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Relationship between serum urate concentration and clinically evident incident gout: an individual participant data analysis
Annals of the Rheumatic Diseases ( IF 20.3 ) Pub Date : 2018-02-20 , DOI: 10.1136/annrheumdis-2017-212288
Nicola Dalbeth 1 , Amanda Phipps-Green 2 , Christopher Frampton 3 , Tuhina Neogi 4 , William J Taylor 5 , Tony R Merriman 2
Affiliation  

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.

中文翻译:

血清尿酸浓度与临床明显痛风事件之间的关系:个体参与者数据分析

目的 根据基线血清尿酸盐估计痛风的累积发病率。方法 使用来自四个公开可用队列(社区研究中的动脉粥样硬化风险、年轻成人研究中的冠状动脉风险发展以及弗雷明汉心脏研究的原始队列和后代队列)的个体参与者数据,根据以下公式计算临床明显痛风的累积发病率到基线血清尿酸类别。Cox 比例风险模型用于评估基线尿酸盐类别与痛风事件风险的关系。结果 该分析包括 18 889 名基线时无痛风的参与者,平均 (SD) 11.2 (4.2) 年,总随访患者年数为 212 363 患者年。每个时间点的累积发生率根据基线血清尿酸浓度而变化,15 年累积发生率 (95% CI) 范围为 <6 mg/dL 的 1.1%(0.9 至 1.4)至 ≥10 mg/dL 的 49%(31 至 67)。与基线血清尿酸 <6 mg/dL 相比,基线血清尿酸 6.0-6.9 mg/dL 的调整 HR 为 2.7,7.0-7.9 mg/dL 为 6.6,8.0-8.9 mg/dL 为 15,9.0- 9.9 mg/dL 为 30,≥10 mg/dL 为 64。 结论 血清尿酸水平是痛风发作的强非线性浓度依赖性预测因子。尽管如此,只有大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,这意味着长期高尿酸血症和其他因素在痛风发病机制中的作用。基线血清尿酸 6.0-6.9 mg/dL 的调整后 HR 为 2.7,7.0-7.9 mg/dL 为 6.6,8.0-8.9 mg/dL 为 15,9.0-9.9 mg/dL 为 30,≥10 mg/dL 为 64。 结论 血清尿酸水平是痛风发作的强非线性浓度依赖性预测因子。尽管如此,只有大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,这意味着长期高尿酸血症和其他因素在痛风发病机制中的作用。基线血清尿酸 6.0-6.9 mg/dL 的调整后 HR 为 2.7,7.0-7.9 mg/dL 为 6.6,8.0-8.9 mg/dL 为 15,9.0-9.9 mg/dL 为 30,≥10 mg/dL 为 64。 结论 血清尿酸水平是痛风发作的强非线性浓度依赖性预测因子。尽管如此,只有大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,这意味着长期高尿酸血症和其他因素在痛风发病机制中的作用。
更新日期:2018-02-20
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