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Annals of the Rheumatic Diseases 2002;61(Supplement 2 ):74; doi:10.1136/ard.61.suppl_2.ii74
Copyright © 2002 BMJ Publishing Group Ltd & European League Against Rheumatism.
Annals of the Rheumatic Diseases 2002;61:ii74-ii77
© 2002 by Annals of the Rheumatic Diseases

REPORT

Effects of anakinra on clinical and radiological outcomes in rheumatoid arthritis

B Bresnihan

St Vincent’s University Hospital, Dublin 4, Republic of Ireland

Correspondence to:
Correspondence to:
Dr B Bresnihan;
c.walsh@st-vincents.ie

Keywords: anakinra; rheumatoid arthritis

Abbreviations: IL, interleukin; RA rheumatoid arthritis; MTX, methotrexate; HAQ, Health Assessment Questionnaire; ACR, American College of Rheumatology

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

Interleukin 1 (IL1) plays a central part in the pathophysiology of rheumatoid arthritis (RA).1,2 The IL1 gene family includes IL1{alpha}, IL1ß, and IL1 receptor antagonist (IL1Ra). IL1{alpha} and IL1ß are both agonist molecules. There are two distinct IL1 receptors, designated type I (IL1RI) and type II (IL1RII). IL1 binding to IL1RI results in signal transduction and cell activation. IL1Ra is the third member of the IL1 gene family. The agonistic effects of IL1 are partially blocked by the interaction between IL1Ra and IL1RI. When IL1Ra binds to IL1RI, it blocks the binding of IL1{alpha} and IL1ß and inhibits signal transduction. Recombinant human IL1Ra, anakinra, has been approved for the treatment of patients with rheumatoid arthritis (RA).

CLINICAL EFFICACY

Conventional response criteria

Five randomised, placebo controlled clinical trials of anakinra in RA have been completed (table 1Go). A total of 2932 patients were recruited. In four studies, the primary end points were related to . . . [Full text of this article]


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