RHEUMATOID-ARTHRITIS - CURRENT CLINICAL AND RESEARCH DIRECTIONS

Citation
Jm. Grossman et E. Brahn, RHEUMATOID-ARTHRITIS - CURRENT CLINICAL AND RESEARCH DIRECTIONS, Journal of women's health, 6(6), 1997, pp. 627-638
Citations number
76
Journal title
ISSN journal
10597115
Volume
6
Issue
6
Year of publication
1997
Pages
627 - 638
Database
ISI
SICI code
1059-7115(1997)6:6<627:R-CCAR>2.0.ZU;2-X
Abstract
Rheumatoid arthritis (RA) is a systemic autoimmune disease characteriz ed by synovitis and joint erosions. It affects approximately 1% of the adult population in a female/male ratio ranging from 2:1 to 4:1. RA i s an insidious disease, typically having an onset of symmetric joint s welling and reaching a peak incidence in the fourth and fifth decades. Extraarticular manifestations include pulmonary, ocular, and vascular disease. The etiology of RA remains unknown. Attempts to discover inf ectious causes have proven unsuccessful, although environmental influe nces may trigger a response leading to the development of this autoimm une disease. Genetic associations have been identified, particularly w ith the major histocompatibility complex class II antigens. Furthermor e, twin studies have shown a 30%-50% concordance rate for monozygotic twins. Approximately 70%-80% of patients with RA have rheumatoid facto r present in the blood, although its role remains unclear. Hormonal st atus may influence RA. The majority of RA patients are women, and in 7 5% of them, the disease improves during pregnancy. RA has significant financial and social implications associated with treatment costs, los t wages, disability, and increased mortality. Mainstays of medical the rapy have included nonsteroidal anti-inflammatory and immunosuppressiv e agents, such as prednisone and methotrexate. Recent advances in the treatment of RA include specific inhibitors of cyclooxygenase II, T ce lls, blood vessels, cytokines (such as tumor necrosis factor-alpha [TN F-alpha] or interleukin-1 [IL-1]), and adhesion molecules. Additional studies are ongoing with combination interventions. It is anticipated that a better understanding of the basic pathophysiologic mechanisms c ritical in RA pathogenesis will provide more precise and efficacious t herapy.