Influence of rheumatoid factor levels and TNF inhibitor structure on secondary nonresponse in rheumatoid arthritis patients.

TNF inhibitors adalimumab certolizumab pegol infliximab monoclonal antibodies rheumatoid arthritis rheumatoid factor

Journal

Frontiers in medicine
ISSN: 2296-858X
Titre abrégé: Front Med (Lausanne)
Pays: Switzerland
ID NLM: 101648047

Informations de publication

Date de publication:
2024
Historique:
received: 08 07 2024
accepted: 15 08 2024
medline: 19 9 2024
pubmed: 19 9 2024
entrez: 19 9 2024
Statut: epublish

Résumé

The EXXELERATE study revealed poorer clinical outcomes in patients treated with adalimumab (ADL) and baseline rheumatoid factor (RF) above 203 IU/mL. However, responses were similar in patients treated with certolizumab pegol (CZP) regardless of RF levels. This study investigated the impact of RF levels >203 IU/mL on TNF inhibitors (TNFi) serum levels and the association with secondary nonresponse in RA patients treated with TNFi. We performed an observational ambispective study with RA patients treated with infliximab (IFX), ADL, or CZP. Patients were stratified according to baseline RF levels: ≤ or >203 IU/mL. After 6 months, serum drug levels and antidrug antibodies were measured, and reasons for discontinuation were collected. We included 170 RA patients: 90 (53%) received IFX, 48 (28%) ADL, and 32 (19%) CZP. While CZP serum levels did not differ between RF groups at 6 months ( Baseline RF above 203 IU/mL is associated with lower serum drug levels and an increased risk of discontinuation due to secondary nonresponse in patients treated with IFX or ADL. In contrast, drug levels and clinical outcomes are not significantly impacted by baseline RF levels in patients under CZP.

Sections du résumé

Background UNASSIGNED
The EXXELERATE study revealed poorer clinical outcomes in patients treated with adalimumab (ADL) and baseline rheumatoid factor (RF) above 203 IU/mL. However, responses were similar in patients treated with certolizumab pegol (CZP) regardless of RF levels.
Objectives UNASSIGNED
This study investigated the impact of RF levels >203 IU/mL on TNF inhibitors (TNFi) serum levels and the association with secondary nonresponse in RA patients treated with TNFi.
Methods UNASSIGNED
We performed an observational ambispective study with RA patients treated with infliximab (IFX), ADL, or CZP. Patients were stratified according to baseline RF levels: ≤ or >203 IU/mL. After 6 months, serum drug levels and antidrug antibodies were measured, and reasons for discontinuation were collected.
Results UNASSIGNED
We included 170 RA patients: 90 (53%) received IFX, 48 (28%) ADL, and 32 (19%) CZP. While CZP serum levels did not differ between RF groups at 6 months (
Conclusion UNASSIGNED
Baseline RF above 203 IU/mL is associated with lower serum drug levels and an increased risk of discontinuation due to secondary nonresponse in patients treated with IFX or ADL. In contrast, drug levels and clinical outcomes are not significantly impacted by baseline RF levels in patients under CZP.

Identifiants

pubmed: 39296891
doi: 10.3389/fmed.2024.1461396
pmc: PMC11410080
doi:

Types de publication

Journal Article

Langues

eng

Pagination

1461396

Informations de copyright

Copyright © 2024 Plasencia-Rodríguez, Martínez-Feito, Novella-Navarro, Pérez De Diego, Bonilla, Gehin, Villalba-Yllán, Nuño, Pascual-Salcedo, Nozal, Almirón and Balsa.

Déclaration de conflit d'intérêts

CP-R has received research grants/honoraria from AbbVie, Pfizer, Novartis, Lilly, and Roche. MN-N has received research grants/honoraria from Galápagos, Janssen, Lilly, Novartis, and UCB. AB received grant/research support and fees for consultancies or as a speaker from AbbVie, Amgen, Pfizer, Novartis, BMS, Nordic, Sanofi, Sandoz, Lilly, UCB, and Roche. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Auteurs

Chamaida Plasencia-Rodríguez (C)

Rheumatology Department, La Paz University Hospital, Madrid, Spain.
Immuno-Rheumatology Research Group, Institute for Health Research (IdiPAZ), Madrid, Spain.

Ana Martínez-Feito (A)

Immuno-Rheumatology Research Group, Institute for Health Research (IdiPAZ), Madrid, Spain.
Immunology Unit, La Paz University Hospital, Madrid, Spain.

Marta Novella-Navarro (M)

Rheumatology Department, La Paz University Hospital, Madrid, Spain.
Immuno-Rheumatology Research Group, Institute for Health Research (IdiPAZ), Madrid, Spain.

Rebeca Pérez De Diego (R)

Laboratory of Immunogenetics of Human Diseases, IdiPAZ Institute for Health Research, La Paz University Hospital, Madrid, Spain.
Innate Immunity Group, IdiPAZ Institute for Health Research, La Paz University Hospital, Madrid, Spain.
Interdepartmental Group of Immunodeficiencies, Madrid, Spain.

Gema Bonilla (G)

Rheumatology Department, La Paz University Hospital, Madrid, Spain.
Immuno-Rheumatology Research Group, Institute for Health Research (IdiPAZ), Madrid, Spain.

Johanna Elin Gehin (JE)

Department of Medical Biochemistry, Oslo University Hospital, Oslo, Norway.

Alejandro Villalba-Yllán (A)

Rheumatology Department, La Paz University Hospital, Madrid, Spain.

Laura Nuño (L)

Rheumatology Department, La Paz University Hospital, Madrid, Spain.

Dora Pascual-Salcedo (D)

Immuno-Rheumatology Research Group, Institute for Health Research (IdiPAZ), Madrid, Spain.

Pilar Nozal (P)

Immunology Unit, La Paz University Hospital, Madrid, Spain.
Center for Biomedical Network Research on Rare Diseases (CIBERER U754), Madrid, Spain.

Mariana Díaz Almirón (MD)

Biostatistics Unit, Institute for Health Research (IdiPAZ), Madrid, Spain.

Alejandro Balsa (A)

Rheumatology Department, La Paz University Hospital, Madrid, Spain.
Immuno-Rheumatology Research Group, Institute for Health Research (IdiPAZ), Madrid, Spain.

Classifications MeSH