title: Serum MMP-1 and TIMP-1 levels are increased in patients with psoriatic arthritis and their siblings.
abstract: OBJECTIVE
  To determine matrix metalloproteinase-1 (MMP-1) and tissue-inhibitor metalloproteinase-1 (TIMP-1) serum levels in patients with psoriatic arthritis (PsA) and to compare this with their siblings and local blood donor controls. PsA is an interesting condition in which to study metalloproteinases because there are variations in the level of destructiveness, including a significant proportion of cases without destructive change. This is unlike rheumatoid arthritis (RA) which is more uniformly destructive and where MMP-1/TIMP-1 levels are known to be elevated.
  
  
  METHODS
  MMP-1 and TIMP-1 serum levels were determined by enzyme-linked immunosorbent assay (ELISA) in (a) index cases with PsA (subtype: RA n = 43, distal interphalangeal disease n = 2, oligoarticular n = 15, spondyloarthropathy n = 9, enthesitis n = 1), (b) siblings with PsA, (c) siblings with psoriasis (Ps), (d) unaffected siblings and (e) local controls. Patients with Ps were divided according to the onset of disease: type I disease, onset before age 40 yr and type II, onset after age 40 yr.
  
  
  RESULTS
  MMP-1 and TIMP-1 levels were significantly increased in both the index cases and the group including all siblings compared with the controls (P < 0.0001). There was no statistical difference in MMP-1 or TIMP-1 levels between index cases and their siblings. There was no difference in serum MMP-1 level between the different subtypes (Moll and Wright) of PsA, but there was an increased level of serum TIMP-1 in patients with rheumatoid pattern (P = 0.05). In the index cases there were increased levels of TIMP-1 in type II onset psoriasis (P = 0.03) but no difference in MMP-1 levels.
  
  
  CONCLUSIONS
  MMP-1 and TIMP-1 serum levels are elevated in PsA. This is greatest in RA pattern PsA. These levels were also elevated in unaffected siblings suggesting that genetic factors may be important. TIMP-1 levels were elevated in psoriasis alone, more so in late onset psoriasis, suggesting that the pathological processes of early and late onset psoriasis may be different.
authors.affiliation: Department of Rheumatology, University of Newcastle upon Tyne, Freeman Hospital, Newcastle Hospitals NHS Trust, High Heaton, Newcastle-upon-Tyne NE7 7DN, UK. andrea.myers@ncl.ac.uk
authors.forename: A
authors.initials: A
authors.lastname: Myers
authors.forename: R
authors.initials: R
authors.lastname: Lakey
authors.forename: T E
authors.initials: TE
authors.lastname: Cawston
authors.forename: L J
authors.initials: LJ
authors.lastname: Kay
authors.forename: D J
authors.initials: DJ
authors.lastname: Walker
mesh_terms: D000328:Adult; D017668:Age of Onset; D015535:Arthritis, Psoriatic / Q000201:enzymology*; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D008297:Male; D020781:Matrix Metalloproteinase 1 / Q000097:blood*; D008875:Middle Aged; D011565:Psoriasis / Q000201:enzymology; D035781:Siblings; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000097:blood*
chemical_list: D019715:Tissue Inhibitor of Metalloproteinase-1; D020781:Matrix Metalloproteinase 1