title: Increased Ed-B fibronectin plasma levels in spondyloarthropathies: comparison with rheumatoid arthritis patients and a healthy population.
abstract: OBJECTIVE
  To determine, for the first time, plasma levels of general fibronectin (Fn) and two spliced isoforms, Ed-A and Ed-B, in patients with spondyloarthropathy (SpA) in comparison with rheumatoid arthritis (RA) patients and healthy volunteers (HV).
  
  
  METHODS
  Plasmas (EDTA) as well as clinical data, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels were collected in two groups of 10 patients fulfilling the European Spondylarthropathy Study Group criteria for SpA or the 1987 American College of Rheumatology criteria for RA. Plasmas of 21 blood donors served as controls. Plasma levels of Fns were determined by using an in-house immunocapture ELISA, using monoclonal antibodies (MAbs) against general Fn and its isoforms.
  
  
  RESULTS
  Total Fn plasma levels were significantly higher in the SpA group (mean+/-S.D.=1387+/-569 mg/l) than in the RA group (684+/-196 mg/l; P=0.02) and in HV (303+/-211 mg/l; P<0.0001). Ed-A Fn levels appeared higher in SpA (23+/-10.4 mg/l) and RA (32.5+/-16.5 mg/l) groups than in the HV group (2.8+/-0.9 mg/l; P=0.0003 and P<0.0001, respectively), without a significant difference between SpA and RA groups. Ed-B Fn levels were higher in SpA (6.9+/-2.1 mg/l) than in RA (3.2+/-1.9 mg/l; P=0. 02) and HV (1.1+/-0.8 mg/l; P=0.0003) groups. No significant correlation was observed in SpA patients between each Fn level and clinical activity, ESR or CRP levels.
  
  
  CONCLUSIONS
  This study showed an increase in plasma levels of Fn and Ed-B Fn in SpA patients compared with RA patients and HV, which could not be attributed solely to systemic inflammation. It may be hypothesized that Ed-A and Ed-B Fn might reflect local turnover in inflamed tissues, and that Ed-B Fn might be particularly involved in the musculoskeletal inflammatory process of SpA.
authors.affiliation: Department of Rheumatology, Hôpital Henri Mondor, 94010 Créteil, Paris, France.
authors.forename: P
authors.initials: P
authors.lastname: Claudepierre
authors.forename: Y
authors.initials: Y
authors.lastname: Allanore
authors.forename: L
authors.initials: L
authors.lastname: Belec
authors.forename: B
authors.initials: B
authors.lastname: Larget-Piet
authors.forename: L
authors.initials: L
authors.lastname: Zardi
authors.forename: X
authors.initials: X
authors.lastname: Chevalier
mesh_terms: D000328:Adult; D017398:Alternative Splicing; D001172:Arthritis, Rheumatoid / Q000097:blood*; D018450:Disease Progression; D005353:Fibronectins / Q000097:blood* / Q000737:chemistry; D006801:Humans; D008297:Male; D020033:Protein Isoforms / Q000097:blood; D012016:Reference Values; D013166:Spondylitis / Q000097:blood*
chemical_list: D005353:Fibronectins; D020033:Protein Isoforms