Insulin resistance in patients with rheumatoid arthritis: effect of anti-TNFalpha therapy

Scand J Rheumatol. Mar-Apr 2007;36(2):91-6. doi: 10.1080/03009740601179605.

Abstract

Objectives: 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.

Methods: 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.

Results: 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.

Conclusion: 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.

Publication types

  • Clinical Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adalimumab
  • Adult
  • Aged
  • Antibodies, Monoclonal / pharmacology*
  • Antibodies, Monoclonal, Humanized
  • Antirheumatic Agents / pharmacology*
  • Arthritis, Rheumatoid / drug therapy*
  • Arthritis, Rheumatoid / metabolism
  • C-Reactive Protein / drug effects
  • Female
  • Glucose Clamp Technique
  • Humans
  • Inflammation / drug therapy
  • Insulin Resistance / physiology*
  • Interleukin-6 / blood
  • Male
  • Middle Aged
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors
  • Tumor Necrosis Factor-alpha / drug effects*

Substances

  • Antibodies, Monoclonal
  • Antibodies, Monoclonal, Humanized
  • Antirheumatic Agents
  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • C-Reactive Protein
  • Adalimumab