BACKGROUND: Studies have suggested that nonspecific nonsteroidal anti-inflammatory drugs may inhibit matrix biosynthesis by articular cartilage, thereby accelerating the progression of osteoarthritis (OA). OBJECTIVE: The objective of this analysis was to determine whether 1-year treatment with the cyclooxygenase-2-specific inhibitor celecoxib at up to twice the recommended and maximally effective dose for OA had any deleterious effects on OA progression by assessing radiographic changes in knee or hip joint morphology in patients with OA. METHODS: In a 12-month, multicenter, prospective, open-label trial, patients with OA of the knee or hip or rheumatoid arthritis receivedcelecoxib at doses ranging from that recommended for the treatment of OA (200 mg/d) to twice the recommended daily dosage (400 mg/d). Available radiographs showing baseline and end-of-treatment status were analyzed using semiquantitative measures of index joint morphology in patients with mild to moderate OA. The morphologic scores were then subjected to mean change and shift-table analysis to determine the extent and rate of disease progression. RESULTS: A total of 2,327 patients (796 with OA of the knee, 1,531 with OA of the hip) were included. A subset of 344 patients (160 with OA of the knee, 184 with OA of the hip) had radiographs from both before and after 12 months' celecoxib treatment. One hundred forty-seven and 158 pairs of knee and hip radiographs, respectively, were available for analysis. These revealed that, with the exception of significant hip joint-space narrowing (P = 0.029), no evidence of disease progression with long-term celecoxib treatment could be detected. The observed increase in hip joint-space narrowing was small (0.14 units/y) (95% CI, 0.08-0.20), was observed prior to celecoxib exposure (by mean change or shift-table analysis), and was not dose related. CONCLUSION: These results are consistent with the hypothesis that long-term therapy with celecoxib does not accelerate progression of OA of the knee or hip.
RCT Entities:
BACKGROUND: Studies have suggested that nonspecific nonsteroidal anti-inflammatory drugs may inhibit matrix biosynthesis by articular cartilage, thereby accelerating the progression of osteoarthritis (OA). OBJECTIVE: The objective of this analysis was to determine whether 1-year treatment with the cyclooxygenase-2-specific inhibitor celecoxib at up to twice the recommended and maximally effective dose for OA had any deleterious effects on OA progression by assessing radiographic changes in knee or hip joint morphology in patients with OA. METHODS: In a 12-month, multicenter, prospective, open-label trial, patients with OA of the knee or hip or rheumatoid arthritis received celecoxib at doses ranging from that recommended for the treatment of OA (200 mg/d) to twice the recommended daily dosage (400 mg/d). Available radiographs showing baseline and end-of-treatment status were analyzed using semiquantitative measures of index joint morphology in patients with mild to moderate OA. The morphologic scores were then subjected to mean change and shift-table analysis to determine the extent and rate of disease progression. RESULTS: A total of 2,327 patients (796 with OA of the knee, 1,531 with OA of the hip) were included. A subset of 344 patients (160 with OA of the knee, 184 with OA of the hip) had radiographs from both before and after 12 months' celecoxib treatment. One hundred forty-seven and 158 pairs of knee and hip radiographs, respectively, were available for analysis. These revealed that, with the exception of significant hip joint-space narrowing (P = 0.029), no evidence of disease progression with long-term celecoxib treatment could be detected. The observed increase in hip joint-space narrowing was small (0.14 units/y) (95% CI, 0.08-0.20), was observed prior to celecoxib exposure (by mean change or shift-table analysis), and was not dose related. CONCLUSION: These results are consistent with the hypothesis that long-term therapy with celecoxib does not accelerate progression of OA of the knee or hip.
Authors: Elke Anklam; Martin Iain Bahl; Robert Ball; Richard D Beger; Jonathan Cohen; Suzanne Fitzpatrick; Philippe Girard; Blanka Halamoda-Kenzaoui; Denise Hinton; Akihiko Hirose; Arnd Hoeveler; Masamitsu Honma; Marta Hugas; Seichi Ishida; George En Kass; Hajime Kojima; Ira Krefting; Serguei Liachenko; Yan Liu; Shane Masters; Uwe Marx; Timothy McCarthy; Tim Mercer; Anil Patri; Carmen Pelaez; Munir Pirmohamed; Stefan Platz; Alexandre Js Ribeiro; Joseph V Rodricks; Ivan Rusyn; Reza M Salek; Reinhilde Schoonjans; Primal Silva; Clive N Svendsen; Susan Sumner; Kyung Sung; Danilo Tagle; Li Tong; Weida Tong; Janny van den Eijnden-van-Raaij; Neil Vary; Tao Wang; John Waterton; May Wang; Hairuo Wen; David Wishart; Yinyin Yuan; William Slikker Journal: Exp Biol Med (Maywood) Date: 2021-11-16
Authors: Allen D Sawitzke; Helen Shi; Martha F Finco; Dorothy D Dunlop; Clifton O Bingham; Crystal L Harris; Nora G Singer; John D Bradley; David Silver; Christopher G Jackson; Nancy E Lane; Chester V Oddis; Fred Wolfe; Jeffrey Lisse; Daniel E Furst; Domenic J Reda; Roland W Moskowitz; H James Williams; Daniel O Clegg Journal: Arthritis Rheum Date: 2008-10
Authors: Wen Shi; Yong Ming Wang; Li Shao Li; Min Yan; Duan Li; Neng Neng Chen; Bin Yan Chen Journal: Clin Drug Investig Date: 2004 Impact factor: 2.859
Authors: Ufuk Tan Timur; Marjolein M J Caron; Ralph M Jeuken; Yvonne M Bastiaansen-Jenniskens; Tim J M Welting; Lodewijk W van Rhijn; Gerjo J V M van Osch; Pieter J Emans Journal: Int J Mol Sci Date: 2020-09-22 Impact factor: 5.923