Autoantibody production in anti-TNF-alpha-treated patients.

Targeting tumor necrosis factor alpha (TNF-alpha) has offered an additional therapeutic strategy against several rheumatic inflammatory disorders. The current use of TNF-alpha inhibitors allows physicians who manage these diseases and patients themselves to testify to an extraordinary efficacy, even though caution for possible adverse events must be maintained. Among these, the occurrence of autoimmune phenomena, encompassing new autoantibody formation and triggering of clinical manifestations, continues to be noted in published reports. Here, we review the current knowledge regarding the autoimmune phenomena linked to anti-TNF-alpha therapy in patients with rheumatic inflammatory disorders.

Switching tumour necrosis factor alpha antagonists in patients with ankylosing spondylitis and psoriatic arthritis: an observational study over a 5-year period.

OBJECTIVE: To evaluate the clinical response after switching from one tumour necrosis factor (TNF)alpha antagonist to another in patients with ankylosing spondylitis (AS) and psoriatic arthritis (PsA). METHODS: In this ongoing, longitudinal, observational study, data were prospectively collected on efficacy and safety since 2000 for patients starting biological treatments. The present analysis was restricted to patients with a diagnosis of spondyloarthropathy (SpA) who switched from one TNFalpha antagonist to another because of inadequate efficacy or adverse events. RESULTS: In total, 589 anti-TNFalpha-naive patients were registered, of whom 165 had a diagnosis of SpA; 7 patients with AS and 15 with PsA received >1 TNFalpha antagonist. Two patients with PsA were treated with all the drugs. In all, 16 subjects switched from infliximab to etanercept, 7 from etanercept to adalimumab and 1 from etanercept to infliximab. Overall, a clinical response was seen in 75% of patients who changed from infliximab to etanercept, and in 57.1% who switched from etanercept to adalimumab. CONCLUSIONS: The findings of this study on a selected population of patients with SpA indicate that the failure of an initial TNFalpha antagonist does not preclude the response to another one. Further trials are needed to confirm this preliminary observation.