title: Circulating leptin and adiponectin concentrations during tumor necrosis factor blockade in patients with active rheumatoid arthritis.
abstract: OBJECTIVE
  Adipocytokines, including leptin and adiponectin, may play an important role in the pathogenesis of rheumatoid arthritis (RA). We investigated the effects of longterm therapeutic tumor necrosis factor (TNF) blockade on adipocytokine concentrations in patients with RA.
  
  
  METHODS
  We studied 58 RA patients starting anti-TNF therapy and 58 healthy controls matched for age, sex, and body mass index (BMI). Fasting blood samples were drawn at baseline, 2 weeks, and 6 months after the start of anti-TNF therapy and serum levels of leptin and adiponectin were measured.
  
  
  RESULTS
  Patients with RA had increased adiponectin (p<0.001) and similar leptin concentrations compared with the controls. Leptin concentrations were significantly higher in patients with high BMI (p<0.001) and correlated positively with BMI at all timepoints (r>0.75). In contrast, serum adiponectin tended to be higher in lean RA patients and did not correlate with BMI at any timepoint. There were no clear correlations between serum concentrations of adipocytokines and disease activity (Disease Activity Score 28). Short or longterm TNF blockade alone had no influence on circulating leptin and adiponectin concentrations. Patients treated with anti-TNF and concomitant corticosteroids on a stable basis showed a significant decrease in adiponectin levels after 6 months of therapy (p<0.025).
  
  
  CONCLUSIONS
  In patients with RA, chronic inflammation and its suppression during anti-TNF therapy have limited influence on plasma leptin concentrations, while significantly decreasing circulating adiponectin levels. Our findings question the suggested key role of inflammatory markers in regulating adipocytokine patterns in RA.
authors.affiliation: Department of Rheumatology, Radboud University Nijmegen Medical Centre, PO Box 9101, 6500 HB Nijmegen, The Netherlands. c.popa@reuma.umcn.nl
authors.forename: Calin
authors.initials: C
authors.lastname: Popa
authors.forename: Mihai G
authors.initials: MG
authors.lastname: Netea
authors.forename: Jacqueline
authors.initials: J
authors.lastname: de Graaf
authors.forename: Frank H J
authors.initials: FH
authors.lastname: van den Hoogen
authors.forename: Timothy R D J
authors.initials: TR
authors.lastname: Radstake
authors.forename: Helga
authors.initials: H
authors.lastname: Toenhake-Dijkstra
authors.forename: Piet L C M
authors.initials: PL
authors.lastname: van Riel
authors.forename: Jos W M
authors.initials: JW
authors.lastname: van der Meer
authors.forename: Anton F H
authors.initials: AF
authors.lastname: Stalenhoef
authors.forename: Pilar
authors.initials: P
authors.lastname: Barrera
mesh_terms: D052242:Adiponectin / Q000097:blood*; D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000188:drug therapy*; D015415:Biomarkers / Q000097:blood; D015992:Body Mass Index; D005260:Female; D006801:Humans; D000069285:Infliximab; D020738:Leptin / Q000097:blood*; D008297:Male; D008875:Middle Aged; D012720:Severity of Illness Index; D013223:Statistics as Topic; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D052242:Adiponectin; D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D015415:Biomarkers; D020738:Leptin; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab