Pregled bibliografske jedinice broj: 229157
The levels of TNF-alpha, cAMP, PGE2 and IL-18 in synovial fluid of patients with rheumatoid arthritis and in patients with osteoarthritis
The levels of TNF-alpha, cAMP, PGE2 and IL-18 in synovial fluid of patients with rheumatoid arthritis and in patients with osteoarthritis // Ann Rheumat Diseases, 64 (2005), Supp III. (podatak o recenziji nije dostupan, kongresno priopcenje, znanstveni)
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Naslov
The levels of TNF-alpha, cAMP, PGE2 and IL-18 in synovial fluid of patients with rheumatoid arthritis and in patients with osteoarthritis
Autori
Čulo, Melanie-Ivana ; Vergles, Domagoj ; Horvat, Gordana ; Morović-Vergles, Jadranka ; Trutin-Ostović, Karmen
Izvornik
Ann Rheumat Diseases (0003-4967) 64
(2005), Supp III;
Vrsta, podvrsta i kategorija rada
Radovi u časopisima, kongresno priopcenje, znanstveni
Ključne riječi
TNF-alpha; cAMP; PGE2; IL-18; synovial fluid; rheumatoid arthritis
Sažetak
Background: 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. Materials and methods: 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. Results: 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. Conclusion: 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.
Izvorni jezik
Engleski
Znanstvena područja
Kliničke medicinske znanosti
Citiraj ovu publikaciju:
Časopis indeksira:
- Current Contents Connect (CCC)
- Web of Science Core Collection (WoSCC)
- Science Citation Index Expanded (SCI-EXP)
- SCI-EXP, SSCI i/ili A&HCI
- Scopus
- MEDLINE
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