title: Insulin resistance in patients with rheumatoid arthritis: effect of anti-TNFalpha therapy.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Rheumatology, The Copenhagen Muscle Research Centre, Rigshospitalet, The Faculty of Health Sciences, University of Copenhagen, Denmark
authors.forename: A
authors.initials: A
authors.lastname: Rosenvinge
authors.forename: R
authors.initials: R
authors.lastname: Krogh-Madsen
authors.forename: B
authors.initials: B
authors.lastname: Baslund
authors.forename: B K
authors.initials: BK
authors.lastname: Pedersen
mesh_terms: D000068879:Adalimumab; D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents / Q000494:pharmacology*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000378:metabolism; D002097:C-Reactive Protein / Q000187:drug effects; D005260:Female; D015309:Glucose Clamp Technique; D006801:Humans; D007249:Inflammation / Q000188:drug therapy; D007333:Insulin Resistance / Q000502:physiology*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008875:Middle Aged; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000187:drug effects*
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D000068879:Adalimumab