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1 Introduction Gout, a prevalent metabolic disorder characterized by hyperuricemic-induced monosodium urate (MSU) crystal deposition in joints and periarticular tissues, elicits intense inflammatory responses that cause significant morbidity ( Escherichia coli and Bacteroides ) that promote urate accumulation and inflammation ( In this review, we synthesized existing information on BA-gout interactions, highlighting: the mechanistic interplay between BA dysregulation and gout pathogenesis across metabolic, immune, and microbial axes

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