This is a post hoc analysis of AVERT-2, a phase 3 trial in DMARD-naive, anti-CCP-positive early rheumatoid arthritis, in which 446 patients received abatacept with methotrexate and 300 received placebo with methotrexate for 56 weeks.
Of 103 biomarkers measured, 47 fell significantly more with abatacept and methotrexate than with methotrexate alone, and 18 of those correlated with baseline disease activity. High baseline interleukin-10 was associated with a greater chance of reaching efficacy endpoints at week 52 on abatacept, and with less bone erosion.
The design limits what this can support. It is exploratory and post hoc, 103 biomarkers were tested, and the analysis was not the trial's stated purpose. With that many comparisons, some associations appear by chance, and the paper is honest that this is hypothesis-generating.
What makes it worth reading is the direction rather than the strength: it is consistent with abatacept's mechanism in seropositive early disease, and it points at a subgroup question worth a prospective answer. It is not a reason to measure interleukin-10 before prescribing.
- Do not order interleukin-10 to guide abatacept: this is exploratory and post hoc.
- Read it as support for abatacept in seropositive early disease, which is where it is already used.
- Note the bone erosion signal separately from the clinical endpoints; structural outcomes and symptom outcomes can diverge.
- Treat any single association drawn from 103 biomarkers with more caution than its p value suggests.
The statistics, in plain English
The p values here, from below 0.03 to below 0.0007, look convincing in isolation and should not be read that way. When 103 biomarkers are tested, several will cross a significance threshold by chance alone, and the paper does not present a correction for that. Post hoc means the question was asked after the results were known, which is a weaker position than a pre-specified analysis even with identical numbers. The finding is a lead for a future trial, not evidence to act on.
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