Rheumatology 1999; 38: 1099-1103
© 1999 British Society for Rheumatology
Increased Ed-B fibronectin plasma levels in spondyloarthropathies: comparison with rheumatoid arthritis patients and a healthy population
Department of Rheumatology, Hôpital Henri Mondor, 94010 Créteil,
1 Department of Virology, Hôpital Broussais, Paris, France and
2 Institute for Cancer Research, Genoa, Italy
Correspondence to:
P. Claudepierre, Service de Rhumatologie, Hôpital Henri Mondor, 51 Avenue du Maréchal de Lattre de Tassigny, 94010 Créteil, France.
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.
KEY WORDS: Spondyloarthropathy, Ankylosing spondylitis, Fibronectin
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