Perturbation of protease inhibitors and substrates in inflammatory arthritis

Semin Thromb Hemost. 1985 Oct;11(4):394-404. doi: 10.1055/s-2007-1004400.

Abstract

Defective systemic fibrinolysis and articular persistence of fibrinlike material are well recognized in RA. Perturbation of the major plasma protease inhibitors, A1AT, A2MG, and AT III, was explored in RA, psoriatic arthritis, and Reiter's syndrome. Experimental evidence is presented and assessed with respect to the potential role of serine esterases and their inhibitors in the pathophysiology of inflammatory arthritis.

MeSH terms

  • Adult
  • Antithrombin III / blood
  • Arthritis, Rheumatoid / blood*
  • Blood Proteins*
  • Female
  • Humans
  • Male
  • Middle Aged
  • Peptide Fragments / analysis
  • Plasminogen / analysis
  • Protease Inhibitors / blood*
  • Rheumatoid Factor / analysis
  • Serine Proteinase Inhibitors
  • alpha 1-Antitrypsin / analysis
  • alpha-Macroglobulins / analysis

Substances

  • Blood Proteins
  • Peptide Fragments
  • Protease Inhibitors
  • Serine Proteinase Inhibitors
  • alpha 1-Antitrypsin
  • alpha-Macroglobulins
  • Antithrombin III
  • Plasminogen
  • Rheumatoid Factor