Serveur d'exploration sur les relations entre la France et l'Australie

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Antidrug antibodies (ADAb) to tumour necrosis factor (TNF)-specific neutralising agents in chronic inflammatory diseases: a real issue, a clinical perspective

Identifieur interne : 004906 ( Main/Exploration ); précédent : 004905; suivant : 004907

Antidrug antibodies (ADAb) to tumour necrosis factor (TNF)-specific neutralising agents in chronic inflammatory diseases: a real issue, a clinical perspective

Auteurs : Fabien B. Vincent [Australie] ; Eric F. Morand [Australie] ; Kim Murphy [Australie] ; Fabienne Mackay [Australie] ; Xavier Mariette [France] ; Christian Marcelli [France]

Source :

RBID : ISTEX:DCAEC499C66FC471323E4B914AC2089B937BFDBE

Descripteurs français

English descriptors

Abstract

The introduction of biologics, especially tumour necrosis factor (TNF) inhibitors, has revolutionized the management of chronic inflammatory diseases. However, at least one third of patients with these diseases, receiving TNF inhibitors either do not respond to treatment, or lose initial responsiveness. For a significant proportion, improvement of clinical response is achieved after switching to another anti-TNF drug, suggesting a basis for failure unrelated to the therapeutic target itself. A likely explanation for this is immunogenicity, as all biologics are potentially immunogenic, and the resulting anti-drug antibodies (ADAb) can theoretically decrease the efficacy of biologics and/or induce adverse events. Indeed, in these chronic inflammatory diseases, many studies have now established correlations between ADAb formation, low serum drug levels, and the failure or loss of response to anti-TNF antibodies. This article will review key findings related to ADAb, and propose a model wherein monitoring of drug levels and ADAb may be a predictive tool leading to a better choice of biologics. Such an approach could improve chronic inflammatory disease management toward a personalized and more cost-effective approach.

Url:
DOI: 10.1136/annrheumdis-2012-202545


Affiliations:


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Le document en format XML

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<term>Clin</term>
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<term>Clinical practice</term>
<term>Clinical response</term>
<term>Clinical response association</term>
<term>Concomitant</term>
<term>Correlated</term>
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<term>Different mechanism</term>
<term>Disease activity</term>
<term>Dose escalation</term>
<term>Elisa</term>
<term>Elisa elisa</term>
<term>Engl</term>
<term>Etanercept</term>
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<term>Golimumab</term>
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<term>Adab</term>
<term>Adab formation</term>
<term>Adab incidence</term>
<term>Adab levels</term>
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<term>Adalimumab treatment</term>
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<term>Antibody formation</term>
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<term>Arthritis rheum</term>
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<term>Clinical improvement</term>
<term>Clinical practice</term>
<term>Clinical response</term>
<term>Clinical response association</term>
<term>Concomitant</term>
<term>Correlated</term>
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<term>Different mechanism</term>
<term>Disease activity</term>
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<front>
<div type="abstract">The introduction of biologics, especially tumour necrosis factor (TNF) inhibitors, has revolutionized the management of chronic inflammatory diseases. However, at least one third of patients with these diseases, receiving TNF inhibitors either do not respond to treatment, or lose initial responsiveness. For a significant proportion, improvement of clinical response is achieved after switching to another anti-TNF drug, suggesting a basis for failure unrelated to the therapeutic target itself. A likely explanation for this is immunogenicity, as all biologics are potentially immunogenic, and the resulting anti-drug antibodies (ADAb) can theoretically decrease the efficacy of biologics and/or induce adverse events. Indeed, in these chronic inflammatory diseases, many studies have now established correlations between ADAb formation, low serum drug levels, and the failure or loss of response to anti-TNF antibodies. This article will review key findings related to ADAb, and propose a model wherein monitoring of drug levels and ADAb may be a predictive tool leading to a better choice of biologics. Such an approach could improve chronic inflammatory disease management toward a personalized and more cost-effective approach.</div>
</front>
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