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高敏C反应蛋白水平的变化与ACEI/D基因多态性的相关性分析 被引量:6

Association between angiotensin converting enzyme I/D polymorphism and high-sensitivity C-reactive protein in type 2 diabetic patients with atherosclerosis treated with ramipril
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摘要 目的分析血管紧张素转换酶(ACE)(I/D)基因多态性与雷米普利治疗2型糖尿病合并动脉粥样硬化(AS)患者高敏C-反应蛋白(hsCRP)水平变化的相关性。方法病例选择:选择2型糖尿病合并颈动脉AS患者,排除明显影响肾素-血管紧张素-醛固酮系统的疾病、严重感染或肝肾疾病、恶性肿瘤、影响随访、半年内有1个月以上血管紧张素转换酶抑制剂(ACEI)或血管紧张素受体拮抗剂(ARB)用药史以及对ACEI过敏患者。样本量估计及分组:随机将患者分为ACEI组(雷米普利5mg,治疗组)99例和对照组(不用ACEI和ARB治疗)21例,其中ACEI组按ACE(I/D)基因型分为DD、ID、II组,每组保证最少20例。药物治疗方案:雷米普利2.5mg开始逐渐加至5mg,疗程至少3个月。收集所有患者心血管危险因素和相关指标作为基线指标。PCR检测ACE(I/D)单核苷酸多态性的频率。ELISA法定量检测治疗前后入选患者hsCRP水平的变化。随访3个月。协方差分析ACE基因DD、ID、II三种基因型患者治疗后hsCRP水平。结果与结论雷米普利5mg治疗2型糖尿病合并AS患者3个月可降低患者hsCRP水平,按ACE(I/D)基因型分型DD、ID、II三组患者之间治疗后hsCRP水平无显著差异。 Objective To explore the relationship between angiotensin converting enzyme (ACE) (I/D) gene polymorphism and the level of high-sensitivity C-reactive protein (hsCRP) in type 2 diabetic patients with atherosclerosis treated with ramipril. Methods A total of 118 in type 2 diabetic patients with atherosclerosis aged 35 years or older without clinical proteinuria, heart failure, or low ejection fraction (<40%), who were not taking ACE inhibitors or (ARB), were randomized into two groups to receive treatment with ramipril (ACEI group, beginning with 2.5 mg/d till reaching 5 mg/d) or placebo for 3 months. The 99 patients in ACEI group were further divided into 3 subgroups according to ACE (I/D) genotypes DD, ID and II, each group consisting of at least 20 patients. The level of hsCRP was detected by enzyme-linked immunosorbent assay before and after the therapy. Result and Conclusion After therapy, hsCRP level significantly decreased, but hsCRP levels showed no significant differences between the groups of different ACE genotypes.
出处 《第一军医大学学报》 CSCD 北大核心 2005年第6期691-695,共5页 Journal of First Military Medical University
基金 广东省自然科学基金(033192)~~
关键词 雷米普利 高敏C-反应蛋白 血管紧张素转换酶 基因多态性 药物基因组学 ramipril high-sensitivity C-reactive protein angiotensin-converting enzyme gene polymorphism pharmacogenomics
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