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Antidrug antibody formation during tumor necrosis factor α inhibitor treatment of severe psoriatic patients in the real-life practice

INTRODUCTION: Antidrug antibody (ADA) production may be the reason behind secondary inefficacy of anti-TNF-α therapy in psoriasis. AIM: To investigate the production of ADA, serum tumor necrosis factor α (TNF-α) and drug levels as predictors of clinical response in real-life circumstances. MATERIAL...

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Detalles Bibliográficos
Autores principales: Herszényi, Krisztina, Jókai, Hajnalka, Rencz, Fanni, Brodszky, Valentin, Nagy, Eszter, Holló, Péter
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Termedia Publishing House 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6906958/
https://www.ncbi.nlm.nih.gov/pubmed/31839776
http://dx.doi.org/10.5114/ada.2019.89507
Descripción
Sumario:INTRODUCTION: Antidrug antibody (ADA) production may be the reason behind secondary inefficacy of anti-TNF-α therapy in psoriasis. AIM: To investigate the production of ADA, serum tumor necrosis factor α (TNF-α) and drug levels as predictors of clinical response in real-life circumstances. MATERIAL AND METHODS: Serum drug concentrations (TNFi), the presence of ADAs and serum TNF-α levels were measured in 158 patients by the ELISA method. Clinical response was evaluated by calculating PASI. Their correlation has been statistically analysed. RESULTS: In adalimumab and infliximab treated patients, ADA formation was observed in 18.4% and 33%, respectively, and the serum TNFi concentration was significantly higher in the ADA negative groups. In contrast there was no ADA formation detected among etanercept treated patients. The serum TNFi concentration was significantly lower among non-responders (n = 33). The serum TNF-α level was also measured and the correlation with the concentration of the serum TNFi level was analysed. Having evaluated the results of all patients together, the serum TNFi and TNF-α concentrations showed a significant negative correlation. However, when groups were analysed separately, in case of adalimumab, a significant negative correlation was detected between serum TNFi and TNF-α concentrations. With respect to infliximab, there was no significant correlation, and an inverse correlation was found in the etanercept group. The TNF-α levels and ADA positivity were significantly higher in non-responders. CONCLUSIONS: This study revealed the major role of ADAs against TNFi in case of secondary inefficacy in real-life circumstances. ADA levels show a stronger correlation with PASI failure than serum TNFi or TNF-α levels.