title: Leptin and visfatin serum levels in non-diabetic ankylosing spondylitis patients undergoing TNF-α antagonist therapy.
abstract: OBJECTIVE
  This paper aims to determine whether disease activity, systemic inflammation and metabolic syndrome are potential determinants of circulating leptin and visfatin levels in ankylosing spondylitis (AS) patients undergoing TNF-α antagonist therapy. We also assessed whether the infusion of infliximab may alter circulating leptin and visfatin concentrations in these patients.
  
  
  METHODS
  We investigated leptin and visfatin serum concentrations in a series of 30 non-diabetic AS patients without history of cardiovascular (CV) events that were treated with the TNF-α antagonist infliximab, immediately prior to an infliximab infusion. Leptin and visfatin levels were also determined immediately after administration of an infliximab dose.
  
  
  RESULTS
  Significant differences in leptin concentrations between men (8.85±5.31 ng/ml) and women (18.96±9.72 ng/ml) were observed (p=0.001). A significant correlation between visfatin concentrations and insulin resistance (HOMA at the time of the study) was found (r= 0.493; p=0.009). Circulating leptin and visfatin concentrations did not correlate with disease duration, erythrocyte sedimentation rate, C-reactive protein, BASDAI and VAS at the time of the study and adiponectin and resistin levels prior to infliximab infusion. Likewise, no differences in leptin and visfatin concentrations were observed when patients with a history of anterior uveitis or presence of syndesmophytes were compared with the remaining patients who did not exhibit these features. Leptin and visfatin levels did not change upon infliximab administration.
  
  
  CONCLUSIONS
  The present study indicates that in non-diabetic patients with AS on treatment with infliximab leptin and visfatin serum levels do not correlate with disease activity or systemic inflammation. Nevertheless, visfatin concentration correlates with insulin resistance.
authors.affiliation: Hospital Xeral-Calde, Lugo, Spain. jose.alberto.miranda.filloy@sergas.es
authors.forename: José A
authors.initials: JA
authors.lastname: Miranda-Filloy
authors.forename: Raquel
authors.initials: R
authors.lastname: López-Mejias
authors.forename: Fernanda
authors.initials: F
authors.lastname: Genre
authors.forename: Beatriz
authors.initials: B
authors.lastname: Carnero-López
authors.forename: Rodrigo
authors.initials: R
authors.lastname: Ochoa
authors.forename: Teresa
authors.initials: T
authors.lastname: Diaz de Terán
authors.forename: Carlos
authors.initials: C
authors.lastname: González-Juanatey
authors.forename: Ricardo
authors.initials: R
authors.lastname: Blanco
authors.forename: Javier
authors.initials: J
authors.lastname: Llorca
authors.forename: Miguel A
authors.initials: MA
authors.lastname: González-Gay
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000008:administration & dosage*; D018501:Antirheumatic Agents / Q000008:administration & dosage; D050197:Atherosclerosis / Q000276:immunology / Q000378:metabolism; D016207:Cytokines / Q000097:blood*; D003920:Diabetes Mellitus; D005260:Female; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000378:metabolism; D000069285:Infliximab; D020738:Leptin / Q000097:blood*; D008297:Male; D024821:Metabolic Syndrome / Q000276:immunology / Q000378:metabolism; D008875:Middle Aged; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood*; D013167:Spondylitis, Ankylosing / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D016207:Cytokines; D020738:Leptin; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D054409:Nicotinamide Phosphoribosyltransferase; C085455:nicotinamide phosphoribosyltransferase, human