Rheumatoid arthritis is a common chronic inflammatory and destructivearthropathy that cannot be cured and that has substantial personal,social, and economic costs. The long-term prognosis is poor:80 percent of affected patients are disabled after 20 years,1and life expectancy is reduced by an average of 3 to 18 years.2The medical cost of rheumatoid arthritis averages $5,919 percase per year in the United States3 and approximately £2,600per case per year in the United Kingdom.4 Current slow-actingantirheumatic drugs have limited efficacy and many side effects.Moreover, they do not improve the long-term prognosis of rheumatoidarthritis.1
Cellular Mediators of Inflammation and Joint Damage
Soluble Mediators of Inflammation and Joint Damage
TNF-
Interleukin-1
Interleukin-6
Antiinflammatory Cytokines
Interleukin-10
Interleukin-4
Joint Damage in Rheumatoid Arthritis
Summary
Inhibition of Cytokines
Neutralization of Cytokines
Receptor Antagonism
Activation of Antiinflammatory Pathways
Clinical Trials of Cytokine Inhibitors
Soluble Human Cytokine-Receptor Proteins
Etanercept
Monoclonal Antibodies against Cytokines
Infliximab
Other Antibodies against TNF-
Cytokine-Receptor Blockers
Recombinant Interleukin-1Receptor Antagonist
Antibody against Interleukin-6 Receptor
Recombinant Interleukin-10 and Interleukin-4
Conclusions
Source Information
From the Department of Rheumatology, Guy's, King's, and St. Thomas' Hospitals School of Medicine, King's College, London.
Address reprint requests to Dr. Choy at the Department of Rheumatology, King's College Hospital, East Dulwich Grove, London SE22 8PT, United Kingdom.
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