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The levels of TNF-alpha and cAMP in synovial fluid of patients with rheumatoid arthritis and patients with osteoarthritis

It is well known that tumor necrosis factor-a (TNF-α ) has a pathogenic role in rhemathoid artthritis (RA) as well as that cyclic adenosine-monophosphate (cAMP) inhibits its production. Therefore, it appeared interesting to investigate posible correlation in concentration of these factors in synovial fluid of patients with RA and in control patients with osteoarthritis (OA). Moreover, there is now a quite lot of drugs, which can influence the synthesis, or degradation of cAMP. Synovial fluid was aseptically taken from joint 9 patients with seropositive RA and 9 patients with OA. The fluid was stored at – 20o C until determination of TNF-α and cAMP concentration. Since most samples were viscous they all were incubated at 37o C for 30 minutes in the presence of hyaluronidase (Sigma) and centrifuged at 12 000 g for 5 minutes before these factors were determined in the supernatants. The concentration TNF-α and cAMP was determined by ELISA assay using Roche and Assay Designs kits, repectively. Generally, the concentration of TNF-α . and cAMP were inversely correlated, both in patients with RA or OA ; r = -0.35, -0.36 and -038, in patients with RA, patients with OA and in all patients combined, respectively. Surprisingly, the concentration of TNF-α somewhat higher in patients with OA than in patients with RA (44, 34 pg/ml ± ; 16.3 SD and 23.31 pg/ml ± ; 31.0, respectively). However, the concentration of cAMP was somewhat higher in synovial fluid of patients with RA than in patients with OA (1, 23 pmol/ml ± ; 0.59 vs 0, 95 pmol/ml ± ; 0.28). Presently, we are determinig the same parameters in higher number of patients, and try to correlate their concentation with concentation PGE2 in synioval fluid as well as with the type of synovial cell effusion. It appears that the concentartion of TNF-α in synovial fluid in patients with RA or OA is inversely correlated with the concentration of cAMP. This may be due to the negative feedback control of TNF-α synthesis by cAMP. However, the presented investigations should be repated in much higher number patients/samples.

TNF-alpha; cAMP; synovial fluid; rheumatoid arthritis

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