Abstract
Anti-tumour necrosis factor (TNF) treatment for rheumatoid arthritis and Crohn’s disease has been introduced over the last few years. Infliximab (Remicade; Schering-Plough), a humanised monoclonal antibody, is licensed for the treatment of both rheumatoid arthritis1 and Crohn’s disease,2 while etanercept (Enbrel; Wyeth Laboratories), a fusion protein binding free TNF-α using the soluble portion of the TNFR-2 receptor,3 and adalimumab (Humira; Abbott Laboratories), a fully humanised monoclonal antibody,4 are licensed for treating rheumatoid arthritis. Post-marketing surveillance in the USA5 has identified cases of tuberculosis (TB) associated with infliximab use and a smaller number with etanercept. TB cases have also been reported in association with adalimumab (Humira prescribing information, Abbott Laboratories, 2002). The cases associated with infliximab occurred within three cycles of treatment, with a median of 12 weeks from commencing treatment,5 and most were in extrapulmonary sites.6 Calculations have suggested that TB rates in patients in the USA treated with infliximab or etanercept are six times that of untreated patients.7

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