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Impact of anti-citrullinated protein antibody on tumor necrosis factor inhibitor or abatacept response in patients with rheumatoid arthritis

OBJECTIVE: To assess the impact of anti-citrullinated protein antibody (ACPA) serostatus on response to treatment with either tumor necrosis factor inhibitors (TNFi) or abatacept in patients with rheumatoid arthritis (RA). METHODS: Data was obtained from the Optimizing Patient outcomes in Australian...

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Detalles Bibliográficos
Autores principales: Tymms, Kathleen, Butcher, Belinda, Smith, Tegan, Littlejohn, Geoffrey
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medical Research and Education Association 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8133894/
https://www.ncbi.nlm.nih.gov/pubmed/32966190
http://dx.doi.org/10.5152/eurjrheum.2020.20024
Descripción
Sumario:OBJECTIVE: To assess the impact of anti-citrullinated protein antibody (ACPA) serostatus on response to treatment with either tumor necrosis factor inhibitors (TNFi) or abatacept in patients with rheumatoid arthritis (RA). METHODS: Data was obtained from the Optimizing Patient outcomes in Australian RheumatoLogy (OPAL) dataset. Patient data were included in the analysis if they commenced treatment with abatacept or TNFi between 01 August 2006 and 30 June 2017 and had at least 12 months’ follow-up. The primary outcome was the mean change in the clinical disease activity index (CDAI) score from baseline to 12 months. RESULTS: A total of 2,052 patients were included of which 1,415 were in the TNFi cohort (n=1,053 ACPA positive) and 637 in the abatacept cohort (n=445 ACPA positive). Patients were predominantly female (75% TNFi; 80% abatacept) with no significant difference in age between cohorts. Patients with ACPA positivity had longer disease duration before commencing treatment in both the TNFi and abatacept cohorts compared to ACPA negative patients. No difference in disease severity was observed in those with ACPA negativity compared to those with ACPA positivity. Patients treated with TNFi and abatacept had significantly improved mean change in CDAI after 12 months; ACPA positivity was associated with greater response to treatment with abatacept compared to that in patients with ACPA negativity (p=0.011). No difference in response was observed based on ACPA serostatus in patients treated with TNFi (p=0.73). CONCLUSION: Baseline ACPA positivity was associated with improved clinical response using CDAI outcome measure at 12 months for abatacept but not for TNFi therapies.