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Association of Anemia and Physical Disability Among Patients with Rheumatoid Arthritis
CHENGLONG HAN, MAHBOOB U. RAHMAN, MITTIE K. DOYLE, JOAN M. BATHON, JOSEF SMOLEN, ARTHUR KAVANAUGH, RENÉ WESTHOVENS, E. WILLIAM St. CLAIR, DANIEL BAKER, and MOHAN BALA
ABSTRACT. Methods. Data were derived from 2495 patients with RA enrolled in 3 clinical trials (ATTRACT, ASPIRE, and START) and treated with infliximab (3 to 10 mg/kg) plus methotrexate (MTX), or MTX plus placebo. The association of hemoglobin and the Health Assessment Questionnaire (HAQ) score was assessed at baseline (n = 2471) and Week 22 (n = 2458) by Spearman correlation, and multivariate linear regression models were employed to control for confounding effects from demographic and other clinical variables. A logistic regression model was used to estimate the odds ratio (OR) for a clinically meaningful improvement (≥ 0.25 point increase) in HAQ associated with a ≥ 1 g/dl improvement in hemoglobin from baseline at Week 22. Results. About 37% of patients with RA had anemia based on World Health Organization criteria: hemoglobin < 12 g/dl in women (39%) and < 13 g/dl in men (32%). Low hemoglobin level was significantly associated with more severe physical disability at baseline (p < 0.001), and both male and female patients with anemia had more severe disability at baseline. Improvement in hemoglobin after treatment at Week 22 was an independent contributor to improvement in HAQ, and a ≥ 1 g/dl improvement in hemoglobin after treatment was associated with a clinically meaningful improvement in the HAQ score at Week 22 (OR 1.43, 95% CI 1.10–1.86; p < 0.01). Conclusion. Anemia is one of the independent factors contributing to physical disability in patients with RA. Improvement in anemia following effective RA treatment may play an independent role in improving physical function. (First Release Oct 15 2007; J Rheumatol 2007;34:2177–82) Key Indexing Terms:
RHEUMATOID ARTHRITIS From Centocor Research and Development, Inc., Malvern, Pennsylvania, USA; Johns Hopkins University, Baltimore, Maryland, USA; Center for Rheumatic Diseases, Krankenhaus der Stadt Wien-Lainz, Vienna, Austria; Department of Rheumatology, University of California, San Diego, La Jolla, California, USA; University Hospital Leuven, Leuven, Belgium; and Duke University Medical Center, Durham, North Carolina, USA. Supported by Centocor, Inc., Malvern, PA, a subsidiary of Johnson & Johnson, New Brunswick, NJ. C. Han, PhD, Associate Director, Outcomes Research; M.U. Rahman, MD, PhD, Senior Director, Immunology Clinical Research; M.K. Doyle, MD, Associate Director, Immunology; D. Baker, MD, Vice President, Clinical Research, Immunology; M. Bala, PhD, Senior Director, Outcomes Research Administration, Centocor Research and Development, Inc.; J.M. Bathon, MD, Professor of Medicine, Johns Hopkins University; J. Smolen, MD, Professor of Medicine, Center for Rheumatic Diseases, Krankenhaus der Stadt Wien-Lainz; A. Kavanaugh, MD, Professor of Medicine, Department of Rheumatology, University of California, San Diego; R. Westhovens, MD, PhD, Professor of Medicine, University Hospital Leuven; E.W. St. Clair, MD, Professor of Medicine, Duke University Medical Center. Address reprint requests to Dr. C. Han, Centocor, Inc., 200 Great Valley Parkway, Malvern, PA 19355. E-mail: chan3@cntus.jnj.com Accepted for publication July 18, 2007. |
