Impact of immunogenicity on response to anti-TNF therapy in moderate-to-severe plaque psoriasis: results of the PREDIR study

Abstract

Purpose: This study was conducted to examine the relationship between loss of clinical response to anti-tumor necrosis factor (TNF) therapy and the production of anti-drug antibodies (ADAs) and the potential effects of biologic immunogenicity.

Materials and methods: This observational, non-interventional, cross-sectional study included patients with moderate-to-severe plaque psoriasis and secondary failure of adalimumab, etanercept and infliximab who were seen in the clinical practice setting. Clinical data and blood samples were collected after patient enrollment at the time that next doses of anti-TNF therapy were scheduled. ADA and serum drug concentrations were detected at a central reference laboratory using ELISA.

Results: Among 137 enrolled patients, ADA were identified in 31/65 (48%), 0/47 and 8/19 (42%) of patients treated with adalimumab, etanercept and infliximab, respectively. The presence of ADA was associated with a slightly worse clinical response in adalimumab-treated patients (Physician Global Assessment score: 3.7 vs. 3.2, ADA-positive vs. ADA-negative patients [p < .05]; correlation between serum ADA titer and body surface area: r = .292 [p = .019]). Concomitant DMARDs were not associated with anti-TNF immunogenicity in any treatment group.

Conclusions: Additional evidence is needed from studies of anti-TNF therapy in psoriasis for clinicians to gain a better understanding of the impact of immunogenicity on clinical response.

Keywords:

• Biologic
• efficacy
• immunogenicity
• psoriasis

Acknowledgements

The authors wish to thank Carmen Garcia-Calvo, MD, PhD, for her valuable contributions to the PREDIR study and development of this manuscript. Editorial/medical writing support was provided by Donna McGuire of Engage Scientific Solutions and was funded by Pfizer.

Disclosure statement

M. Ara-Martín has received honoraria as a consultant, investigator, speaker or advisory board member from AbbVie, Amgen, Celgene, Janssen, Leo Pharma, MSD, Novartis and Pfizer. P. Herranz has received honoraria as a consultant, investigator, speaker or advisory board member from AbbVie, Janssen, Leo Pharma, MSD, Novartis and Pfizer. D. Pascual-Salcedo has received speaker fees from Pfizer, AbbVie and MSD and observational research grants from Pfizer and Novartis.

Additional information

Funding

This study was sponsored by Pfizer.