Tumor Necrosis Factor alpha (TNFɑ) belongs to the proinflammatory cytokines which promote and sustain inflammatory reactions. It is produced by macrophages and T cells and plays a central role in both acute and chronic inflammations. Consequently, chronic inflammatory diseases like Crohn’s disease, ulcerative colitis, rheumatoid arthritis, or psoriasis are increasingly being treated with antibodies against TNFɑ, which target directly the underlying inflammatory process.
During recent years, reports of an association between anti-drug antibodies (ADAs) and adverse effects of treatments both in CD and UC have surfaced. Development of ADAs is usually considered to be associated to immunogenicity of monoclonal antibodies. The clinical efficacy of an anti-TNFɑ therapy usually correlates with the trough level of the therapeutic antibody, or the drug level just before the next application of the anti-TNFɑ antibody. Several factors influence the trough level, among them dosage and frequency of anti-TNFɑ blocker infusion, disease activity, individual pharmacokinetics and immune reaction (formation of anti-drug antibodies, ADA). It is thought that ADA functionally neutralize the therapeutic antibodies or induce their rapid elimination. Consequences of ADA formation can be therapy failure and allergic reactions during anti-TNFɑ antibody application.
The IDKmonitor® Infliximab total ADA ELISA for the detection of total antibodies against infliximab measures free and bound antibodies against infliximab. This assay allows a reliable determination of ADA even in the presence of infliximab; therefore, it is ideal for therapy monitoring when a measurable infliximab concentration is expected, for example shortly after last infusion. In combination with the drug level determination, the IDKmonitor® Infliximab total ADA ELISA is an opportunity for the treating physician to monitor and optimize treatment early on.
Preparation of Patient: No special preparation.
