Editorials

Treating rheumatoid arthritis with tumour necrosis factor α blockade

BMJ 2002; 324 doi: https://doi.org/10.1136/bmj.324.7333.312 (Published 09 February 2002) Cite this as: BMJ 2002;324:312

May be a giant therapeutic leap or a small expensive step

  1. Paul Emery, professor,
  2. Maya Buch, research fellow
  1. Academic Unit, Musculoskeletal Disease, Leeds Teaching Hospitals Trust, Leeds LS2 9NZ

    Rheumatoid arthritis is one of the commonest autoimmune diseases, with a prevalence of about 1%, and it is perhaps the most common reversible disability in the Western world. After 10 years, 50% of people with rheumatoid arthritis in employment no longer work, most losing their jobs in the first 12 months after diagnosis.1 Excessive amounts of the pro-inflammatory cytokines, tumour necrosis factor, TNF β interleukin-1 (IL-1β), and interleukin-6 (IL-6), mediate most of the pathogenic features of rheumatoid arthritis. Infliximab, the chimeric antibody to tumour necrosis factor alpha, and etanercept, a fusion protein p75 tumour necrosis factor alpha receptor immunoglobulin, have been shown to be very effective in reducing the chronic symptoms and signs of rheumatoid arthritis in patients who fail to respond to conventional treatment with disease modifying drugs.2 Both these molecules produce response rates which are at least as high as those seen with other treatments given for milder disease. Importantly, these drugs have been shown to be effective in patients who were thought to be resistant to all treatment. Before these new drugs such patients were left to deteriorate, resulting in cachexic individuals with destroyed joints, a picture all too familiar to physicians.

    Most physicians believed that because of the redundancy of the …

    View Full Text

    Sign in

    Log in through your institution

    Free trial

    Register for a free trial to thebmj.com to receive unlimited access to all content on thebmj.com for 14 days.
    Sign up for a free trial

    Subscribe