The geometric mean fold rise ratio came in at 0.96, with a 95% confidence interval of 0.36 to 2.56. A ratio of 1.0 would mean the two groups had identical responses; 0.96 means essentially no separation. The wide confidence interval reflects variability between patients, but the point estimate sits squarely on "no effect."

The pattern held up across every drug class and across short- and long-half-life drugs alike. Half-life is the time it takes the body to clear half a given dose.

How big was the flare risk?

The downside was real. Patients who paused therapy were 2.27 times more likely to experience a disease flare than those who kept taking their meds (95% CI, 1.41 to 3.65). In other words, the odds of a flare more than doubled. The risk was sharpest among patients on JAKi therapies.

Adverse events overall looked similar between groups, though they cropped up more frequently in the hold arm. That tracks with the flare signal: stopping treatment tends to let inflammation rebound.

What do the authors recommend?

Curtis's team put it bluntly in the paper. "Given the increased flare risk and absence of humoral immunogenicity benefit, these findings do not support routine temporary interruption for COVID-19 vaccine optimization," they wrote.

The practical message: for most inflammatory arthritis patients on these drug classes, keep taking your medication around booster time. Any change should be a conversation with a rheumatologist, not a default move.

What are the limits?

A few caveats. The trial enrolled only patients on biologic or JAKi therapies, so results may not transfer to other DMARDs. The antibody analysis also carried wide confidence intervals, meaning the study can't rule out a small effect in either direction. Researchers measured antibodies only — not T-cell protection, a separate arm of the immune system.

The DOI is 10.1001/jamainternmed.2026.4894. The study appeared online Oct. 5 in JAMA Internal Medicine.