The relationship between serum uric acid and non alcoholic fatty liver disease: a cross-sectional retrospective study

Background and aim: Non alcoholic fatty liver disease (NAFLD) is considered as the hepatic manifestation of metabolic syndrome (MS). Previous studies have linked hyperuricemia with cardiovascular diseases and their risk factors, including MS. Aim of this study was to investigate the relationship between serum uric acid (UA) levels and the presence of NAFLD among our outpatients. Material and methods: We analyzed data of 322 patients (122M-200F with a mean age of 54.5±16.4 yrs) referring to our ambulatory of gastrointestinal disease between January 2012 and December 2012. The subjects were divided into 2 groups according to the presence (n=176) or the absence (n=146) of NAFLD. Hepatic steatosis was diagnosed based on abdominal ultrasonographic findings, after exclusion of any other etiological liver disease and alcohol consumption. The UA levels were categorized according to the quartiles, considered separately for both sexes, as follows: (M) Q1 4.4 mg/dL, Q2 4.5–5.2 mg/dL, Q3 5.3–6-3 mg/dL and Q4 >6.3 mg/dL; (F) Q1 3.6 mg/dL, Q2 3.7–4.5 mg/dL, Q3 4.6–4.9 mg/dL and Q4 >4.9 mg/dL. Multivariate logistic regression was performed across the UA quartiles to determine the ORs for NAFLD. Results: Metabolic abnormalities (hypertension, obesity, diabetes, hypertriglyceridemia) and UA levels were found significantly higher in subjects with NAFLD. The OR (95% CI), for the presence of NAFLD in the subjects with the highest UA levels (Q4) was 4.12 (2.07–8.18), as compared to the subjects within Q1. After adjustment for sex and MS components, the adjusted OR was 3.01 (1.4–6.49). The prevalence rate of NAFLD increased with progressively higher UA levels (P value for trend <0,0001). Conclusions: Our results are consistent with other studies that assert UA levels are significantly associated with NAFLD. These findings suggest that elevated UA concentrations may be an independent risk factor for NAFLD. Furthermore, some studies demonstrated that increased UA levels may be related to hepatic ATP depletion, which arrests protein synthesis and evocates inflammatory and pro-oxidative changes. In conclusion, if UA proves to be in the casual pathway for NAFLD, the prevention or treatment of hyperuricemia may reduce the risk of development or progression of NAFLD.