Hepatic steatosis and liver stiffness in patients with gout: a controlled cross-sectional elastography study

Gout shares cardiometabolic risk factors with metabolic dysfunction-associated steatotic liver disease (MASLD). We aimed to compare elastography-defined hepatic steatosis and liver stiffness between patients with gout and metabolically stringent controls, and to identify independent determinants of controlled attenuation parameter (CAP) and liver stiffness measurement (LSM).

In this single-center cross-sectional study (April 2024-January 2026), 201 adults with gout and 80 controls free of hypertension, diabetes mellitus, chronic kidney disease, and coronary artery disease underwent vibration-controlled transient elastography (FibroScan®). Multivariable linear and logistic regression models identified independent predictors of CAP, LSM, and binary elastographic outcomes.

Patients with gout had significantly higher CAP (279 vs. 251.5 dB/m; p < 0.001) and LSM (6.1 vs. 5.1 kPa; p < 0.001). In unadjusted analyses, the odds of hepatic steatosis (CAP ≥ 238 dB/m; OR 2.42, 95% CI 1.40-4.20; p = 0.001) and of increased liver stiffness (LSM ≥ 7.0 kPa; OR 2.46, 95% CI 1.27-4.78; p = 0.007) were higher in the gout group, and LSM ≥ 9.6 kPa was more frequent (12.9% vs. 1.3%; p = 0.001). On multivariable analysis, BMI and ALT were the principal determinants of CAP, whereas BMI and age independently predicted continuous LSM. Gout status was not independently associated with CAP, continuous LSM, hepatic steatosis, or increased liver stiffness (adjusted OR 1.83, 95% CI 0.84-4.01; p = 0.131). Serum uric acid and disease activity measures were not associated with any elastographic outcome.

Patients with gout exhibit a substantially higher burden of elastography-defined hepatic steatosis and increased liver stiffness than metabolically stringent controls. This excess was accounted for by adiposity and age rather than by gout status or urate levels, suggesting that non-invasive liver assessment in gout should be guided by cardiometabolic risk profile rather than by the diagnosis of gout itself. Key Points • In unadjusted analyses, patients with gout had more than twofold higher odds of both hepatic steatosis and increased liver stiffness on transient elastography compared with metabolically stringent controls. • BMI and ALT were the strongest independent determinants of CAP; BMI and age were the strongest determinants of continuous LSM. • After adjustment for age, BMI and cardiometabolic covariates, gout status was not independently associated with any elastographic outcome, including increased liver stiffness (LSM ≥ 7.0 kPa). • Serum uric acid, disease activity scores, and urate-lowering or anti-inflammatory therapies were not associated with elastographic liver measures, indicating that hepatic involvement in gout reflects adiposity-driven metabolic burden rather than urate-specific mechanisms.