Presence of anti-cyclic citrullinated peptide antibodies is associated with better treatment response to abatacept but not to TNF inhibitors in patients with rheumatoid arthritis: a meta-analysis

• Published in: Clinical and experimental rheumatology 2020-05, Vol.38 (3), p.455-466
• Main Authors: Alemao, Evo, Postema, Roelien, Elbez, Yedid, Mamane, Carole, Finckh, Axel
• Format: Article
• Language: English
• ISSN: 0392-856X

The objective of this study was to investigate whether anti-cyclic citrullinated peptide antibody (ACPA) status is associated with clinical responses to abatacept or TNF-α-inhibitors (TNF-α-i) in RA patients. A systematic literature review (SLR) was performed in January 2018 to identify published studies and conference abstracts evaluating biologic DMARD response according to ACPA status. Mantel-Haenszel meta-analysis methods were used to pool risk ratios (RRs). In the base-case, treatment response was assessed using EULAR measure, while a scenario analysis assessed response by combining ACR20, DAS28 and EULAR measures. Subgroup analyses were performed for duration of study follow-up. Eighteen of the 30 SLR studies were included in the meta-analysis. The base-case showed a statistically significant positive association between ACPA positivity and EULAR response for patients treated with abatacept (RR: 1.13 [95% CI: 1.00, 1.26]), while ACPA positivity was associated with lower EULAR responses to TNF-α-i (RR: 0.91 [95% CI: 0.84, 0.98]). For the scenario analysis, results were consistent with the base-case for abatacept (RR 1.18 [95% CI 1.03, 1.35]), while for TNFα-i, no significant difference by ACPA status was observed (RR 0.97 [95% CI 0.86, 1.10]). Subgroups analyses showed results similar to the base-case for both abatacept and TNF-α-i. This meta-analysis confirms that ACPA-positive RA patients are marginally more likely to achieve EULAR and ACR20 response to abatacept compared to ACPA-negative patients. Additionally, the analysis demonstrates that there is no association between ACPA status and response to TNF-α-i, consistent with findings of previously published studies.