Accortt Neil A, Chung James B, Bonafede Machaon, Limone Brendan L, Mannino David M
Amgen, Inc., Center for Observational Research, Thousand Oaks, CA.
Amgen, Inc., US Medical Organization, Thousand Oaks, CA.
Int J Chron Obstruct Pulmon Dis. 2017 Jul 19;12:2085-2094. doi: 10.2147/COPD.S127815. eCollection 2017.
Limited information exists on the impact of tumor necrosis factor inhibition on COPD exacerbations. This retrospective study characterized this impact among COPD patients with underlying autoimmune conditions, exposed to tumor necrosis factor inhibitors (TNFi) and/or non-biologic disease-modifying antirheumatic drugs (DMARDs).
Adult COPD patients with ≥1 diagnosis for rheumatoid arthritis (RA), psoriasis (PsO), psoriatic arthritis (PsA), or ankylosing spondylitis (AS) before or within 6 months following the index COPD diagnosis were identified from the Truven Health MarketScan databases. Patients were required to have a second claim for RA, PsO, PsA, AS, or DMARD use (biologic or non-biologic) prior to or up to 6 months following the index date. Incidence of COPD-related hospitalizations and emergency room (ER) visits was evaluated in relation to treatment with TNFi and/or DMARDs and other potential risk factors.
The study cohort included 40,687 patients (untreated, 37.7%; non-biologic DMARD, 35.4%; TNFi + non-biologic DMARD, 18%; TNFi, 8.8%). The proportion of patients with a COPD-related hospitalization and the incidence of COPD-related hospitalization (per 100 person-years) were lowest in the TNFi cohort (8.6%; 3.54, 95% confidence interval [CI]: 3.16-3.95) and the TNFi + non-biologic DMARD cohort (8.4%; 2.85, 95% CI: 2.63-3.08). In multivariate models, treatment with TNFi + non-biologic DMARD reduced the risk of COPD-related hospitalization or ER visits by 32% relative to non-biologic DMARDs (hazard ratio: 0.68; 95% CI: 0.61-0.75).
In real-world settings, TNFi monotherapy confers similar risk for COPD-related hospitalization or ER visits as a non-biologic DMARD. Decreased risk was found among those treated with both TNFi and a non-biologic DMARD.
关于肿瘤坏死因子抑制对慢性阻塞性肺疾病（COPD）急性加重的影响，现有信息有限。这项回顾性研究描述了在患有自身免疫性基础疾病、接受肿瘤坏死因子抑制剂（TNFi）和/或非生物性改善病情抗风湿药（DMARDs）治疗的COPD患者中这种影响。
从Truven Health MarketScan数据库中识别出在首次诊断COPD之前或之后6个月内至少诊断过1次类风湿关节炎（RA）、银屑病（PsO）、银屑病关节炎（PsA）或强直性脊柱炎（AS）的成年COPD患者。要求患者在索引日期之前或之后6个月内有第二次RA、PsO、PsA、AS或使用DMARD（生物性或非生物性）的记录。评估与TNFi和/或DMARD治疗以及其他潜在风险因素相关的COPD相关住院和急诊就诊发生率。
研究队列包括40687名患者（未治疗，37.7%；非生物性DMARD，35.4%；TNFi + 非生物性DMARD，18%；TNFi，8.8%）。在TNFi队列（8.6%；3.54，95%置信区间[CI]：3.16 - 3.95）和TNFi + 非生物性DMARD队列（8.4%；2.85，95%CI：2.63 - 3.08）中，COPD相关住院患者的比例和COPD相关住院发生率（每100人年）最低。在多变量模型中，与非生物性DMARD相比，TNFi + 非生物性DMARD治疗使COPD相关住院或急诊就诊风险降低了32%（风险比：0.68；95%CI：0.61 - 0.75）。
在现实环境中，TNFi单药治疗导致COPD相关住院或急诊就诊的风险与非生物性DMARD相似。在同时接受TNFi和非生物性DMARD治疗的患者中发现风险降低。
