In the treatment of rheumatic diseases (rheumatoid arthritis, spondylarthritides), chronic inflammatory bowel diseases (Crohn’s disease and ulcerative colitis) and psoriasis, TNF-α inhibitors such as adalimumab (ADL; commercial name Humira^®) and infliximab (IFX; commercial name Remicade^®) are given when patients respond insufficiently to conventional disease-modifying antirheumatic drugs (DMARDs) or these are contraindicated.
Increasing ADL or IFX levels in the treatment lead to continuous improvement of the clinical symptoms. After reaching the optimal concentration range, further increase of the active ingredient no longer significantly improves the symptoms, but may lead to side effects. In order to reach the optimal range, the drug dosage must be adjusted individually.
If the drug level drops significantly, this indicates the production of body-own anti-drug antibodies (ADA), a frequent problem in the treatment with TNF-α inhibitors. These endogenous antibodies complex the drug, which leads to its premature elimination from the body and/or interruption of the effect mechanism. In patients who do not respond to the treatment, ADA occur more frequently and in higher concentrations than in patients who are being successfully treated with ADL and IFX.