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Case report reveals interleukin-1β blockade effectively resolves severe gout during arsenic therapy, highlighting inflammatory mechanisms.
We report a 49‐year‐old male patient with a normal serum uric acid and recent diagnosis of acute promyelocytic leukemia (APL) who developed a severe polyarticular gout flare during treatment with arsenic trioxide (ATO). Unlike conventional chemotherapies, ATO acts through the generation of reactive oxygen species (ROS), leading to APL cell apoptosis. The gout flare in our patient was initially treated with high‐dose intravenous glucocorticoids with no clinical response and was subsequently treated with interleukin‐1β receptor blockade, which resulted in complete clinical resolution of his gout. Our case offers insights into inflammatory pathways in gout, including the evolving role of ROS in autoinflammation.
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Hamilton et al. (2026) studied this question.
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