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Longterm Safety, Efficacy, and Radiographic Outcome with Etanercept Treatment in Patients with Early Rheumatoid Arthritis MARK C. GENOVESE, JOAN M. BATHON, ROY M. FLEISCHMANN, LARRY W. MORELAND, RICHARD W. MARTIN, JAMES B. WHITMORE, WAYNE H. TSUJI, and JONATHAN A. LEFF ABSTRACT. Objective. To evaluate safety, efficacy, and radiographic progression in patients with early rheumatoid arthritis (RA) undergoing longterm treatment with etanercept. Methods. Patients with early RA (disease duration of 3 years or less) who had completed a 2-year efficacy study comparing etanercept and methotrexate (MTX) were followed in an extension where they received 25 mg etanercept twice weekly. Safety was summarized descriptively and compared with data from the efficacy study. Efficacy and radiographic progression were assessed using American College of Rheumatology response criteria, disease activity scores, and Total Sharp Score (TSS). Results. Rates of serious adverse events and serious infections did not increase with longterm exposure to etanercept, and were similar to rates reported for the blinded portion of the efficacy study. Efficacy was sustained in patients who completed 5 years of etanercept treatment at the time of this report (N = 201), even in those who decreased or discontinued use of MTX or corticosteroids. No radiographic progression (change in TSS ≥ 0) was seen in 55% of patients with 5-year radiographs; negative change (TSS < 0) was seen in 11%. Conclusion. Etanercept treatment in patients with early RA was generally well tolerated for up to 5 years. The results indicate sustained efficacy and decreased rate of radiographic progression. The rate of radiographic progression was low compared with other studies, emphasizing the benefit gained in patients with early aggressive RA who undergo longterm treatment with etanercept. (J Rheumatol 2005;32:1232-42) Key Indexing Terms:
BIOLOGICAL RESPONSE MODIFIERS From the Division of Rheumatology, Stanford University Medical Center, Palo Alto, California; Division of Rheumatology, Johns Hopkins University, Baltimore, Maryland; Division of Rheumatology, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas; Clinical Immunology and Rheumatology, University of Alabama at Birmingham, Birmingham, Alabama; College of Human Medicine, Michigan State University, Grand Rapids, Michigan; and Amgen Inc., Thousand Oaks, California, USA. Supported by Immunex Corporation, a wholly owned subsidiary of Amgen Inc., and by Wyeth, Collegeville, PA, USA. M.C. Genovese, MD, Division of Rheumatology, Stanford University Medical Center; J.M. Bathon, MD, Division of Rheumatology, Johns Hopkins University; R.M. Fleischmann, MD, Division of Rheumatology, University of Texas Southwestern Medical Center at Dallas; L.W. Moreland, MD, Clinical Immunology and Rheumatology, University of Alabama at Birmingham; R.W. Martin, MD, MA, College of Human Medicine, Michigan State University; J.B. Whitmore, PhD; W.H. Tsuji, MD; J.A. Leff, MD, Amgen Inc. Address reprint requests to Dr. M.C. Genovese, Division of Rheumatology, Stanford University Medical Center, 1000 Welch Road, Suite 203, Palo Alto, CA 94304. E-mail: genovese@stanford.edu Accepted for publication February 11, 2005. |