| Summary: | New therapeutic options bring new problems and also new knowledge about disease mechanisms. Ten years ago the first antagonist to tumor necrosis factor was first used to treat inflammatory diseases and the use of anti-cytokines has proved to be a revolution in therapeutics. The natural history of rheumatoid arthritis, psoriasis, ankilosing spondilitis and juvenile rheumatoid arthritis changed after those products were introduced in therapy. Today, there are three different antitumor necrosis factor antibodies and one antibody antitumor necrosis factor receptor. All of them increase the risk of tuberculosis, but there is a clear difference between them: the risk for inflaximab is 12 times the risk for etanercept. One of the receptors for tumor necrosis factor, TNFR1 is essential to activate macrophages, and probably this is the place in which antitumor necrosis factor monoclonal antibodies do interfere with defense against tuberculosis.
|
|---|