Higher levels of serum uric acid influences hepatic damage in patients with non-alcoholic fatty liver disease (NAFLD).

Abstract

recent evidence suggests a causal link between serum uric acid and the metabolic syndrome , diabetes mellitus , arterial hypertension , and renal and cardiac disease . Uric acid is an endogenous danger signal and activator of the inflammasome , and has been independently associated with an increased risk of cirrhosis . Aim and methods : six hundred and thirty-four patients from the nation-wide HEPAMET registry with biopsy -proven NAFLD (53% NASH) were analyzed to determine whether hyperuricemia is related with advanced liver damage in patients with non-alcoholic fatty liver disease ( NAFLD ). Patients were divided into three groups according to the tertile levels of serum uric acid and gender . Results: the cohort was composed of 50% females , with a mean age of 49 years (range 19-80). Patients in the top third of serum uric acid levels were older (p = 0.017); they had a higher body mass index (p < 0.01), arterial blood pressure (p = 0.05), triglyceridemia (p = 0.012), serum creatinine (p < 0.001) and total cholesterol (p = 0.016) and lower HDL- cholesterol (p = 0.004). According to the univariate analysis, the variables associated with patients in the top third were more advanced steatosis (p = 0.02), liver fibrosis (F2-F4 vs F0-1; p = 0.011), NASH (p = 0.002) and NAS score (p = 0.05). According to the multivariate logistic regression analysis, the top third of uric acid level was independently associated with steatosis (adjusted hazard ratio 1.7; CI 95%: 1.05-2.8) and NASH (adjusted hazard ratio 1.8; CI 95%: 1.08-3.0) but not with advanced fibrosis (F2-F4) (adjusted hazard ratio 1.09; CI 95%: 0.63-1.87). Conclusion: higher levels of serum uric acid were independently associated with hepatocellular steatosis and NASH in a cohort of patients with NAFLD . Serum uric acid levels warrants further evaluation as a component of the current non-invasive NAFLD scores of histopathological damage.