Association between serum uric acid and non-alcoholic fatty liver disease (NAFLD): an observational cross-sectional study in an Egyptian outpatient cohort.

BACKGROUND

Hepatic steatosis, characterized by excessive triglyceride accumulation within hepatocytes, is the central feature of non-alcoholic fatty liver disease (NAFLD). This spectrum encompasses simple steatosis, non-alcoholic steatohepatitis (NASH), progressive fibrosis, and cirrhosis. NAFLD pathogenesis involves an intricate interplay between nutritional factors, metabolic dysregulation, and genetic predisposition. Evidence suggests hyperuricemia is an independent risk factor for NAFLD, with elevated serum uric acid (SUA) levels associated with increased steatosis severity and fibrosis advancement. This study investigated the association between SUA levels and liver involvement—specifically ultrasound-assessed steatosis grading and elastography-measured liver stiffness—in patients with NAFLD.

METHODS

This cross-sectional study enrolled 70 patients aged ≥18 years with ultrasound-diagnosed NAFLD (Group I) and 70 age-, sex-, and residence-matched healthy controls (Group II). Participants were recruited from Minia University Liver Hospital between March 2022 and February 2023. Exclusion criteria included excessive alcohol consumption, viral or autoimmune hepatitis, established cirrhosis, and medications affecting uric acid metabolism. The primary outcome was presence of NAFLD. Evaluations comprised detailed medical history, anthropometric measurements, laboratory testing (including SUA), abdominal ultrasonography for steatosis grading, and two-dimensional shear wave elastography for liver stiffness assessment.

RESULTS

Hyperuricemia prevalence reached 55.7% (n=39) among NAFLD patients compared to 0% in controls (p=0.001). Mean SUA concentrations were significantly elevated in the NAFLD group versus controls (5.98 ± 1.9 mg/dL vs. 4.34 ± 0.7 mg/dL, p=0.001). A significant association emerged between hyperuricemia and hepatic steatosis grades (p=0.032). Multivariate logistic regression identified SUA as independently associated with NAFLD after adjustment for confounders (Adjusted OR 1.45; 95% CI: 1.12–1.88, p=0.005 per 1 mg/dL increment), alongside BMI, waist circumference, triglycerides, and creatinine. Receiver operating characteristic (ROC) analysis demonstrated an optimal 5.3 mg/dL SUA cut-off for NAFLD discrimination (AUC 0.74, 64% sensitivity, 94% specificity, p=0.001).

CONCLUSION

Elevated SUA levels were consistently associated with NAFLD presence, steatosis severity, and increased liver stiffness. The 5.3 mg/dL threshold warrants further validation. Notable limitations include single-center recruitment potentially limiting generalizability, a cross-sectional design precluding temporal relationship and causality determination, and the possibility of residual confounding from unmeasured variables.