Chen Haoran, Wang Meng, Yang Lin, Li Jiao, Li Zixiao
Institute of Medical Information/Library, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, People's Republic of China.
Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, People's Republic of China.
J Inflamm Res. 2024 Nov 11;17:8681-8694. doi: 10.2147/JIR.S494487. eCollection 2024.
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.
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.
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.
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.
炎症生物标志物(高敏C反应蛋白,hsCRP)与抗氧化剂(尿酸,UA)之间关于缺血性中风或短暂性脑缺血发作(TIA)后预后的相互作用仍未得到充分研究。本研究旨在评估(1)hsCRP和UA的个体及联合作用,以及(2)在hsCRP水平升高的患者中,UA对90天时功能预后不良的神经保护作用。
进行了一项前瞻性队列研究,纳入2140例连续的缺血性中风或TIA患者,检测其hsCRP和UA水平。主要结局定义为功能预后不良,以90天时改良Rankin量表(mRS)评分为3 - 6分表示,mRS评分变化作为次要结局。采用逻辑回归和倾向评分(PS)分析以确保结果的稳健性。
345例(16.1%)患者出现功能预后不良。个体效应发现,hsCRP最高四分位数(调整后OR = 3.090;95%CI 2.150 - 4.442)和UA最高四分位数(调整后OR = 0.671;95%CI 0.551 - 0.883)分别与功能预后不良风险增加或降低相关。hsCRP和UA对主要结局的联合效应(调整后OR = 3.994;95%CI 2.758 - 5.640)在hsCRP水平高(hsCRP > 1.60 mg/L)且UA水平低(UA ≤ 291.85 µmol/L)的患者中更为明显。对于hsCRP水平高的患者,未调整或调整hsCRP后,UA水平低的患者与UA水平高的患者相比,主要和次要结局的风险更高。在基于PS的模型中观察到了相似且可靠的结果。
在缺血性中风或TIA患者中,hsCRP高水平和UA低水平联合与90天时功能预后不良风险增加显著相关。此外,高UA水平可降低hsCRP水平高的患者功能预后不良的风险。