Published online Jun 15, 2022. doi: 10.4239/wjd.v13.i6.454
Peer-review started: January 14, 2022
First decision: April 18, 2022
Revised: April 18, 2022
Accepted: May 28, 2022
Article in press: May 28, 2022
Published online: June 15, 2022
Processing time: 144 Days and 18.3 Hours
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.
This study examined the effect of JAKi treatment on the reduction of IR in RA with active disease.
A retrospective study was carried out in non-diabetic active RA patients under tofacitinib (TOF) therapy with 5 mg twice-daily immediate-release formulation from 2017 to 2021.
Fifty-six RA patients aged 30 years to 75 years (52.3 ± 11.1) with DAS 28 values 4.54 to 7.37 (5.82 ± 0.74), were classified into high- and low-IR groups based on the baseline homeostatic model assessment (HOMA)-IR levels. For the 30 patients naive to biologics, after a 24-wk therapeutic period, reduced levels of HOMA-IR were observed in the high-IR group (3.331 ± 1.036 vs 2.292 ± 0.707, P < 0.001). In another 26 patients exposed to tumor necrosis factor-α or interleukin-6 blockers, despite showing a decrease with lower magnitude than that observed in the naïve patients, reduced HOMA-IR levels were also identified in the high-IR group (2.924 ± 0.790 vs 2.545 ± 1.080, P = 0.018).
In this retrospective study, our results demonstrated reduced IR following 24-wk TOF therapy in non-diabetic active RA patients.
Further prospective studies can be performed in both non-diabetic patients and those with comorbid diabetes to clearly elucidate the effect of TOF on IR in active RA.