Intestinal Microbiome May Influence Gout and Hyperuricemia Outcomes
Emerging research suggests the intestinal microbiome’s role in gout and hyperuricemia may have therapeutic implications according to a review published online in Inflammation. The authors highlight key microbial shifts in patients with gout and experimental models, pointing to potential avenues for microbiome-targeted interventions in clinical contexts.
Study Findings: Microbiome Features in Gout and Hyperuricemia
Gout, a crystal arthropathy driven by hyperuricemia (HU) and subsequent monosodium urate (MSU) crystal deposition, affects millions globally and frequently leads to acute inflammatory arthritis and chronic joint damage. The reviewed literature indicates that patients with gout and HU consistently exhibit reduced gut microbial diversity and a higher Bacteroidetes:Firmicutes ratio compared with healthy controls. Notably, beneficial genera such as Akkermansia, Bifidobacterium, and butyrate producers such as Coprococcus and Roseburia were depleted in affected individuals.
Human cohort data from >300 participants in China and a separate Seoul cohort showed these dysbiotic patterns, which also correlated with elevated serum urate and inflammatory markers. Preclinical animal studies reported that probiotic supplementation with Lactobacillus strains and prebiotic inulin altered gut composition, increased short-chain fatty acids (SCFAs), and in some models reduced serum urate levels and proinflammatory cytokines versus controls.
However, the authors caution that methodological limitations — modest sample sizes, regional biases, and inconsistent controls — temper the certainty of these findings.
Clinical Implications for Gout Management
For clinicians treating gout and HU, these insights underscore the potential relevance of gut microbiota modulation as an adjunctive strategy alongside established urate-lowering therapies. Dysbiosis characterized by reduced diversity and loss of butyrate-producing species may contribute to systemic inflammation and impaired urate metabolism, offering a biological rationale for exploring dietary, probiotic, or prebiotic approaches in targeted patient populations.
However, translation to practice remains preliminary: large, controlled human trials are lacking, and most interventional evidence derives from animal models that may not fully recapitulate human physiology. Clinicians should interpret current data as hypothesis-generating, not practice-changing, while remaining alert to emerging trials testing microbiome-centered therapies.
Reference
Renton N, Pillinger MH, Toprover M. Gout, hyperuricemia, and the intestinal microbiome. Inflammation. 2025;48:3776–3784. doi:10.1007/s10753-025-02337-x.
