title: Apelin serum levels in non-diabetic ankylosing spondylitis patients undergoing TNF-α antagonist therapy.
abstract: OBJECTIVE
  To determine whether disease activity, systemic inflammation and metabolic syndrome are potential determinants of circulating apelin in ankylosing spondylitis (AS) patients undergoing TNF-α antagonist-infliximab therapy.
  
  
  METHODS
  We investigated apelin 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. Correlations of apelin serum levels with disease activity, systemic inflammation and metabolic syndrome were assessed. Also, potential changes in apelin concentration following an infusion of the anti-TNF-α monoclonal antibody-infliximab were analysed.
  
  
  RESULTS
  No significant correlation between apelin concentration and demographic features, inflammation, adiposity and metabolic syndrome features was seen. Neither differences were seen in basal apelin in different categorical variables associated to AS. Following infliximab infusion, a reduction of apelin serum levels was observed. In this regard, the median (interquartile range) values of apelin decreased from 0.99 (0.74-1.25) ng/ml immediately prior to infliximab infusion to 0.92 (0.72-1.39) ng/ml at the end of the infusion (time 120 minutes). However, the reduction in apelin serum levels following administration of the drug did not achieve statistical significance.
  
  
  CONCLUSIONS
  The present study shows that in non-diabetic patients with AS on treatment with infliximab apelin serum levels do not correlate with disease activity or metabolic syndrome. A single infusion of infliximab does not yield a significant change of apelin serum levels in AS patients.
authors.affiliation: Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IFIMAV, Santander, Spain. fernandagenre@gmail.com
authors.forename: Fernanda
authors.initials: F
authors.lastname: Genre
authors.forename: José A
authors.initials: JA
authors.lastname: Miranda-Filloy
authors.forename: Raquel
authors.initials: R
authors.lastname: López-Mejias
authors.forename: Beatriz
authors.initials: B
authors.lastname: Carnero-López
authors.forename: Rodrigo
authors.initials: R
authors.lastname: Ochoa
authors.forename: Javier
authors.initials: J
authors.lastname: Rueda
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: D054392:Adipokines / Q000097:blood; D000273:Adipose Tissue / Q000378:metabolism; D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000008:administration & dosage*; D018501:Antirheumatic Agents / Q000008:administration & dosage; D000073861:Apelin; D050197:Atherosclerosis / Q000276:immunology / Q000378:metabolism; D003920:Diabetes Mellitus; D005260:Female; D006801:Humans; D000069285:Infliximab; D036341:Intercellular Signaling Peptides and Proteins / Q000097:blood*; D008297:Male; D024821:Metabolic Syndrome / Q000276:immunology / Q000378:metabolism; D008875:Middle Aged; D013167:Spondylitis, Ankylosing / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000276:immunology
chemical_list: C115436:APLN protein, human; D054392:Adipokines; D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D000073861:Apelin; D036341:Intercellular Signaling Peptides and Proteins; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab