Biologic agents may induce immune responses that could impact drug action.
The aims of this study were to assess antidrug antibodies (ADAs) in patients with rheumatoid arthritis (RA) from Argentina treated with etanercept, adalimumab, or infliximab at a single visit and correlate it with efficacy outcomes.
In this subset analysis of a noninterventional, multinational, cross-sectional study (NCT01981473), adult patients with RA treated continuously for 6 to 24 months with etanercept, adalimumab, or infliximab were evaluated for ADAs and trough drug concentrations of 2 days or less prior to the next scheduled dose. Efficacy measurements included Disease Activity Score based on a 28-joint count–erythrocyte sedimentation rate, low disease activity, and Health Assessment Questionnaire—Disability Index. Targeted medical history of injection site/infusion reactions, serum sickness, and thromboembolic events were reported.
Baseline demographics, disease characteristics, and duration of treatment of the 119 patients (etanercept: n = 54, adalimumab: n = 52, infliximab: n = 13) were similar across all groups. No etanercept-treated patient tested positive for ADAs compared with 19 (36.5%) of 52 patients and 4 (30.8%) of 13 patients treated with adalimumab and infliximab, respectively. In adalimumab- and infliximab-treated patients, ADA presence correlated negatively with trough drug levels. A greater proportion of ADA-negative patients achieved Health Assessment Questionnaire—Disability Index of 0.5 or less and had better composite efficacy measures compared with ADA-positive patients. The rate of targeted medical events reported was low.
In this subset analysis, RA patients from Argentina treated with adalimumab or infliximab, but not etanercept, tested positive for ADAs. Antidrug antibody–negative patients showed a tendency toward better clinical outcomes compared with ADA-positive patients.
From the *Centro de Investigación en Enfermedades Reumáticas, Buenos Aires, Argentina;
†Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil;
‡Pfizer, Collegeville, PA;
§Pfizer, San José, Costa Rica;
∥Pfizer, Buenos Aires, Argentina; and
¶Clínica Enfermedades Reumatoideas San Juan, San Juan, Argentina.
This study was sponsored by Pfizer. Medical writing support was provided by Mukund Nori, PhD, MBA, CMPP, of Engage Scientific Solutions and was funded by Pfizer.
P.J.M. has received research grants from AbbVie, Centocor, Eli Lilly, and Pfizer. R.X. is a consultant for AstraZeneca, Hospira, Janssen, and Pfizer and on the speaker's bureau for AbbVie, AstraZeneca, Janssen, Pfizer, and Roche. R.M.R. was employed by Pfizer at the time of the study and owns stock in Pfizer. R.P., Q.S., L.M., G.S., and C.E.B. are employed by Pfizer and own stock in Pfizer. R.P.H. declares no conflict of interest.
Correspondence: Pablo J. Maid, MD, Centro de Investigación en Enfermedades Reumáticas, Av. Cordoba 1525, 12th Floor, Buenos Aires, Argentina. E-mail: firstname.lastname@example.org.