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Abstract
Paf-acether (platelet-activating factor) is a phospholipid described as a potent mediator of inflammatory response. We have recently shown that the level of paf bound to lipoproteins was significantly higher in the serum from patients with rheumatic diseases, compared to that of control subjects. In serum, paf is inactivated in part by a paf acetylhydrolase that catalyses the hydrolysis of the acetate residue. Acetylhydrolase activity was measured in the serum and synovial fluid of patients with rheumatoid arthritis and other arthritides, i.e. osteoarthritis and chondrocalcinosis. In serum, the activity of acetylhydrolase was significantly increased in patients with rheumatic diseases when compared with that in the control group. However, it was enhanced to a lesser degree in rheumatoid arthritis than in non inflammatory rheumatic diseases. These results suggest a role for acetylhydrolase in controlling paf levels in rheumatic diseases.