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Annals of the Rheumatic Diseases 2002;61(Supplement 2 ):70; doi:10.1136/ard.61.suppl_2.ii70
Copyright © 2002 BMJ Publishing Group Ltd & European League Against Rheumatism.
Annals of the Rheumatic Diseases 2002;61:ii70-ii73
© 2002 by Annals of the Rheumatic Diseases

REPORT

Adalimumab (a fully human anti-tumour necrosis factor {alpha} monoclonal antibody) in the treatment of active rheumatoid arthritis: the initial results of five trials

R Rau

Department of Rheumatology, Evangelisches Fachkrankenhaus Ratingen, Ratingen, Germany

Correspondence to:
Correspondence to:
Dr R Rau, Rheumaklinik, Evangelisches Fachkrankenhaus, Rosenstr 2 D-40882 Ratingen, Germany;
rrau@uni-duesseldorf.de

Keywords: rheumatoid arthritis; adalimumab

Abbreviations: RA, rheumatoid arthritis; TNF{alpha}, tumour necrosis factor {alpha}; MTX, methotrexate; DMARD, disease modifying antirheumatic drug

The first 150 words of the full text of this article appear below.

Rheumatoid arthritis (RA), a common, chronic, idiopathic autoimmune disease, is characterised by symmetrical synovitis, inflammatory exudates in the joint cavity, and erosion of articular cartilage and marginal bone.1 Standard treatment for RA typically consists of traditional disease modifying antirheumatic drugs (DMARDs), corticosteroids, non-steroidal anti-inflammatory drugs, and analgesics.2 Despite these various treatments, many patients with RA continue to experience substantial disease activity, with progressive joint damage and accompanying functional loss. In recent years, insights into the pathophysiology of RA have lead to the development of novel therapeutic strategies that target underlying disease processes, the most promising of which entails neutralisation of tumour necrosis factor {alpha} (TNF{alpha}).3

ANTI-TNF{alpha} TREATMENTS

TNF{alpha} is a potent proinflammatory cytokine that plays a critical part in the progression of inflammatory synovitis and articular matrix degradation in RA.3 Increased concentrations of TNF{alpha} are found in the synovial fluid and serum of patients with active RA.4 Derived primarily from activated monocytes . . . [Full text of this article]


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