Arthritis Research UK Centre for Epidemiology, Centre for Musculoskeletal Research, Institute of Inflammation and Repair, The University of Manchester and Salford Royal Hospital NHS Foundation Trust.
Arthritis Research UK Centre for Epidemiology, Centre for Musculoskeletal Research, Institute of Inflammation and Repair, The University of Manchester.
Arthritis Rheumatol. 2016 Jun;68(6):1337-45. doi: 10.1002/art.39582.
Patients with rheumatoid arthritis (RA) are at an increased risk of ischemic stroke. Tumor necrosis factor inhibitors (TNFi) may influence risk and mortality after ischemic stroke by reducing inflammation. This study was undertaken to examine the association of TNFi with the risk of incident ischemic stroke and with 30-day and 1-year mortality after ischemic stroke.
Patients with RA starting therapy with TNFi and a biologics-naive comparator group treated with synthetic disease-modifying antirheumatic drugs (DMARDs) only were recruited to the British Society for Rheumatology Biologics Register for Rheumatoid Arthritis from 2001 to 2009. Patients were followed up via clinical and patient questionnaires as well as the national death register. Incident strokes were classified as ischemic if brain imaging reports suggested ischemia or if ischemic stroke was reported as the underlying cause of death on a death certificate. Patients with a previous stroke were excluded. Risk of ischemic stroke was compared between patients receiving synthetic DMARDs only and those ever-exposed to TNFi using a Cox proportional hazards regression model adjusted for potential confounders. Mortality after ischemic stroke was compared between synthetic DMARD-treated patients and TNFi-treated patients using logistic regression, adjusted for age and sex.
To April 2010, 127 verified incident ischemic strokes (21 in 3,271 synthetic DMARD-treated patients and 106 in 11,642 TNFi-treated patients) occurred during 11,973 and 61,226 person-years of observation, respectively (incidence rate 175 versus 173 per 100,000 person-years). After adjustment for confounders, there was no association between ever-exposure to TNFi and ischemic stroke (hazard ratio 0.99 [95% confidence interval (95% CI) 0.54-1.81]). Mortality 30 days or 1 year after ischemic stroke was not associated with concurrent TNFi exposure (odds ratio 0.18 [95% CI 0.03-1.21] and 0.60 [95% CI 0.16-2.28], respectively).
Exposure to TNFi does not appear to influence the occurrence of ischemic stroke in the medium term in patients with RA. The impact on mortality after ischemic stroke remains inconclusive.
类风湿关节炎（RA）患者发生缺血性卒中的风险增加。肿瘤坏死因子抑制剂（TNFi）可通过减轻炎症来影响缺血性卒中和死亡率。本研究旨在探讨 TNFi 与缺血性卒中事件风险以及缺血性卒中后 30 天和 1 年死亡率之间的关系。
从 2001 年至 2009 年，我们招募了开始接受 TNFi 治疗和生物制剂初治比较组的仅接受合成疾病修饰抗风湿药物（DMARDs）治疗的 RA 患者，入组英国风湿病学会生物制剂登记处进行 RA 研究。通过临床和患者问卷调查以及国家死亡登记处对患者进行随访。如果脑部影像学报告提示缺血或死亡证明中报告缺血性卒中是死亡的根本原因，则将卒中事件分类为缺血性。排除既往有卒中的患者。使用 Cox 比例风险回归模型，根据潜在混杂因素对仅接受合成 DMARD 治疗的患者和曾经接受过 TNFi 治疗的患者进行比较，评估缺血性卒中的风险。使用 logistic 回归，根据年龄和性别，对接受合成 DMARD 治疗的患者和接受 TNFi 治疗的患者进行缺血性卒中后死亡率的比较。
截至 2010 年 4 月，在 11973 和 61226 人年的观察期间，分别发生了 127 例经证实的缺血性卒中（3271 例接受合成 DMARD 治疗的患者中有 21 例，11642 例接受 TNFi 治疗的患者中有 106 例）（发病率分别为 175 例和 173 例/100,000 人年）。在校正混杂因素后，曾接受 TNFi 治疗与缺血性卒中之间无关联（风险比 0.99 [95%置信区间（95%CI）0.54-1.81]）。缺血性卒中后 30 天或 1 年的死亡率与同时接受 TNFi 暴露无关（比值比分别为 0.18 [95%CI 0.03-1.21]和 0.60 [95%CI 0.16-2.28]）。
RA 患者接受 TNFi 治疗似乎不会在中期内影响缺血性卒中的发生。对缺血性卒中后死亡率的影响仍不确定。
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