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血清尿酸浓度与临床明显痛风发作的关系:一项个体参与者数据分析。

Relationship between serum urate concentration and clinically evident incident gout: an individual participant data analysis.

机构信息

Department of Medicine, University of Auckland, Auckland, New Zealand.

Department of Biochemistry, University of Otago, Dunedin, New Zealand.

出版信息

Ann Rheum Dis. 2018 Jul;77(7):1048-1052. doi: 10.1136/annrheumdis-2017-212288. Epub 2018 Feb 20.

Abstract

OBJECTIVES

To provide estimates of the cumulative incidence of gout according to baseline serum urate.

METHODS

Using individual participant data from four publicly available cohorts (Atherosclerosis Risk in Communities Study, Coronary Artery Risk Development in Young Adults Study, and both the Original and Offspring cohorts of the Framingham Heart Study), the cumulative incidence of clinically evident gout was calculated according to baseline serum urate category. Cox proportional hazards modelling was used to evaluate the relation of baseline urate categories to risk of incident gout.

RESULTS

This analysis included 18 889 participants who were gout-free at baseline, with mean (SD) 11.2 (4.2) years and 212 363 total patient-years of follow-up. The cumulative incidence at each time point varied according to baseline serum urate concentrations, with 15-year cumulative incidence (95% CI) ranging from 1.1% (0.9 to 1.4) for <6 mg/dL to 49% (31 to 67) for ≥10 mg/dL. Compared with baseline serum urate <6 mg/dL, the adjusted HR for baseline serum urate 6.0-6.9 mg/dL was 2.7, for 7.0-7.9 mg/dL was 6.6, for 8.0-8.9 mg/dL was 15, for 9.0-9.9 mg/dL was 30, and for ≥10 mg/dL was 64.

CONCLUSIONS

Serum urate level is a strong non-linear concentration-dependent predictor of incident gout. Nonetheless, only about half of those with serum urate concentrations ≥10mg/dL develop clinically evident gout over 15 years, implying a role for prolonged hyperuricaemia and additional factors in the pathogenesis of gout.

摘要

目的

根据基线血尿酸水平估算痛风的累积发病率。

方法

利用四项公开队列研究(动脉粥样硬化风险研究、年轻人冠状动脉风险发展研究以及弗雷明汉心脏研究的原始队列和子代队列)的个体参与者数据,根据基线血清尿酸类别计算临床明显痛风的累积发病率。采用 Cox 比例风险模型评估基线尿酸类别与痛风发病风险的关系。

结果

这项分析纳入了 18889 名基线时无痛风且血尿酸正常的参与者,平均(SD)年龄为 11.2(4.2)岁,总随访患者年数为 212363 年。各时间点的累积发病率因基线血清尿酸浓度而异,15 年累积发病率(95%CI)从<6mg/dL 的 1.1%(0.9 至 1.4)到≥10mg/dL 的 49%(31 至 67)。与基线血尿酸<6mg/dL 相比,基线血尿酸 6.0-6.9mg/dL、7.0-7.9mg/dL、8.0-8.9mg/dL、9.0-9.9mg/dL 和≥10mg/dL 的调整后 HR 分别为 2.7、6.6、15、30 和 64。

结论

血清尿酸水平是痛风发病的强非线性、浓度依赖性预测指标。尽管如此,只有约一半的血清尿酸浓度≥10mg/dL 的患者在 15 年内出现临床明显的痛风,这表明高尿酸血症持续时间延长和其他因素在痛风发病机制中起作用。

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