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Vincent et al present a thorough review of available clinical research on antidrug antibodies to tumour necrosis factor (TNF) blocking agents.1 We agree to a large extent with their interpretation of the data with regard to pathophysiology, assay characteristics and variation in drug and antidrug antibody serum levels. However, the conclusion that measurement of (anti)drug levels should therefore be used for clinical decision making in non-responding biological patients with inflammatory diseases to save costs, prevent adverse events and improve disease activity, including their proposed algorithm, seems flawed and is thus far insufficiently supported by evidence. In our comment we will focus on rheumatoid arthritis (RA), but for other inflammatory disease the same comments can be made.
First, we would argue that the most promising application for therapeutic drug monitoring (TDM) to save costs or adverse events is not to predict response to the next treatment option in non-responding patients, but rather to predict successful dose reduction and stopping in patients who are doing well. All treatment alternatives in non-responding patients employ either another biological or a higher dose of the same biological, so even optimal channelling of patients can only lead to better disease control, not to saved costs or prevented adverse events. In patients doing well however, it could …