Department of Geriatrics, Peking University First Hospital, Beijing, China.
Eur Rev Med Pharmacol Sci. 2020 Mar;24(5):2719-2724. doi: 10.26355/eurrev_202003_20544.
Uric acid is considered a biomarker for cardiovascular risk. Only a few studies have investigated the effect of aspirin on serum uric acid (SUA) levels with contradictory results. The present study evaluated the effect of aspirin on SUA levels in Chinese individuals over 60 years of age.
Subjects over 60 with coronary artery disease or multiple cardiovascular risk factors were enrolled in a multicentre randomized clinical trial. Eligible subjects were randomized to receive 50 mg or 100 mg aspirin daily. Levels of arachidonic acid-induced platelet aggregation performed by light transmission aggregometry (LTA-AA) and SUA were measured at randomization and two weeks thereafter. In this subanalysis, subjects without aspirin use prior to enrolment were chosen.
A total of 446 subjects were analysed, of which 151 subjects took 50 mg aspirin, and 295 took 100 mg aspirin. Hyperuricaemia was present in 23.3% (104/446) of subjects at baseline. LTA-AA levels were significantly reduced in subjects after taking aspirin for two weeks (both 50 mg and 100 mg, p < 0.001). SUA levels were decreased after aspirin administration (311 μmol/L vs. 302 μmol/L, p < 0.001). Further analysis showed SUA levels were unchanged in normouricaemic subjects (284 μmol/L vs. 280 μmol/L, p > 0.05), while slightly decreased in hyperuricaemic subjects (429 μmol/L vs. 392 μmol/L, p < 0.001).
Our study showed that both 50 mg and 100 mg aspirin significantly inhibited platelet aggregation. Aspirin treatment for two weeks showed no hyperuricaemic effect in people over 60. SUA levels were unchanged after taking aspirin in normouricaemic subjects but decreased in hyperuricaemic subjects. This trial was registered at www. chictr.org.cn as ChiCTR1800018517.
尿酸被认为是心血管风险的生物标志物。只有少数研究调查了阿司匹林对血清尿酸(SUA)水平的影响,结果存在矛盾。本研究评估了阿司匹林对中国 60 岁以上人群 SUA 水平的影响。
患有冠状动脉疾病或多种心血管危险因素的 60 岁以上患者参加了一项多中心随机临床试验。合格的患者被随机分配接受每日 50mg 或 100mg 阿司匹林治疗。在随机分组时和两周后,通过光传输聚集计(LTA-AA)测量花生四烯酸诱导的血小板聚集水平和 SUA 水平。在这项亚分析中,选择了在入组前没有使用阿司匹林的患者。
共分析了 446 名患者,其中 151 名患者服用 50mg 阿司匹林,295 名患者服用 100mg 阿司匹林。在基线时,23.3%(446/1904)的患者存在高尿酸血症。在服用阿司匹林两周后,血小板聚集水平明显降低(50mg 和 100mg 均 p<0.001)。SUA 水平在服用阿司匹林后降低(311μmol/L 比 302μmol/L,p<0.001)。进一步分析显示,在血尿酸正常的患者中,SUA 水平没有变化(284μmol/L 比 280μmol/L,p>0.05),而在高尿酸血症患者中,SUA 水平略有降低(429μmol/L 比 392μmol/L,p<0.001)。
本研究表明,50mg 和 100mg 阿司匹林均能显著抑制血小板聚集。服用阿司匹林两周后,60 岁以上人群无高尿酸血症作用。在血尿酸正常的患者中,服用阿司匹林后 SUA 水平没有变化,但在高尿酸血症患者中,SUA 水平下降。本试验在中国临床试验注册中心注册,注册号为 ChiCTR1800018517。