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Previous Volume 344:907-916 March 22, 2001 Number 12 Next

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Rheumatoid arthritis is a common chronic inflammatory and destructive arthropathy 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,¹ and life expectancy is reduced by an average of 3 to 18 years.² The medical cost of rheumatoid arthritis averages $5,919 per case per year in the United States³ and approximately £2,600 per case per year in the United Kingdom.⁴ Current slow-acting antirheumatic drugs have limited efficacy and many side effects. Moreover, they do not improve the long-term prognosis of rheumatoid arthritis.¹

. . . [Full Text of this Article]

Pathogenesis of Rheumatoid Arthritis

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-1–Receptor 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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