Li Nanxin, Betts Keith A, Messali Andrew J, Skup Martha, Garg Vishvas
Analysis Group Inc, Boston, Massachusetts.
AbbVie Inc, North Chicago, Illinois.
Clin Ther. 2017 Aug;39(8):1618-1627. doi: 10.1016/j.clinthera.2017.06.009. Epub 2017 Jul 17.
The purpose of this study was to assess the real-world effectiveness of patients with rheumatoid arthritis (RA) who discontinued etanercept treatment and subsequently received another tumor necrosis factor α (TNF-α) inhibitor or a non-TNF-α biologic in the United Kingdom, France, and Germany.
Medical record data of patients with RA were collected from a panel of rheumatologists in the United Kingdom, France, and Germany. Patients were required to have a diagnosis of RA, be ≥18 years old, and have initiated use of another TNF-α inhibitor (adalimumab, certolizumab pegol, golimumab, or infliximab) or a non-TNF-α biologic (abatacept or tocilizumab) between January 2014 and May 2015 after discontinuing use of etanercept. Reasons for discontinuing use of etanercept and selecting a second biologic disease-modifying antirheumatic drug (DMARD) were described. Study outcomes included European League Against Rheumatism (EULAR) response and change in Clinical Disease Activity Index (CDAI) score. The study outcomes were compared among treatment groups (ie, TNF-α inhibitors and non-TNF-α biologics) using descriptive and multivariable-adjusted analyses. As a secondary analysis, the study outcomes were also descriptively compared between each of the TNF-α inhibitors. Because adalimumab is one of the most commonly used TNF-α inhibitor to treat RA, a secondary analysis was conducted to compare the outcomes among adalimumab, other TNF-α inhibitors, and non-TNF-α inhibitors.
Patient characteristics before initiating treatment with a second DMARD were similar across treatment groups (all TNF-α inhibitors [n = 296] and non-TNF-α biologics [n = 276]). The most common reasons for discontinuing etanercept treatment were inadequate response, adverse effects, and patient preference. After etanercept, TNF-α inhibitors overall were associated with a significantly lower EULAR good response rate (56.0% vs. 64.4%, P < 0.05) and smaller CDAI score change (-6.3 vs -7.3, P = .06) relative to non-TNF-α biologics. However, the proportion of patients achieving an EULAR good response was numerically higher for adalimumab versus other TNF-α inhibitors (61.1% vs 51.6%, P = 0.11) and comparable versus non-TNF-α biologics (61.1% vs 64.4%, P = 0.52). Adalimumab was also associated with a CDAI score change significantly greater than that of other TNF-α inhibitors (-7.1 vs -5.8, P < 0.05) and comparable to that of non-TNF-α biologics (-7.1 vs -7.3, P = 0.79). The results were consistent in the multivariable-adjusted analysis and secondary analysis.
In this retrospective analysis of patients with RA in the United Kingdom, France, and Germany, after discontinuation of etanercept treatment, TNF-α inhibitors as a class were overall less effective as second biologic DMARDs relative to non-TNF-α biologics; however, adalimumab was more or as effective as other TNF-α inhibitors and non-TNF-α biologics.
本研究旨在评估在英国、法国和德国,停用依那西普治疗后继而接受另一种肿瘤坏死因子α(TNF-α)抑制剂或非TNF-α生物制剂的类风湿关节炎(RA)患者的实际疗效。
从英国、法国和德国的一组风湿病专家处收集RA患者的病历数据。患者需确诊为RA,年龄≥18岁,且在2014年1月至2015年5月停用依那西普后开始使用另一种TNF-α抑制剂(阿达木单抗、赛妥珠单抗、戈利木单抗或英夫利昔单抗)或非TNF-α生物制剂(阿巴西普或托珠单抗)。描述了停用依那西普及选择第二种改善病情抗风湿生物制剂(DMARD)的原因。研究结局包括欧洲抗风湿病联盟(EULAR)反应及临床疾病活动指数(CDAI)评分的变化。使用描述性分析和多变量调整分析对各治疗组(即TNF-α抑制剂和非TNF-α生物制剂)的研究结局进行比较。作为次要分析,还对每种TNF-α抑制剂之间的研究结局进行了描述性比较。由于阿达木单抗是治疗RA最常用的TNF-α抑制剂之一,因此进行了次要分析以比较阿达木单抗、其他TNF-α抑制剂和非TNF-α抑制剂之间的结局。
各治疗组(所有TNF-α抑制剂[n = 296]和非TNF-α生物制剂[n = 276])在开始使用第二种DMARD治疗前的患者特征相似。停用依那西普治疗最常见的原因是疗效不佳、不良反应和患者偏好。与非TNF-α生物制剂相比,停用依那西普后,总体而言TNF-α抑制剂的EULAR良好反应率显著较低(56.0%对64.4%,P < 0.05),CDAI评分变化较小(-6.3对-7.3,P = 0.06)。然而,阿达木单抗达到EULAR良好反应的患者比例在数值上高于其他TNF-α抑制剂(61.1%对51.6%,P = 0.11),与非TNF-α生物制剂相当(61.1%对64.4%,P = 0.52)。阿达木单抗的CDAI评分变化也显著大于其他TNF-α抑制剂(-7.1对-5.8,P < 0.05),与非TNF-α生物制剂相当(-7.1对-7.3,P = 0.79)。多变量调整分析和次要分析的结果一致。
在这项对英国、法国和德国RA患者的回顾性分析中,停用依那西普治疗后,作为一个类别,TNF-α抑制剂作为第二种生物DMARD相对于非TNF-α生物制剂总体疗效较差;然而,阿达木单抗与其他TNF-α抑制剂和非TNF-α生物制剂的疗效相当或更优。