Conrado M Fernández Rodríguez1, Rocío Aller2, María Luisa Gutiérrez García3, Javier Ampuero4, Judith Gómez-Camarero5, Rosa M ª Martín-Mateos6, Diego Burgos-Santamaría7, José Miguel Rosales8, Patricia Aspichueta9, Xabier Buque9, Mercedes Latorre10, Raúl J Andrade11, Manuel Hernández-Guerra12, Manuel Romero-Gómez13. 1. Digestivo, Hospital Universitario Fundacion Alcorcon, España. 2. Digestivo, Hospital Clínico Universitario de Valladolid, España. 3. Aparato Digestivo, Hospital Universitario Fundacion Alcorcon, Spain. 4. UNIT for the clinical Management of Digestive Dise, Virgen del Rocio University Hospital CIBEReh. 5. Aparato Digestivo, Hospital Universitario de Burgos. 6. Gastroenterologia, Hospital Universitario Ramon y Cajal. Universidad de ALcala de Henares. CIBERehd. 7. Gastroenterologia, Hospital Universitario Ramon y Cajal. Universidad de ALcala de Henares. CIBERehd, España. 8. Aparato Digestivo, Hospital Costa del Sol, España. 9. Biocruces Health Research Institute, University of Basque Country UPV/EHU, Bizkaia, Spain. 10. Unidad de hepatología, Consorcio Hospital General Universitario de Valencia. 11. Unidad Aparato Digestivo. Complejo Hospitalario de Especialidades Virgen de la Victoria, Málaga. 12. Gastroenterology, Tenerife University Hospital. Canary Island, Spain. 11. 13. UGC Aparato Digestivo. Hospital Virgen del Rocío, Sevilla.
Abstract
BACKGROUND: 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.
BACKGROUND: 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.
Authors: Sebastian Zenovia; Carol Stanciu; Catalin Sfarti; Ana-Maria Singeap; Camelia Cojocariu; Irina Girleanu; Mihaela Dimache; Stefan Chiriac; Cristina Maria Muzica; Robert Nastasa; Laura Huiban; Tudor Cuciureanu; Anca Trifan Journal: Diagnostics (Basel) Date: 2021-04-27