TY - JOUR T1 - Infliximab efficiency and failure JF - Annals of the Rheumatic Diseases JO - Ann Rheum Dis SP - 751 LP - 752 VL - 63 IS - 6 AU - A P Rozin Y1 - 2004/06/01 UR - http://ard.bmj.com/content/63/6/751.abstract N2 - I would like to comment on an interesting letter in the Annals about anti-tumour necrosis factor (TNF) monotherapy for giant cell arteritis (GCA).1 The suggestion that vasculitis may be cured by anti-TNF treatment may seem to be reasonable. The factors sustaining autoimmune inflammation may include new target antigen production, immune system activation, and a vicious cycle of lymphocyte cascade activation. This mechanism has been recently suggested2 after a report of long term remission (6–24 months) of Wegener’s granulomatosis as a result of infliximab treatment,3 but unfortunately, it is not relevant in this case.The authors considered overcoming infliximab failure with an increased dose and frequency,1 but “such an approach is by no means cost effective and should not be attempted”. There is another way of dealing with a loss of infliximab efficiency, which may be explained by examining the generation of human antichimeric antibodies (HACA). The following information should be considered: Second line treatment should be added at the start of infliximab treatment to prevent HACA production. HACA may be related to a shortened duration of response after repeated infliximab doses as was first described in patients with rheumatoid arthritis (RA).4 The assay used to determine HACA is affected by the presence of infliximab itself,5 and HACA levels have to be measured after the drug has been stopped. In the ATTRACT study, 27 patients who discontinued infliximab treatment were tested for the presence of HACA: three (11%) were positive, two with a titre of 1/10 and one with a titre of 1/40.6 Formation of HACA may be inversely related to the infliximab dose. HACA were found in 53, 21, … ER -