title: Anti-TNF-alpha therapy does not modulate leptin in patients with severe rheumatoid arthritis.
abstract: OBJECTIVE
  The adipocytokine leptin regulates weight centrally and participates in the regulation of the immune and inflammatory responses. Chronic systemic inflammation is of major importance in the development of atherosclerosis in rheumatoid arthritis (RA). In the present study we investigated whether inflammation, obesity or both of these characteristics are potential determinants of circulating leptin concentrations in a group of RA patients on periodical treatment with the TNF-alpha-blocker-infliximab due to severe disease. We also assessed whether the infusion of infliximab may alter circulating leptin concentrations in patients with severe RA.
  
  
  METHODS
  We investigated 33 patients with RA on periodical treatment with infliximab. Serum leptin levels were determined immediately prior to and after infliximab infusion.
  
  
  RESULTS
  There was a positive correlation between body mass index of RA patients and baseline serum level of leptin (rho=0.665, p<0.001). Apart from a significant correlation with VCAM-1 (rho=0.349, p=0.04), no significant correlations between baseline leptin levels and the age at the time of the study or at the onset of the disease, disease duration, ESR and CRP levels, DAS28, lipids, insulin sensitivity, adhesion molecules, resistin, adiponectin, ghrelin or the cumulative prednisone dose at the time of the study were found. Leptin levels did not change upon infliximab infusion (p=0.48).
  
  
  CONCLUSIONS
  In RA patients on TNF-alpha blocker treatment, circulating leptin levels are unrelated to disease activity but constitute a manifestation of adiposity. The beneficial effect of anti-TNF-alpha therapy on cardiovascular mortality in RA does not seem to be mediated by reduction in serum levels of leptin.
authors.affiliation: Division of Rheumatology, Hospital Xeral Calde, Lugo, Spain. miguelaggay@hotmail.com
authors.forename: M A
authors.initials: MA
authors.lastname: Gonzalez-Gay
authors.forename: M T
authors.initials: MT
authors.lastname: Garcia-Unzueta
authors.forename: A
authors.initials: A
authors.lastname: Berja
authors.forename: C
authors.initials: C
authors.lastname: Gonzalez-Juanatey
authors.forename: J A
authors.initials: JA
authors.lastname: Miranda-Filloy
authors.forename: T R
authors.initials: TR
authors.lastname: Vazquez-Rodriguez
authors.forename: J M
authors.initials: JM
authors.lastname: de Matias
authors.forename: J
authors.initials: J
authors.lastname: Martin
authors.forename: P H
authors.initials: PH
authors.lastname: Dessein
authors.forename: J
authors.initials: J
authors.lastname: Llorca
mesh_terms: D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000188:drug therapy* / Q000276:immunology; D001799:Blood Sedimentation; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000032:analysis; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood; D000069285:Infliximab; D020738:Leptin / Q000097:blood* / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000097:blood*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D020738:Leptin; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D000069285:Infliximab