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Insulin sensitivity improved in rheumatoid arthritis patients after anti-TNF therapy
Anti-tumor necrosis factor therapy improved insulin sensitivity and reversed insulin signaling cascade defects in patients with rheumatoid arthritis and high insulin resistance, according to prospective study results.
Researchers studied 61 patients (mean age, 60 years; 43 women) with active rheumatoid arthritis (RA) and a mean Disease Activity Score 28 (DAS28) of 5.8. The patients were assigned infliximab (n=49), adalimumab (n=11) or eternercept (n=1) for anti-tumor necrosis factor (TNF) therapy. Seven control patients with RA were assigned abatacept to study insulin signaling.
Patients with high insulin resistance (homeostasis model assessment [HOMA-IR] above median, n=30) displayed significantly higher mean DAS28 (P=.011), serum triglycerides (P=.015) and systolic blood pressure levels (P=.024) than patients with low insulin resistance at baseline. After 12 weeks of therapy, the high insulin resistance group showed significant reduction in HOMA-IR (P<.001), HOMA-B (P=.001), serum triglycerides (P=.039), along with increases in quantitative insulin sensitivity check index (P<.001) and serum high-density lipoprotein cholesterol (P=.022). Seven high insulin resistant patients displayed reduction in p-Ser312 insulin receptor substrate-1 (IRS-1) (P=.043) through Western blot analysis. Abatacept’s effect on p-Ser312 IRS-1 and p-AKT varied among the controls.
“We found that 12 weeks of treatment with anti-TNF agents may improve insulin resistance in patients with active RA and high insulin resistance,” the researchers concluded. “Treatment with anti-TNF was shown to restore the phosphorylation status of Ser312-IRS-1 and AKT, which are important mediators in the insulin signaling cascade. The impact of these biochemical changes in modifying the burden of cardiovascular diseases in patients with chronic inflammatory arthritis remains to be seen.”