Abstract

Spondyloarthritis (SpA) patients do not respond uniformly to TNF inhibitor therapy, some of them losing their beneficial evolution and becoming primary or secondary non-responders. Hence, questions have been raised whether this situation is linked to predictive genetic factors, individual characteristics or to disease activity. Studies have incriminated immunogenicity as being responsible for the loss or lack of response. It appears that the development of anti-drug antibodies leads to a decrease in drug levels with further impact on patients’ clinical state. This brief review aims to clarify some of the processes involved in the immunogenic phenomenon for patients with SpA, based on the current published literature.

Highlights

  • Introducing anti-TNF therapy has significantly improved the outcome of patients with spondyloarthritis (SpA) by diminishing the clinical symptoms and lowering the global disease activity [1]

  • Secondary non-responders are patients who lose their initial benefit from anti-TNF therapy and this state can be attributed to anti-drug antibodies (ADA) formation

  • Loss of response when there is a sub-therapeutic drug level and negative ADA. This result can be due to an inadequate bioavailability or a disturbance in the drug pharmacokinetics, with an increased turnover. This can be caused by a high level of inflammation with excessive TNF amounts in the affected tissues or in patients with inflammatory enteral disorders that lead to drug elimination

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Summary

Introduction

Introducing anti-TNF (tumor necrosis factor) therapy has significantly improved the outcome of patients with spondyloarthritis (SpA) by diminishing the clinical symptoms and lowering the global disease activity [1]. An increasing number of studies indicate that the lack or loss of response in SpA patients might be due to immune reactions against the drugs, by forming neutralizing antibodies. TNFs has been incriminated in the therapeutic failure in non-responder patients by lowering the level of active substance or in those with adverse events occurrence [6].

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