Abstract
ObjectivesTo determine the impact of celecoxib and etoricoxib therapy on serum and synovial fluid levels of IL-1β, IL-6, TNF-α, sTNFR1, sTNFR2 and IL-1Ra in patients with inflammatory arthritis. To determine the correlation between cytokine changes and synovial membrane penetration index of the study drugs, and pain VAS change.MethodsFifty-one patients with inflammatory synovial fluid accumulation in a knee joint (33 women), randomized on 3 groups of 17 each: 100 mg b.i.d. celecoxib treated group, 90 mg o.d. etoricoxib treated group, and the control group with no NSAID treatment. Cytokines serum and synovial fluid levels as well as membrane penetration index were assessed prior and after treatment.ResultsCelecoxib led to decrease of both synovial fluid and serum levels of IL-6 (p=0.017 and p=0.003, respectively). In the etoricoxib treated group synovial fluid IL-6 concentration was significantly decreased after treatment (p=0.019). Correlating the study drugs penetration index with the change of cytokines and their receptors levels, positive correlation was found with the reduction of synovial fluid IL-1β for the celecoxib (p=0.032) and with the increase of synovial fluid sTNFR1 for the etoricoxib group (p=0.028). Pain VAS reduction was positively correlated with decrease of synovial fluid IL-1β (p=0.041) and IL-6 levels (p<0.005) and negative with synovial fluid sTNFR1 changes (p=0.045) in celecoxib group, and negative with serum TNF-α decrease (p=0.044) in the etoricoxib group.ConclusionOur results suggest that celecoxib and etoricoxib inhibit the inflammatory cytokines, mostly in synovial fluid but also in serum, causing through this mechanism, decrease of inflammation, irrespective to COX-2 inhibition.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.