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Increased DHEAS Levels in Patients with Rheumatoid Arthritis After Treatment with Tumor Necrosis Factor Antagonists: Evidence for Improved Adrenal Function
SOFIA ERNESTAM, INGIÄLD HAFSTRÖM, SIGBRITT WERNER, KJELL CARLSTRÖM, and BIRGITTA TENGSTRAND
ABSTRACT. Methods. Forty-eight patients with RA were treated with infliximab or etanercept for 2 years. Disease activity, clinical response, and physical function were evaluated and serum levels of high sensitivity C-reactive protein and interleukin 6 were analyzed before start of treatment and after 1 and 2 years. At the same timepoints adrenocorticotropic hormone (ACTH), cortisol, and dehydroepiandrosterone sulfate (DHEAS) were analyzed; luteinizing hormone (LH), estradiol, and testosterone were analyzed as well in 18 male patients. Results. DHEAS increased (p < 0.05) after 1 and 2 years of treatment with TNF antagonists. No change in serum levels of ACTH, cortisol, LH, estradiol, or testosterone was recorded during the 2 years. The increased levels of DHEAS correlated with improved physical function measured by Health Assessment Questionnaire (p < 0.01). There was no correlation between hormone levels and clinical response or inflammatory markers. A longitudinal stability in individual hormone levels was found between baseline and 2 years, most markedly for DHEAS levels (rs = 0.90, p < 0.01). A female subgroup characterized by low levels of DHEAS had a lower age at disease onset. Conclusion. The increased DHEAS levels may indicate an improved adrenal function during 2 years' treatment with TNF antagonists. Improved physical function, correlated to increased DHEAS levels, may be an effect of better adrenal function during powerful antiinflammatory treatment. The stability in individual hormone levels suggests a stable hormonal homeostasis, independent of inflammatory activity. (First Release May 1 2007; J Rheumatol 2007;34:1451-8) Key Indexing Terms:
RHEUMATOID ARTHRITIS From the Department of Rheumatology, Department of Endocrinology, Metabolism and Diabetes, and Division of Clinical Chemistry, Department of Laboratory Medicine, Karolinska Institute at Karolinska University Hospital, Huddinge, Stockholm, Sweden. Supported by The Swedish Association Against Rheumatism and King Gustaf V 80 Years Foundation. S. Ernestam, MD, PhD; I. Hafström, MD, PhD, Professor; B. Tengstrand, MD, PhD, Department of Rheumatology; S. Werner, MD, PhD, Professor, Department of Endocrinology; K. Carlström, PhD, Professor, Division of Clinical Chemistry. Address reprint requests to Dr. S. Ernestam, Department of Rheumatology, R92, Karolinska University Hospital, Huddinge, SE-141 86 Stockholm, Sweden. E-mail: sofia.ernestam@karolinska.se Accepted for publication February 27, 2007. |
