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Continued Inhibition of Radiographic Progression in Patients with Psoriatic Arthritis Following 2 Years of Treatment with Etanercept PHILIP J. MEASE, ALAN J. KIVITZ, FRANCIS X. BURCH, EVAN L. SIEGEL, STANLEY B. COHEN, PETER ORY, DAVID SALONEN, JOEL RUBENSTEIN, JOHN T. SHARP, MELEANA DUNN, and WAYNE TSUJI ABSTRACT. Methods. Patients were previously randomized to receive placebo or etanercept in a double-blind study and chose to participate in the current open-label extension phase. All patients received etanercept 25 mg twice weekly. Radiographic progression was determined at baseline, 1 year, and 2 years using the Sharp method modified to include joints frequently affected in PsA. Arthritis and psoriasis responses were determined using American College of Rheumatology 20% (ACR20) improvement criteria, PsA response criteria (PsARC), and the psoriasis area severity index (PASI). Results. Of 205 patients randomized, 169 entered open-label, and 141 [71 randomized to receive placebo (placebo/etanercept) and 70 randomized to receive etanercept (etanercept/etanercept)] had radiographic data available for analysis at 2 years. ACR20 criteria, PsARC, and PASI 50 criteria were met by 64%, 84%, and 62%, respectively, of etanercept/etanercept patients at the end of the 48-week open-label period. Placebo/etanercept patients achieved comparable results within 12 weeks that were sustained at 48 weeks (63%, 80%, and 73%). Radiographic progression was inhibited in the etanercept/ etanercept patients (mean adjusted change in total Sharp score of –0.38 from baseline to 2 yrs). In placebo/etanercept patients, disease progression was inhibited once patients began receiving etanercept (mean adjusted change of –0.22 from 1 year to 2 years). Adverse event rates were similar to those observed during randomized phase, with only one serious adverse event deemed possibly related to etanercept. Conclusion. These data demonstrate a sustained benefit of etanercept treatment, including inhibition of radiographic progression, in patients with PsA. (First Release Feb 1, 2006; J Rheumatol 2006;33:712–21)
Key Indexing Terms: PSORIATIC ARTHRITIS
From Seattle Rheumatology Associates, Seattle, Washington; Altoona Center for Clinical Research, Duncansville, Pennsylvania; San Antonio Center for Clinical Research, San Antonio, Texas; The Center for Rheumatology and Bone Research, Wheaton, Maryland; St. Paul University Medical Center, Dallas, Texas; University of Washington, Seattle, Washington, USA; University of Toronto, Toronto, Ontario, Canada; and Amgen Inc., Thousand Oaks, California, USA. Supported by Immunex Corporation, a wholly owned subsidiary of Amgen Inc. Drs. Mease, Siegel, Cohen, and Ory have received consulting fees and honoraria from Amgen. Drs. Mease, Kivitz, and Siegel have stock ownership or options in Amgen. Drs. Ory, Salonen, Rubenstein, and Sharp were compensated for reading radiographs in this study. P.J. Mease, MD, Seattle Rheumatology Associates; A.J. Kivitz, MD, Altoona Center for Clinical Research; F.X. Burch, MD, San Antonio Center for Clinical Research; E.L. Siegel, MD, The Center for Rheumatology and Bone Research; S.B. Cohen, MD, St. Paul University Medical Center; P. Ory, MD; J.T. Sharp, MD, University of Washington; D. Salonen, MD; J. Rubenstein, MD, University of Toronto; M. Dunn, MS; W. Tsuji, MD, Amgen Inc. Address reprint requests to Dr. P.J. Mease, Seattle Rheumatology Associates, 1101 Madison Street, Seattle, WA 98104, USA. E-mail: pmease@nwlink.com Accepted for publication October 19, 2005.
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