Corrona Research Foundation, Albany, NY, United States; Vagelos College of Physicians & Surgeons, Columbia University, New York, NY, United States; CorEvitas, Waltham, MA, United States.
Corrona Research Foundation, Albany, NY, United States; University of Massachusetts, Worcester, MA, United States.
Semin Arthritis Rheum. 2024 Oct;68:152504. doi: 10.1016/j.semarthrit.2024.152504. Epub 2024 Jun 29.
Cardiovascular disease (CVD) is the main cause of mortality in Rheumatoid Arthritis (RA).
To investigate the effect of biologic disease modifying anti-rheumatic drugs (bDMARDs) on lipids and CVD risk and evaluate associations with changes in systemic inflammation.
Patients with RA initiating a bDMARD were evaluated at baseline, 3 and 6 months later. Longitudinal mixed effects models examined the association of individual biologics with changes in lipid levelsm Reynolds Risk Score (RRS) and Framingham risk score. Mediation by CRP, clinical disease activity index (CDAI) or swollen joint count on lipid changes were modeled using structural equation models. The correlation between CRP changes and LDL changes was estimated. Changes of LDL-C at 6 months among patients with low baseline LDL-C (<90 mg/dl) vs higher baseline LDL-C(90-130, and >130 mg/dl) were compared. The association between LDL-C changes across baseline LDL-C groups and disease activity improvement was evaluated.
1698 bDMARD initiations were analyzed. Patients initiating tocilizumab had a significant increase in lipid levels but RRS at 3 and 6 months was similar across all biologics. Framingham risk score increased for patients treated with tocilizumab. Mediator analyses were statistically significant for the effects of CRP on lipid levels. Increases in LDL-C from baseline were independent of clinical response. An association of changes from baseline CRP and LDL-C were observed across all of the bDMARDs studied.
Moderate increases in lipid levels on bDMARD treatment were not associated with an increased CVD risk by RRS regardless of the bDMARD initiated. Changes in CRP were significantly associated with changes in lipids in a mediator analysis.
心血管疾病（CVD）是类风湿关节炎（RA）患者的主要致死原因。
本研究旨在探讨生物制剂改善病情抗风湿药（bDMARDs）对血脂和 CVD 风险的影响，并评估其与全身炎症变化的关系。
评估了起始 bDMARD 治疗的 RA 患者在基线、3 个月和 6 个月时的情况。采用纵向混合效应模型研究了个体生物制剂与血脂水平、Reynolds 风险评分（RRS）和 Framingham 风险评分变化的相关性。采用结构方程模型对 CRP、临床疾病活动指数（CDAI）或肿胀关节计数对血脂变化的中介作用进行建模。估计了 CRP 变化与 LDL-C 变化之间的相关性。比较了基线 LDL-C 较低（<90mg/dl）与较高（90-130 和>130mg/dl）患者在 6 个月时 LDL-C 的变化。评估了 LDL-C 变化与疾病活动改善的相关性。
共分析了 1698 例 bDMARD 起始治疗。起始使用托珠单抗的患者血脂水平显著升高，但所有生物制剂在 3 个月和 6 个月时的 RRS 相似。接受托珠单抗治疗的患者Framingham 风险评分增加。CRP 对血脂水平的影响中介分析有统计学意义。与基线相比，LDL-C 的增加独立于临床反应。在所有研究的 bDMARD 中，均观察到 CRP 和 LDL-C 从基线的变化之间存在关联。
无论起始使用何种 bDMARD，bDMARD 治疗时血脂水平的适度升高与 RRS 评估的 CVD 风险增加无关。中介分析显示，CRP 的变化与血脂的变化显著相关。
