The Effects of 5-year Etanercept Therapy on Cardiovascular Risk Factors in Patients with Psoriatic Arthritis

The Effects of 5-year Etanercept Therapy on Cardiovascular Risk Factors in Patients with Psoriatic Arthritis
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DOI:
10.3899/jrheum.161418
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发表时间:
2017-09-01
影响因子:
3.9
通讯作者:
Nurmohamed, Michael T.
Nurmohamed, Michael T.
中科院分区:
医学2区
文献类型:
--
作者:
Agca, Rabia;Heslinga, Maaike;Nurmohamed, Michael T.

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目标。目的探讨依那西普(ETN)对银屑病关节炎(PSA)患者脂代谢及心血管疾病(CVD)危险因素的影响。在118名连续接受PSA治疗的患者的观察队列中,对5年内的心血管危险因素进行了评估。采用混合模型分析研究ETN治疗对心脑血管疾病危险因素的影响。在ETN治疗期间,28个关节的疾病活动性评分、C反应蛋白(CRP)和血沉下降。总胆固醇(TC)、高密度脂蛋白胆固醇(HDLc)和低密度脂蛋白胆固醇(LDLc)有所增加。TC/HDLc比率保持不变。载脂蛋白B/载脂蛋白A-I(apoB/apoA-I)比值明显降低。C反应蛋白升高与apoB/apoA-1比值升高相关。在ETN治疗的5年期间,血脂浓度显示出微小的变化,并且与炎症标记物呈负相关。其他心血管危险因素保持稳定。ApoB/apoA-1比率随着时间的推移而下降,疾病活动性的增加与这一比率的增加有关。然而,这种温和的血脂调节不能解释ETN的有益心血管效应,ETN可能通过炎症相关机制发挥这些作用。
Objective. To investigate the effects of etanercept (ETN) on lipid metabolism and other known cardiovascular disease (CVD) risk factors in patients with psoriatic arthritis (PsA).Methods. In an observational cohort of 118 consecutive patients with PsA, CVD risk factors were assessed over 5 years. Mixed-model analyses were performed to investigate the effects of ETN therapy on CVD risk factors over time.Results. Disease Activity Score in 28 joints, C-reactive protein (CRP), and erythrocyte sedimentation rate decreased during therapy with ETN. There was an increase in total cholesterol (TC), high-density lipoprotein cholesterol (HDLc), and low-density lipoprotein cholesterol. The TC/HDLc ratio remained unaltered. The apolipoprotein B to apolipoprotein A-I (apoB/apoA-I) ratio decreased significantly. An increase in CRP was associated with an increase in the apoB/apoA-1 ratio.Conclusion. Serum lipid concentrations showed small changes over a 5-year period of ETN therapy and were inversely associated with inflammatory markers. Other CVD risk factors remained stable. The apoB/apoA-1 ratio decreased over time and an increase in disease activity was associated with an increase in this ratio. However, this modest lipid modulation cannot explain the observed beneficial CV effects of ETN, and ETN likely exerts those effects through inflammation-related mechanisms.