We undertook this study to test the hypotheses that patients with active rheumatoid arthritis (RA) are insulin resistant and that anti-tumour necrosis factor-alpha (TNFalpha) therapy improves not only the clinical state of these patients but also their glucose metabolism.
Nine RA patients with active disease and nine healthy subjects, matched for sex, age, and body mass index (BMI), underwent a hyperinsulinaemic euglycaemic clamp. The RA patients received anti-TNFalpha therapy with Humira(adalimumab) and had the insulin clamp re-evaluated after 8 weeks of treatment.
Patients with RA had marked insulin resistance (glucose infusion rate (GIR) area under the curve (AUC) was 499+/-55 mg/kg in the RA group compared to 710+/-77 mg/kg in the control group; p<0.05). However, insulin sensitivity did not differ before and after 8 weeks of adalimumab therapy. The RA patients demonstrated a reduction in C-reactive protein (CRP) and interleukin-6 (IL-6) levels after the therapy as compared to pretreatment values, but there was no concomitant effect on plasma levels of TNFalpha.
RA patients with active disease showed marked insulin resistance that was not influenced by anti-TNFalpha therapy despite a reduction in systemic inflammation during the treatment.