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1.
Chinese Medical Journal ; (24): 2461-2465, 2009.
Article in English | WPRIM | ID: wpr-266046

ABSTRACT

<p><b>BACKGROUND</b>Marked interindividual variation exists in blood pressure response to benazepril, which is considered to have genetic basis. Our objectives were to evaluate whether the E112D polymorphism in the prolylcarboxypeptidase (PRCP) gene has impact on blood pressure response to benazepril.</p><p><b>METHODS</b>Hypertensive patients from Huoqiu County and Yuexi County of Anhui Province received daily treatment with an oral dosage of 10 mg benazepril for 15 days. Genotypes of the E112D polymorphism in the PRCP gene were determined by TaqMan SNP genotyping assay. Multivariate linear and Logistic regressions using generalized estimating equation model were performed in a total of 1092 patients to evaluate the association of PRCP genotypes and blood pressure response to benazepril.</p><p><b>RESULTS</b>Patients carrying ED or DD genotype had a less systolic blood pressure reduction (adjusted beta = -3.7 + or - 1.1, P < 0.001), a less diastolic blood pressure reduction (adjusted beta = -3.1 + or - 0.8, P < 0.001) and a lower percentage of reaching target blood pressure defined as SBP lower than 140 mmHg and DBP lower than 90 mmHg (adjusted OR = 0.6, P = 0.005) than those patients carrying EE genotype. In addition, the results from stratified analysis by county (Huoqiu or Yuexi) were similar to those observed in the pooled population.</p><p><b>CONCLUSIONS</b>Our data suggest that the E112D polymorphism in the PRCP gene may be a useful genetic marker to predict the antihypertensive effect of short-term benazepril treatment in hypertensive patients of Anhui Province, China.</p>


Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Young Adult , Antihypertensive Agents , Therapeutic Uses , Benzazepines , Therapeutic Uses , Blood Pressure , Carboxypeptidases , Genetics , Genetic Predisposition to Disease , Genetics , Genotype , Hypertension , Drug Therapy , Genetics , Polymerase Chain Reaction , Polymorphism, Single Nucleotide , Genetics , Physiology
2.
Chinese Medical Journal ; (24): 172-175, 2004.
Article in English | WPRIM | ID: wpr-235809

ABSTRACT

<p><b>BACKGROUND</b>Inflammation is a major cause of restenosis after coronary stenting. Intercellular adhesion molecule-1 (ICAM-1) is an important adhesion molecule that plays a key role in the tight adhesion between leukocytes and vascular endothelium. The object of this study was to investigate the association between the K469E polymorphism of the ICAM-1 gene and restenosis after coronary stenting in North Chinese population.</p><p><b>METHODS</b>The ICAM-1 K469E polymorphism was genotyped using polymerase chain reaction-restriction fragment length polymorphism method in 124 patients who had undergone coronary stenting and coronary angiography at least 3 months earlier. Information on clinical risk factors and procedure-related data were also collected.</p><p><b>RESULTS</b>Of 124 enrolled patients in total, there were 72 cases of in-stent restenosis. The restenosis rate in this population was 58.1%. The frequencies of the three possible genotypes of the ICAM-1 K469E polymorphism were: KK genotype 50.8%, EE genotype 41.9%, and EK genotype 41.9%. Among restenosis patients, the frequency of the KK genotype was 58.3% and the frequency of E allele carriers was 41.7%. Among non-restenosis patients, the frequency of the KK genotype was 40.4%, and the frequency of E allele carriers was 59.6%. The distribution of these two genotype groups between restenosis and non-restenosis patients was significantly different (P = 0.049). Using multivariate logistic regression, the difference between the two groups was more apparent. The odds ratio of KK homozygotes vs E allele carriers was 2.6, with 95% confidence interval 1.2 - 5.8 (P = 0.018). After grading of risk factors, we found that the KK genotype was a stronger predictor of in-stent restenosis in obesity or hyperlipemia patients, with an odds ratio of 9.3 and 3.7, respectively (P < 0.05).</p><p><b>CONCLUSION</b>In our study population, KK homozygotes of the ICAM-1 codon 469 mutation had a higher risk of restenosis after coronary stenting, especially in the case of obese or hyperlipemia patients.</p>


Subject(s)
Female , Humans , Male , Middle Aged , Asian People , Genetics , China , Codon , Coronary Restenosis , Genetics , Genotype , Hyperlipidemias , Intercellular Adhesion Molecule-1 , Genetics , Obesity , Polymorphism, Genetic , Stents
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