Wang Chrong-Reen, Tsai Hung-Wen
Department of Internal Medicine, National Cheng Kung University Hospital, Tainan 70403, Taiwan.
Department of Pathology, National Cheng Kung University Hospital, Tainan 70403, Taiwan.
World J Diabetes. 2022 Jun 15;13(6):454-465. doi: 10.4239/wjd.v13.i6.454.
An increased risk of insulin resistance (IR) has been identified in rheumatoid arthritis (RA), a chronic inflammatory disorder with elevated levels of pathogenic cytokines. Biologics targeting proinflammatory cytokines can control the disease and improve insulin sensitivity in RA. Although Janus kinase (JAK) signaling can regulate cytokine receptors and participate in RA pathogenesis, it remains to be elucidated whether there is a reduction of IR in such patients under JAK inhibitor (JAKi) therapy.
To study the effect of JAKi treatment on the reduction of IR in RA patients with active disease.
A retrospective study was carried out from April 1, 2017 to March 31, 2021 in a population of non-diabetic patients with active RA who were undergoing tofacitinib (TOF) therapy with 5 mg twice-daily immediate-release formulation.
Fifty-six RA patients, aged 30 years to 75 years (mean ± SD: 52.3 ± 11.1) with disease activity score 28 values ranging from 4.54 to 7.37 (5.82 ± 0.74), were classified into high-IR (> 2.0) and low-IR (≤ 2.0) groups based on their baseline homeostatic model assessment (HOMA)-IR levels. They had no previous exposure to JAKi, and received TOF therapy for no less than 6 mo. In 30 patients who were naïve to biologics, after a 24-week therapeutic period, the high-IR group showed reduced HOMA-IR levels (3.331 ± 1.036 2.292 ± 0.707, < 0.001). In another 26 patients who were exposed to tumor necrosis factor-α or interleukin-6 blockers, the high-IR group, despite having achieved a decrease but with lower magnitude than in naïve patients, showed reduced HOMA-IR levels (2.924 ± 0.790 2.545 ± 1.080, = 0.018).
In this retrospective study, reduced IR was achieved in non-diabetic active RA patients following 24 wk of TOF therapy.
胰岛素抵抗（IR）风险增加已在类风湿关节炎（RA）中得到确认，RA是一种慢性炎症性疾病，其致病细胞因子水平升高。靶向促炎细胞因子的生物制剂可控制疾病并改善RA患者的胰岛素敏感性。尽管 Janus 激酶（JAK）信号传导可调节细胞因子受体并参与RA发病机制，但JAK抑制剂（JAKi）治疗此类患者时IR是否降低仍有待阐明。
研究JAKi治疗对活动性疾病的RA患者降低IR的影响。
对2017年4月1日至2021年3月31日期间，一组正在接受托法替布（TOF）5mg每日两次速释制剂治疗的非糖尿病活动性RA患者进行回顾性研究。
56例年龄在30岁至75岁（平均±标准差：52.3±11.1）、疾病活动度评分28值在4.54至7.37（5.82±0.74）之间的RA患者，根据其基线稳态模型评估（HOMA）-IR水平分为高IR（>2.0）和低IR（≤2.0）组。他们既往未接触过JAKi，且接受TOF治疗不少于6个月。在30例未使用过生物制剂的患者中，经过24周治疗期后，高IR组的HOMA-IR水平降低（3.331±1.036比2.292±0.707，P<0.001）。在另外26例曾接触过肿瘤坏死因子-α或白细胞介素-6阻滞剂的患者中，高IR组尽管HOMA-IR水平有所下降，但下降幅度低于未使用过生物制剂的患者，其HOMA-IR水平降低（2.924±0.790比2.5 45±1.080，P=0.018）。
在这项回顾性研究中，非糖尿病活动性RA患者接受24周TOF治疗后IR降低。
