Early diagnosis and treatment of rheumatoid arthritis for improved outcomes: Focus on etanercept, a new biologic response modifier

被引:11
作者
Fleischmann, RM [1 ]
机构
[1] St Paul Med Ctr, Dallas, TX 75235 USA
关键词
rheumatoid arthritis; biologic response modifiers; early diagnosis; etanercept; joint damage;
D O I
10.1016/S0149-2918(00)80002-8
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Early diagnosis and prompt treatment can improve outcomes in rheumatoid arthritis (RA). Significant joint damage occurs early in the course of the disease, when RA is most aggressive. Many rheumatologists now advocate an inverted pyramid approach to therapy, in which treatment with disease-modifying antirheumatic drugs is initiated on diagnosis. The goals of this approach are to preserve patient function and to slow disease progression. Current therapies exhibit varying degrees of efficacy and cumulative toxicity that frequently limit their usefulness, particularly with long-term use. New biologic response modifiers (BRMs) that target specific cells or cytokines involved in the inflammatory response hold great promise for RA therapy because of their improved efficacy and limited toxicity. The first BRM to be approved by the US Food and Drug Administration for use in RA is etanercept, a soluble tumor necrosis factor-receptor fusion protein. Etanercept is highly effective in relieving RA symptoms and has a good safety profile. The availability of well-tolerated therapies may encourage clinicians to diagnose and treat RA more promptly, thereby ensuring patients the best possible outcomes.
引用
收藏
页码:1429 / 1442
页数:14
相关论文
共 57 条
[1]   MJA practice essentials .8. Rheumatology - Rheumatoid arthritis [J].
Ahern, MJ ;
Smith, MD .
MEDICAL JOURNAL OF AUSTRALIA, 1997, 166 (03) :156-161
[2]  
ALBANI S, 1997, TXB RHEUMATOLOGY, P979
[3]  
AMETT FC, 1988, ARTHRITIS RHEUM, V31, P315
[4]   CYTOKINES AND CYTOKINE INHIBITORS OR ANTAGONISTS IN RHEUMATOID-ARTHRITIS [J].
AREND, WP ;
DAYER, JM .
ARTHRITIS AND RHEUMATISM, 1990, 33 (03) :305-315
[5]  
BELZA BL, 1993, NURS RES, V42, P93
[6]   RHEUMATOID-ARTHRITIS, COPING AND WELL-BEING - CROSS-SECTIONAL SUBGROUP COMPARISONS AND CORRELATIONAL ANALYSES [J].
BENDTSEN, P ;
HORNQUIST, JO .
SCANDINAVIAN JOURNAL OF SOCIAL MEDICINE, 1994, 22 (02) :97-106
[7]  
BLACKBURN WD, 1997, TXB THEUMATOLOGY, P1089
[8]   The mechanisms of action of disease-modifying antirheumatic drugs: A review with emphasis on macrophage signal transduction and the induction of proinflammatory cytokines [J].
Bondeson, J .
GENERAL PHARMACOLOGY-THE VASCULAR SYSTEM, 1997, 29 (02) :127-150
[9]  
Brennan FM, 1997, BRIT J RHEUMATOL, V36, P643
[10]   TNF INHIBITORS ARE PRODUCED SPONTANEOUSLY BY RHEUMATOID AND OSTEOARTHRITIC SYNOVIAL JOINT CELL-CULTURES - EVIDENCE OF FEEDBACK-CONTROL OF TNF ACTION [J].
BRENNAN, FM ;
GIBBONS, DL ;
COPE, AP ;
KATSIKIS, P ;
MAINI, RN ;
FELDMANN, M .
SCANDINAVIAN JOURNAL OF IMMUNOLOGY, 1995, 42 (01) :158-165