%可信度区间0.078-0.466,χ2=14.416,P<0.005,两组IFN-γ等位基因频率有明显差异。结论本研究证实小儿哮喘易感性与IFN-γ基因启动子多态性相关联。     

中国苏州地区汉族人群MCP-1基因多态性与急性胰腺炎相关性研究

目的探讨中国苏州地区汉族人群单核细胞趋化因子蛋白-1(monocyte chemoattractant protein-1,MCP-1)基因-2518A/G多态性与急性胰腺炎的相关性。方法采用聚合酶链反应-限制性片段长度多态性方法检测中国苏州汉族人群急性胰腺炎(acute pancreatitis,AP)患者101例[其中包括轻症急性胰腺炎(mildAP,MAP)78例,重症急性胰腺炎(servere AP,SAP)23例]和120名健康对照的MCP-1基因-2518位点基因型分布及基因频率,并评价基因多态性与AP易感性之间的相关性。结果对照组MCP-1-2518A/G位点的AA基因型频率较SAP组和MAP组高,差异有统计学意义(P<0.01),携AG及GG基因型者患MAP的风险度约是AA基因型的5.896倍(P<0.01,OR=5.896),患SAP的风险度约为7.011倍(P<0.05,OR=7.011)。而在MAP与SAP组间AA基因型频率差异无统计学意义(P=0.997)。对照组G等位基因频率明显低于MAP(P<0.01,OR=0.318)和SAP组(P<0.01,OR=0.309)。但G等位基因频率在MAP与SAP组间基因型分布差异无统计学意义(P=0.623,OR=1.211)。结论中国苏州地区汉族人群MCP-1-2518位点AA基因型可能有助于保护机体避免发生AP,G等位基因频率较高的人可能易患AP。但AA基因型和G等位基因频率不能预测SAP的发生。     

APOA5基因单核苷酸多态性与冠心病相关性研究

目的　探讨APOA5基因多态性与冠状动脉粥样硬化性心脏病 (coronaryheartdisease ,CHD)的相关性、与血脂关系及其在中国汉族人群中的分布。方法　用聚合酶链反应 限制性片段长度多态性分析APOA5与APOA4交界区域的T/C单核苷酸多态。结果　T/C单核苷酸多态位点等位基因T、C频率在CHD组和正常对照组分别为 0 .43 5、0 .5 65和 0 .3 74、0 .62 6。等位基因频率和基因型频率分布均符合Hardy Weinberg平衡定律。T/C基因多态性基因型频率 ,等位基因T、C频率在两组间差异有显著性(P <0 .0 5 ) ,且基因型CC的冠心病患者其血浆高密度脂蛋白水平显著高于其他基因型患者 (P <0 .0 1)。中国人T/C单核苷酸多态位点T、C等位基因频率与欧洲白人比较 ,差异存在非常显著性 ( 0 .3 74vs 0 .663、0 62 6vs 0 .3 3 7;P <0 .0 0 1)。结论　T/C单核苷酸多态性与CHD存在相关性 (P <0 .0 5 ) ,患者组CC基因型与血浆高密度脂蛋白水平密切相关 (P <0 .0 1)。     

单胺氧化酶B和NAD(P)H醌氧化还原酶基因多态性与帕金森病的关系

目的 探讨参与多巴胺代谢的单胺氧化酶B（monoamine oxidase B,MAO-B)内含子13A／G多态性,NAD（P）H醌氧化还原酶基因[NAD(P)H:quinone oxidoreductase,NQO1]cDNA609C/T多态性与帕金森病（Parkinson's disease,PD)遗传易感性的关系。方法 应用等位基因特异PCR扩增分析MAO－B基因的多态性,用PCR－RFLP分析NQO1基因多态性。结果 MAO－BA／G等位基因频率、各基因型频率PD组与对照组差异无显著性。NQO1基因T等位基因频率PD组（52％）高于正常对照组（43％）带T碱基的NQO1基因型频率PD组显著高于正常对照组（P＜0．05）,其患PD的相对危险度（odds ratio,OR)为3．8。在带有A等位基因MAO－B基因型的个体,带有T碱基因的T等位基因是PD的危险因素。MAO－B基因的A等位基因型与NQO1基因的T等位基因的基因型可相互协同,增加PD发生的风险。     

广西人群中IL-33 基因rs10975521A / T、rs1929992A / G 多态性的分布特点

目的：研究探讨IL-33基因rs10975521A/T、rs1929992A/G的基因多态性在广西人群中的分布特点。分析两位点的基因型及基因频率在不同种族间的分布差异。方法：采用单碱基延伸法(PCR-SEB)及DNA测序法对283例受试者IL-33基因rs10975521A/T、rs1929992A/G位点进行多态性分析。用统计学方法分析其分布频率及组间差异。结果： rs10975521A/T 存在AA、AT、TT三种基因型,分布频率分别为12.7%、53.0%、34.3%。其各基因型及等位基因频率在广西人群中男女性别之间无显著差异( P >0.05)。其等位基因频率与人类基因组计划公布的欧洲人( P <0.05)、北京汉族人( P <0.05)及日本人群( P <0.01)之间均有显著差异。rs1929992A/G存在AA、AG、GG三种基因型,分布频率分别为23.9%、53.7%、13.4%。其各基因型及等位基因频率在广西地区人群中男女之间也无统计医学意义( P >0.05)。其基因型与欧洲人( P <0.01)、北京汉族人( P <0.05)和日本人( P <0.01)之间差异有统计学意义。等位基因频率与欧洲人( P <0.01) 、北京汉族人( P <0.05) 相比差异有统计学意义。结论： IL-33基因rs10975521A/T、rs1929992A/G的基因多态性在种族和地区间存在不同程度的差异。     

The role of genetic variants of matrix metalloproteinases in coronary and carotid atherosclerosis

Current evidence suggests that matrix metalloproteinases (MMPs) have a role in early atherosclerosis, plaque rupture and myocardial infarction. Polymorphisms in MMP genes have been examined for associations with atherosclerosis, but interpretation is complicated by methodological issues. This article presents a systematic review of these association studies and a meta-analysis of available data for polymorphisms where a sufficient number of studies was available. The 5A allele of the MMP3 5A/6A polymorphism was associated with acute myocardial infarction (odds ratio (OR) 1.26, 95% confidence interval (CI) 1.1 to 1.4, p<0.001), suggesting its role in plaque rupture. There was no association with the functional MMP9 -1562C/T polymorphism (OR 1.11, 95% CI 1.0 to 1.3, p = 0.18). Current data provide evidence for the role of MMP3 polymorphism in plaque destabilisation, but elucidation of the role of other MMP gene variants in atherosclerosis will depend on better study design, including a larger sample size, extensive screening of individual genes with haplotype analysis and replication of studies to avoid publication bias.     

Ischaemic stroke in hypertensive patients is associated with variations in the PDE4D genome region

Previous Icelandic studies reported that single nucleotide polymorphisms (SNPs) in the phosphodiesterase 4D (PDE4D) region and the 5-lipoxygenase activating protein ALOX5AP were associated with ischaemic stroke, whereas other studies reported ambiguous findings. We examined 932 ischaemic stroke patients from a Swedish population-based stroke register, and 396 control subjects. We assessed possible associations between ischaemic stroke and nine preselected SNPs in the chromosome regions of the PDE4D gene, including rs12188950 (SNP45) and rs3887175 (SNP39); the ALOX5AP gene, including rs17222814 (SG13S25) and the promoter region of the MHC class II transactivator, MHC2TA. The T allele of SNP45 showed negative association with ischaemic stroke (odds ratio, OR=0.72; 95% confidence interval (CI): 0.58-0.91; P=0.0055). Among hypertensive subjects, this influence of the T allele of SNP45, and the T allele of SNP39, were more pronounced (with OR=0.52; 95% CI: 0.37-0.73; P=0.0001 and OR=0.57; 95% CI: 0.41-0.79; P=0.0007, respectively). These SNPs also interacted with hypertension with a relative excess risk due to interaction of -1.66 (P=0.0002) for SNP45 and -1.65 (P=0.0005) for SNP39. The P-values remained significant after correction for multiple testing. Among nonhypertensives, the A allele of SG13S25 indicated increased stroke risk (OR=1.82; 95% CI: 1.21-2.74; P=0.0039; not significant after Bonferroni correction). SNP45 was associated with ischaemic stroke even when controlling for hypertension, diabetes, heart disease and smoking. Our meta-analysis of 13 studies (including ours) showed no overall influence of SNP45 on ischaemic stroke. However, the 13 studies may differ because of nonrandom causes, as suggested by the heterogeneity test (P=0.042). This might support previously undetected mechanisms causing fluctuating ischaemic stroke risk.European Journal of Human Genetics (2008) 16, 1117-1125; doi:10.1038/ejhg.2008.62; published online 9 April 2008.     

彩色多普勒超声对颈动脉粥样硬化与脑梗死的相关性分析

目的探讨颈动脉粥样硬化与脑梗死的关系。方法应用彩色多普勒超声检测82例脑梗死患者和46例非脑梗死患者颈动脉内-中膜厚度（intima-media thickness,IMT）、斑块检出率、管腔狭窄率,并观察斑块性质。结果脑梗死组斑块检出率及颈动脉内膜厚度较对照组明显增加,两组比较差异有统计学意义（P〈0.01）,脑梗死组斑块检出率（70.7%）明显高于对照组（32.6%）;脑梗死组颈总动脉（CCA）内膜厚度（1.38±0.14）明显高于对照组（0.89±0.16）,脑梗死组颈内动脉（ICA）内膜厚度（1.16±0.27）明显高于对照组（0.78±0.17）。斑块多发生于颈动脉分叉处（44.4%）,以软斑块、溃疡斑块（59.2%）居多。结论颈动脉粥样硬化程度与脑梗死的发病关系密切,彩超评估颈动脉粥样硬化程度,对脑梗死的早期预防和治疗具有重要的临床价值。     

A functional Sp1/Egr1-tandem repeat polymorphism in the 5-lipoxygenase gene is not associated with myocardial infarction

Arachidonate 5-lipoxygenase is an enzyme encoded by the ALOX5 gene, and plays an important role in the synthesis of leukotrienes. These are inflammatory mediators, and have been involved in atherosclerosis and other pathological processes that require proinflammatory activities. Human and animal studies have suggested a role for the ALOX5 gene in atherosclerosis, including a significant association between a promoter polymorphism and a carotid intimal-medial thickness in response to dietary fat. This polymorphism was three- to six-tandem repeats of a Sp1/Egr1 binding motif (GGGCGG)(n), and the number of repeats has been linked with the amount of gene expression. We hypothesized that this ALOX5 polymorphism could influence the risk for myocardial infarction (MI). First, we analysed the effect of the four alleles on gene expression by transfecting the HEK-293 cell line with luciferase reporter-constructs. We found that luciferase activities are dependent on the number of the Sp1/Egr1 repeats, with the three and six repeats having the lowest and highest values. We genotyped 312 male MI survivors, aged < 55 years, and 376 healthy controls matched with patients for sex, age, and ethnicity. Ninety-six per cent of the patients were smokers, compared to only 42% among the controls (P < 0.001; OR = 31.84). The 55 + 56 repeat genotypes were less frequent in patients (55 = 56%, 56 = 0.6%) compared to controls (55 = 60%, 56 = 3%). However, these were non-significantly different frequencies. In addition, no difference in MI-onset age and biochemical values was found between the allele and genotypes. In conclusion, we confirmed the effect of the ALOX5-promoter polymorphism on gene expression, but our data did not support a significant effect of this functional variation on MI risk.     

The role of LTA4H and ALOX5AP polymorphism in asthma and allergy susceptibility

Background: Leukotrienes (LTs) have been identified as central mediators in asthma and allergy. Pharmacological inhibition of cysteinyl‐LT activity improves asthma symptoms and control. Accumulating evidence suggests a role for the dihydroxy leukotriene LTB₄ in airway disease. LTA₄ hydrolase and 5‐lipoxygenase activating protein have key roles in LTB₄ production. Single nucleotide polymorphism (SNPs) and haplotypes spanning the LTA4H and ALOX5AP genes have been associated with LTB₄ production and myocardial infarction (MI). Objective: To assess the contribution of LTA4H and ALOX5AP polymorphism to asthma and allergy susceptibility. Methods: Three hundred and forty‐one Caucasian families (two asthmatic siblings) were genotyped for eight SNPs spanning ALOX5AP and five SNPs spanning LTA4H. Association analyses of asthma and related phenotypes (total IgE, atopy, bronchial hyper‐responsiveness, FEV₁) were undertaken using the Family Based Association Test. Results: Single point analyses identified association (P < 0.05) between SNPs SG13S114, SG13S89, SG13S41 (ALOX5AP), rs1978331 (LTA4H) and asthma and/or related phenotypes. Haplotype analyses using all LTA4H SNPs identified a single key risk haplotype for the development of asthma (P = 0.006) and related phenotypes (P = 0.042–0.005). Haplotype analyses using all ALOX5AP SNPs identified several asthma and atopy risk and protective haplotypes. There was limited correlation with previously identified MI risk haplotypes in both genes. Carriers of both ALOX5AP SG13S41 and LTA4H rs1978331 alleles had an increased risk of developing asthma (OR 2.17, CI 1.41–3.32). Conclusions: These data provide evidence for the role of SNPs spanning the ALOX5AP and LTA4H genes in asthma and atopy susceptibility in the Caucasian population and support a role for LTB₄ in disease pathogenesis.     

The roles of stromelysin-1 and the gelatinase B gene polymorphism in stable angina

Matrix metalloproteinases contribute to vascular remodeling by breaking down extracellular-matrix while new matrix is synthesized. Of the variety of MMPs, stromelysin-1 and gelatinase B may have key roles in coronary artery atherosclerosis. Moreover, The 5A/6A polymorphism in the promoter region of the stromelysin-1 gene may be a pathogenetic risk factor for acute myocardial infarction. Gelatinase B (92-kDa type IV collagenase and MMP-9) is one of the MMPs found to be highly expressed in the disruption-prone regions of atherosclerotic plaques. C- to T substitution at the promoter site (-1562) resulted in the higher promoter activity of the T-allelic promoter. The R279Q polymorphism in exon 6 led to the substitution of adenosine by guanine, and was a common polymorphism in the general population. We evaluated the relation between these polymorphisms and stable angina, the severity of atherosclerosis in coronary artery disease, and in-stent restenosis after percutaneous coronary angioplasty. The study population was composed of 131 patients with stable angina (mean age 61.3 years, 89 males) and 117 control subjects (mean age 59.3 years, 59 males). Coronary angiographies were performed in all cases at Yonsei University Cardiovascular Hospital from February 1998 to June 2000. The genotype for each polymorphism was determined using a SNaPshotTM kit and by restriction fragment length polymorphism (RFLP). The prevalence of 5A containing a polymorphism of the stromelysin-1 gene was higher in the stable angina group than in control patients, but no difference in the two polymorphisms of the gelatinase B gene was found between the two groups. By multiple logistic analysis, the 5A-allele of the stromelysin-1 gene was found to be an independent risk factor of stable angina with an odds ratio of 2.29 (95% CI; 1.19-4.38). However, the severity of atherosclerosis in coronary artery or in stent restenosis was not related to any polymorphism of stromelysin-1 or gelatinase B. Our results show that functional genetic variation of stromelysin-1 could be a significant risk factor for stable angina, and might play an important role in coronary atherosclerosis involving vascular remodeling.     

5-Lipoxygenase (ALOX5) and FLAP (ALOX5AP) gene polymorphisms as factors in vascular pathology and Alzheimer's disease

We first hypothesized in 2000 that a polymorphism of the human gene encoding the enzyme 5-lipoxygenase (5-LOX) might be associated with Alzheimer's disease. Only a little progress has been made in directly testing our proposal. However, additional important new data lead us to hypothesize that genetic variability not only in the 5-LOX gene, i.e., ALOX5, but also in polymorphism of the five-lipoxygenase activating protein (FLAP) gene, i.e., ALOX5AP, may be associated with Alzheimer's pathology. Studies in mice followed by several extensive clinical studies have identified ALOX5 and ALOX5AP polymorphisms as strong risk factors for atherosclerosis and cerebrovascular pathologies. New data point to a significant aggregation of vascular risk factors and risk of Alzheimer's disease. Preliminary findings in postmortem brain of Alzheimer's patients identified elevated 5-LOX immunostaining in this disease. We suggest that our hypothesis of a link between the ALOX5 and ALOX5AP gene polymorphisms and Alzheimer's disease could be tested in a clinical setting and in animal models, i.e., transgenic mice could be produced by crossing the available 5-LOX-deficient mice with the available transgenic mice models of Alzheimer's disease.     

Association of interleukin‐10 promoter region polymorphisms with risk factors of Atherosclerosis

Atherosclerosis is considered as an inflammatory disease, and carotid artery intima‐media thickness (IMT) and carotid plaque are generally used as intermediated phenotype of atherosclerosis. The aim of this study was to investigate whether carotid IMT and plaque are associated with promoter region polymorphisms of interleukin 10 (IL‐10) gene. We recruited 135 subjects from a rural area of south‐eastern part of South Korea. Three polymorphisms in the promoter region of IL‐10 (?1082 A/G, ?819 T/C and ?592 A/C) were genotyped by pyrosequencing. Carotid IMT was measured at common carotid arteries, and carotid bulbs and cardiovascular risk factors such as cholesterol, blood pressure, uric acid and homocysteine were measured using blood samples. Subjects with the minor allele (C) of ?819 T/C or the minor allele (C) of ?592A/C showed lower values in carotid IMT than those with major allele homozygote of each polymorphism (P = 0.018 and P = 0.031, respectively). Subjects with carotid plaque were significantly older and showed higher values in carotid IMT, uric acid and homocysteine than those without plaque (P < 0.01, respectively). In conclusion, the promoter region polymorphisms of IL‐10 gene associate with carotid IMT and plaque. Further studies with larger samples are needed to provide stronger evidence to justify anti‐atheromatous properties of IL‐10.