Pathogenesis and treatment of kidney disease and hypertension - Effect of statins versus untreated dyslipidemia on serum uric acid levels in patients with coronary heart disease: A subgroup analysis of the GREek Atorvastatin and Coronary-heart-disease Evaluation (GREACE) study

Pathogenesis and treatment of kidney disease and hypertension - Effect of statins versus untreated dyslipidemia on serum uric acid levels in patients with coronary heart disease: A subgroup analysis of the GREek Atorvastatin and Coronary-heart-disease Evaluation (GREACE) study
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DOI:
10.1053/j.ajkd.2003.12.023
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发表时间:
2004-04-01
影响因子:
13.2
通讯作者:
Mikhailidis, DP
Mikhailidis, DP
中科院分区:
医学1区
文献类型:
--
作者:
Athyros, VG;Elisaf, M;Mikhailidis, DP

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背景:血脂异常对血尿酸(SUA)水平的影响知之甚少,他汀类药物治疗对其影响也知之甚少。希腊的阿托伐他汀和冠心病评估研究表明,与常规治疗相比,每天24毫克的平均阿托伐他汀剂量实现了国家胆固醇教育计划的治疗目标,显著降低了冠心病(CHD)患者的发病率和死亡率。在这里,我们报告了未接受血脂异常治疗的普通护理患者(12%接受他汀类药物治疗)与绝大多数接受阿托伐他汀治疗的结构性护理患者(98%)的血尿酸水平的时间进程。方法:通过使用方差分析来评估治疗组内和治疗组之间随时间的差异,比较研究中的平均尿酸水平(长达48个月)与基线时的水平。使用COX多变量分析来调查研究期间血尿酸水平的变化是否与临床相关。结果:所有患者治疗前肾功能正常,血肌酐(Scr)<1.3mgdL(115mU/L),血尿酸水平中度升高(平均值7.10+-0.9mgdL[42552mU/L];正常上限7.0mgdL[415mU/L])。常规护理患者(n=800)的血尿酸水平增加了3.3%(P&lt;0.0001)。结构化护理患者(n=800)的血尿酸水平降低了8.2%(P&lt;0.0001)。在所有未服用利尿剂的患者(n=1,407)中,血尿酸水平的变化与Scr水平的变化呈正相关(r=0.82p&lt;0.0001),与估计的肾小球滤过率(r=-0.77p&lt;0.0001)呈负相关。在调整了所有冠心病相关事件的19个预测因素后,COX多因素回归分析显示,血尿酸水平每降低0.5 mg(30mU/L),危险比(HR)为0.89(95%可信区间[CI],0.78~0.96;P=0.03),HR为0.76(95%CI,0.62~0.89);P=0.001),血尿酸水平每增加1 mg,心率增加1.29(95%氯,1.17~1.43;P=0.001)。结论:数据表明,血尿酸水平是冠心病复发事件的独立预测因子。阿托伐他汀治疗显著降低了冠心病患者的血尿酸水平,从而抵消了与冠心病风险相关的另一个因素。
Background: Little is known about the effect of dyslipidemia on serum uric acid (SUA) levels, and less is known about the effect of statin treatment on them. The GREek Atorvastatin and Coronary-heart-disease Evaluation study suggested that a mean atorvastatin dose of 24 mg/d achieves the National Cholesterol Educational Program treatment goals and significantly reduces morbidity and mortality in patients with coronary heart disease (CHD) in comparison to the usual care. Here, we report the time course of SUA levels in usual-care patients undertreated for their dyslipidemia (12% were administered statins) in comparison to structured-care patients treated with atorvastatin in the vast majority (98%). Methods: Mean on-study SUA levels (up to 48 months) were compared with those at baseline by using analyses of variance to assess differences over time within and between treatment groups. Cox multivariate analysis was used to investigate whether changes in SUA levels during the study were clinically relevant. Results: All patients had normal renal function at baseline; serum creatinine (SCr) levels less than 1.3 mg/dL (< 115 mu mol/L) and moderately elevated SUA levels (mean, 7.1 +/- 0.9 [SD] mg/dL [425 52 mu mol/L]; upper normal limit, 7.0 mg/dL [415 mu mol/L]). Usual-care patients (n = 800) showed an increase in SUA levels by 3.3% (P < 0.0001). Structured-care patients (n = 800) had an 8.2% reduction in SUA levels (P < 0.0001). In all patients not administered diuretics (n = 1,407), SUA level changes showed a positive correlation with changes in SCr levels (r = 0.82; P < 0.0001) and an inverse correlation with estimated glomerular filtration rate (r = -0.77; P < 0.0001). After adjustment for 19 predictors of all CHD-related events, Cox multivariate analysis involving backward stepwise logistic regression showed a hazard ratio (HR) of 0.89 (95% confidence interval [CI], 0.78 to 0.96; P = 0.03) with every 0.5-mg (30-mu mol/L) reduction in SUA level, an HR of 0.76 (95% Cl, 0.62 to 0.89; P = 0.001) with every 1-mg (60-mu mol/L) reduction, an HR of 1.14 (95% Cl, 1.03 to 1.27; P = 0.02) with every 0.5-mg increase, and an HR of 1.29 (95% Cl, 1.17 to 1.43; P = 0.001) with every 1-mg increase in SUA levels. Conclusion., Data suggest that SUA level is an independent predictor of CHD recurrent events. Atorvastatin treatment significantly reduces SUA levels in patients with CHD, thus offsetting an additional factor associated with CHD risk.