Tumor necrosis factor-α antagonists for the treatment of rheumatic diseases

被引:136
作者
Criscione, LG [1 ]
St Clair, EW [1 ]
机构
[1] Duke Univ, Med Ctr, Div Rheumatol Allergy & Clin Immunol, Dept Med, Durham, NC 27710 USA
关键词
D O I
10.1097/00002281-200205000-00002
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Tumor necrosis factor-alpha (TNF-alpha) antagonists have rapidly emerged as a valuable class of antirheumatic agents. Etanercept, a dimerized version of the soluble tumor necrosis factor receptor II, and infliximab, a chimeric anti-TNF-alpha monoclonal antibody, are currently approved for the treatment of rheumatoid arthritis (RA) based on their proven beneficial effects in clinical trials, New insights into the role of TNF-alpha in disease pathogenesis have expanded our understanding about the possible mechanisms by which these agents reduce synovial inflammation and inhibit bone and cartilage degradation. The enlarging safety experience has revealed growing concerns about TNF-alpha inhibition and increased risk for opportunistic infection, most notably the reactivation of latent Mycobacterium tuberculosis infection. Recent recommendations have addressed this risk by calling for pretreatment screening for previous exposure to tuberculosis. The success of etanercept and infliximab therapy for RA has prompted the development of other TNF-alpha antagonists and extended the investigation of this therapeutic approach to other inflammatory diseases. TNF-alpha antagonists promise to shape the care of RA and other rheumatic diseases for many years to come. (C) 2002 Lippincott Williams Wilkins, Inc.
引用
收藏
页码:204 / 211
页数:8
相关论文
共 94 条
[1]  
Baeten D, 2001, ARTHRITIS RHEUM-US, V44, P186, DOI 10.1002/1529-0131(200101)44:1<186::AID-ANR25>3.0.CO
[2]  
2-B
[3]   A comparison of etanercept and methotrexate in patients with early rheumatoid arthritis [J].
Bathon, JM ;
Martin, RW ;
Fleischmann, RM ;
Tesser, JR ;
Schiff, MH ;
Keystone, EC ;
Genovese, MC ;
Wasko, MC ;
Moreland, LW ;
Weaver, AL ;
Markenson, J ;
Finck, BK .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 343 (22) :1586-1593
[4]  
Brandt J, 2000, ARTHRITIS RHEUM-US, V43, P1346, DOI 10.1002/1529-0131(200006)43:6<1346::AID-ANR18>3.0.CO
[5]  
2-E
[6]  
Brandt J, 2001, ARTHRITIS RHEUM, V44, pS89
[7]   USE OF IMMUNOHISTOLOGIC AND IN-SITU HYBRIDIZATION TECHNIQUES IN THE EXAMINATION OF SACROILIAC JOINT BIOPSY SPECIMENS FROM PATIENTS WITH ANKYLOSING-SPONDYLITIS [J].
BRAUN, J ;
BOLLOW, M ;
NEURE, L ;
SEIPELT, E ;
SEYREKBASAN, F ;
HERBST, H ;
EGGENS, U ;
DISTLER, A ;
SIEPER, J .
ARTHRITIS AND RHEUMATISM, 1995, 38 (04) :499-505
[8]   Severe inflammatory arthritis and lymphadenopathy in the absence of TNF [J].
Campbell, IK ;
O'Donnell, K ;
Lawlor, KE ;
Wicks, IP .
JOURNAL OF CLINICAL INVESTIGATION, 2001, 107 (12) :1519-1527
[9]  
Cavagna L, 2001, CLIN EXP RHEUMATOL, V19, P329
[10]  
Charles PJ, 2000, ARTHRITIS RHEUM, V43, P2383, DOI 10.1002/1529-0131(200011)43:11<2383::AID-ANR2>3.0.CO