title: Serum COMP-C3b complexes in rheumatic diseases and relation to anti-TNF-α treatment.
abstract: BACKGROUND
  Cartilage oligomeric matrix protein (COMP) is found at elevated concentrations in sera of patients with joint diseases such as rheumatoid arthritis (RA) and osteoarthritis (OA). We recently showed that COMP activates complement via the alternative pathway and that COMP-C3b complexes are present in sera of RA patients, but not in healthy controls. We now set out to elaborate on the information provided by this marker in a variety of diseases and larger patient cohorts.
  
  
  METHODS
  COMP-C3b levels in sera were measured by using an enzyme-linked immunosorbent assay (ELISA) capturing COMP and detecting C3b. Serum COMP was measured by using ELISA.
  
  
  RESULTS
  COMP-C3b levels were significantly elevated in patients with RA as well as in systemic lupus erythematosus (SLE), compared with healthy controls. SLE patients with arthritis had significantly higher COMP-C3b levels than did those without. COMP-C3b was furthermore elevated in patients with ankylosing spondylitis (AS), psoriatic arthritis (PsA), reactive arthritis, systemic sclerosis, and OA. COMP-C3b did not correlate with COMP in any of the patient groups. COMP-C3b correlated with disease activity in RA, but not in other diseases. COMP-C3b levels in RA patients decreased on treatment with tumor necrosis factor (TNF)-α inhibitors, whereas the levels increased in patients with AS or PsA. The changes of COMP-C3b did not parallel the changes of C-reactive protein (CRP).
  
  
  CONCLUSIONS
  COMP-C3b levels are elevated in several rheumatologic diseases and correlate with inflammatory measures in RA. COMP-C3b levels in RA decrease during TNF-α inhibition differently from those of CRP, suggesting that formation of COMP-C3b relates to disease features not reflected by general inflammation measures.
authors.affiliation: Department of Laboratory Medicine Malmö, Section of Medical Protein Chemistry, Lund University, Wallenberg Laboratory floor 4, SE-205 02 Malmö, Sweden.
authors.forename: Kaisa E
authors.initials: KE
authors.lastname: Happonen
authors.forename: Tore
authors.initials: T
authors.lastname: Saxne
authors.forename: Pierre
authors.initials: P
authors.lastname: Geborek
authors.forename: Maria
authors.initials: M
authors.lastname: Andersson
authors.forename: Anders A
authors.initials: AA
authors.lastname: Bengtsson
authors.forename: Roger
authors.initials: R
authors.lastname: Hesselstrand
authors.forename: Dick
authors.initials: D
authors.lastname: Heinegård
authors.forename: Anna M
authors.initials: AM
authors.lastname: Blom
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001168:Arthritis / Q000097:blood / Q000188:drug therapy / Q000473:pathology; D015535:Arthritis, Psoriatic / Q000097:blood / Q000188:drug therapy / Q000473:pathology; D016918:Arthritis, Reactive / Q000097:blood / Q000188:drug therapy / Q000473:pathology; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000188:drug therapy / Q000473:pathology; D002097:C-Reactive Protein / Q000378:metabolism; D064236:Cartilage Oligomeric Matrix Protein; D003179:Complement C3b / Q000378:metabolism*; D004797:Enzyme-Linked Immunosorbent Assay; D016326:Extracellular Matrix Proteins / Q000097:blood*; D005260:Female; D006023:Glycoproteins / Q000097:blood*; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000097:blood* / Q000188:drug therapy / Q000473:pathology; D008297:Male; D064235:Matrilin Proteins; D008875:Middle Aged; D013167:Spondylitis, Ankylosing / Q000097:blood / Q000188:drug therapy / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000097:blood*; D055815:Young Adult
chemical_list: D064236:Cartilage Oligomeric Matrix Protein; D016326:Extracellular Matrix Proteins; D006023:Glycoproteins; D064235:Matrilin Proteins; C577553:TSP5 protein, human; D014409:Tumor Necrosis Factor-alpha; D003179:Complement C3b; D002097:C-Reactive Protein