6533b859fe1ef96bd12b8122

RESEARCH PRODUCT

Hyperuricaemia: another metabolic feature affecting the severity of chronic hepatitis because of HCV infection.

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Background Several works observed a link between uric acid serum levels and clinical and histological features of nonalcoholic fatty liver disease. An association between chronic hepatitis C (CHC) and uric acid levels has been poorly investigated. Aims To assess the potential association between uric acid serum levels and both histological features of liver damage and sustained virological response (SVR) in a homogeneous cohort of CHC patients. Methods Consecutive biopsy-proven CHC patients were included. Hyperuricaemia was diagnosed with uric acid serum levels >7 mg/dl in men, and >6 mg/dl in women. Patients underwent therapy with pegylated interferon plus ribavirin. Results Hyperuricaemia, observed in 7.5% of patients, was associated with low density lipoprotein cholesterol (OR 1.015, 95% CI 1.004–1.026, P = 0.008), arterial hypertension (OR 3.024, 95% CI 1.290–7.088, P = 0.01), estimated glomerular filtration rate (OR 0.942, 95% CI 0.919–0.965, P < 0.001) and severity of steatosis (OR 3.176, 95% CI 1.828–5.517, P < 0.001) by multivariate logistic regression analysis. The following features were independently linked to the severity of liver steatosis (<5% vs. ≥5% to <30% vs. ≥30%) using ordinal regression analysis: age (OR 1.027, 95% CI 1.011–1.044, P = 0.01), body mass index (OR 1.088, 95% CI 1.039–1.138, P < 0.001), triglycerides (OR 1.005, 95% CI 1.001–1.009, P = 0.02), homeostasis model assessment (OR 1.095, 95% CI 1.014–1.184, P = 0.02), hyperuricaemia (OR 2.751, 95% CI 1.423–5.322, P = 0.003), hepatitis C virus genotype 3 (OR 4.567, 95% CI 1.515–13.763, P = 0.007) and severe necroinflammatory activity (OR 1.584, 95% CI 1.067–2.349, P = 0.02). No independent association was found among uric acid levels and necroinflammatory activity, fibrosis and SVR. Conclusions In CHC patients, hyperuricaemia was independently associated with severity of steatosis, representing, in this setting, via steatosis induction, an indirect factor affecting both liver damage and poor response to therapy, and thus a novel potential therapeutic target in CHC management.