Slone Epidemiology Center, Boston University, Boston University Medical Campus, 72 East Concord Street, L-7, Boston, MA, 02118, USA.
Department of Rheumatology and Immunology, Kailuan General Hospital, Tangshan, China.
Arthritis Res Ther. 2020 Apr 15;22(1):84. doi: 10.1186/s13075-020-02173-4.
Longitudinal evidence on change of serum urate level with mortality risk is limited as prior studies have a measurement of serum urate at a single time point. Further, the combined effect of serum urate and systemic inflammation on mortality is unknown.
We conducted a prospective cohort study of 152,358 participants (122,045 men and 30,313 women) with repeated measurements of serum urate in 2006, 2008, 2010, and 2012 (107,751 participants had all four measurements of serum urate). We used the Cox proportional hazard model to examine the association between cumulative average and changes in serum urate with mortality. The combined effect of serum urate and systemic inflammation was determined by testing the interaction of serum urate and high-sensitive C-reactive protein (hs-CRP) in relation to mortality risk.
During a median follow-up of 8.7 (interquartile range 6.3-9.2) years, we identified 7564 all-cause deaths, 1763 CVD deaths, 1706 cancer deaths, and 1572 other deaths. We observed U-shaped relationships of cumulative average serum urate with all-cause mortality, cardiovascular mortality, and other mortalities. Compared with participants with stable serum urate, those with greater increases in serum urate had a 1.7-fold elevated mortality (hazard ratio (HR) = 1.66, 95% confidence interval (CI) = 1.49-1.84), and those with decreased serum urate had a 2-fold elevated mortality risk (HR = 2.14, 95% CI 1.93-2.37). Participants with both hyperuricemia and hs-CRP had 1.6 times higher mortality, compared with those with low serum urate and hs-CRP levels (HR = 1.56, 95% CI 1.37-1.76).
We observed a U-shaped relationship of long-term cumulative average serum urate with all-cause mortality, cardiovascular mortality, and other mortalities. Compared with participants with relatively stable serum urate levels, a greater increase or decrease in serum urate was associated with elevated mortality. Participants with both hyperuricemia and high systemic inflammation had the greatest mortality risk compared with those with low serum urate and low hs-CRP levels.
既往研究多基于单次血清尿酸测量，因此关于血清尿酸水平随死亡率变化的纵向证据有限。此外，血清尿酸和全身炎症对死亡率的综合影响尚不清楚。
我们进行了一项前瞻性队列研究，纳入了 152358 名参与者（122045 名男性和 30313 名女性），这些参与者在 2006 年、2008 年、2010 年和 2012 年进行了重复的血清尿酸测量（107751 名参与者进行了所有 4 次血清尿酸测量）。我们使用 Cox 比例风险模型来检验累积平均血清尿酸和血清尿酸变化与死亡率之间的关联。通过检验血清尿酸与高敏 C 反应蛋白（hs-CRP）交互作用与死亡率风险的关系，确定血清尿酸和全身炎症的综合影响。
在中位数为 8.7 年（四分位间距 6.3-9.2 年）的随访期间，我们共确定了 7564 例全因死亡、1763 例心血管疾病死亡、1706 例癌症死亡和 1572 例其他死亡。我们观察到累积平均血清尿酸与全因死亡率、心血管死亡率和其他死亡率呈 U 形关系。与血清尿酸稳定的参与者相比，血清尿酸升高幅度较大者的死亡率升高 1.7 倍（风险比[HR] = 1.66，95%置信区间[CI] = 1.49-1.84），而血清尿酸降低者的死亡率升高 2 倍（HR = 2.14，95%CI 1.93-2.37）。与低血清尿酸和 hs-CRP 水平的参与者相比，同时患有高尿酸血症和 hs-CRP 的参与者的死亡率高 1.6 倍（HR = 1.56，95%CI 1.37-1.76）。
我们观察到长期累积平均血清尿酸与全因死亡率、心血管死亡率和其他死亡率呈 U 形关系。与血清尿酸水平相对稳定的参与者相比，血清尿酸升高或降低与死亡率升高相关。与低血清尿酸和低 hs-CRP 水平的参与者相比，同时患有高尿酸血症和全身炎症的参与者的死亡率风险最高。
