Association of Uric Acid, High-Sensitivity C-Reactive Protein, and 90-Day Risk of Poor Function Outcome in Patients with Ischemic Stroke or Transient Ischemic Attacks.
Haoran Chen, Meng Wang, Lin Yang, Jiao Li, Zixiao Li
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引用次数: 0
Abstract
Aim: The interaction between inflammatory biomarkers (high-sensitivity C-reactive protein, hsCRP) and antioxidants (uric acid, UA) regarding prognosis after ischemic stroke or transient ischemic attack (TIA) remains inadequately explored. This study aimed to assess (1) the individual and joint effects of hsCRP and UA, and (2) the neuroprotective role of UA in patients with elevated hsCRP levels concerning poor functional outcomes at 90 days.
Methods: A prospective cohort study was conducted involving 2140 consecutive ischemic stroke or TIA patients with hsCRP and UA levels. The primary outcome was defined as a poor functional outcome, indicated by a modified Rankin Scale (mRS) score of 3-6 at 90 days, with a shift in the mRS score as a secondary outcome. Logistic regression and propensity score (PS) analyses were employed to ensure robustness.
Results: Poor functional outcome occurred in 345 (16.1%) patients. Individual effects found that the highest quartiles of hsCRP (adjusted OR = 3.090; 95% CI 2.150-4.442) and UA (adjusted OR = 0.671; 95% CI 0.551-0.883) were associated with increased or decreased risk of poor functional outcome, respectively. Joint effects (adjusted OR = 3.994; 95% CI 2.758-5.640) between hsCRP and UA on the primary outcome were more apparent in patients with high hsCRP levels (hsCRP > 1.60 mg/L) and low UA levels (UA ≤ 291.85 µmol/L). For the patients with high hsCRP levels, patients with low UA levels had a higher risk of primary and secondary outcomes, compared with those with high UA levels, after unadjusted or adjusted for hsCRP. Similar and reliable results were observed in PS-based models.
Conclusion: In patients with ischemic stroke or TIA, joint high levels of hsCRP and low UA levels significantly correlate with increased risk of poor functional outcome at 90 days. In addition, high UA levels could reduce the risk of poor functional outcome for patients with high hsCRP levels.
目的：关于缺血性中风或短暂性脑缺血发作（TIA）后预后的炎症生物标志物（高敏C反应蛋白，hsCRP）与抗氧化剂（尿酸，UA）之间的相互作用仍未得到充分探讨。本研究旨在评估：(1) hsCRP 和 UA 的个体和联合作用；(2) UA 对 hsCRP 水平升高且 90 天后功能预后不佳的患者的神经保护作用：这项前瞻性队列研究涉及 2140 名连续缺血性脑卒中或 TIA 患者，他们的 hsCRP 和 UA 水平都很高。主要结果定义为不良功能预后，即 90 天时改良 Rankin 量表（mRS）评分为 3-6 分，mRS 评分的变化为次要结果。为确保稳健性，采用了逻辑回归和倾向得分（PS）分析：结果：345 名（16.1%）患者出现功能障碍。个体效应发现，hsCRP（调整后 OR = 3.090；95% CI 2.150-4.442）和 UA（调整后 OR = 0.671；95% CI 0.551-0.883）的最高四分位数分别与功能预后不良风险的增加或降低有关。在高 hsCRP 水平（hsCRP > 1.60 mg/L）和低 UA 水平（UA ≤ 291.85 µmol/L）的患者中，hsCRP 和 UA 对主要预后的联合影响（调整后 OR = 3.994；95% CI 2.758-5.640）更为明显。对于 hsCRP 水平较高的患者，与 UA 水平较高的患者相比，未经调整或调整 hsCRP 后，UA 水平较低的患者发生主要和次要结局的风险更高。在基于 PS 的模型中也观察到了类似且可靠的结果：结论：在缺血性卒中或 TIA 患者中，高 hsCRP 水平和低 UA 水平与 90 天后不良功能预后风险的增加密切相关。此外，高 UA 水平可降低高 hsCRP 水平患者功能预后不良的风险。
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