Does autophagy have a role in the pathogenesis of pediatric hepatic steatosis?

Abstract

Abstract Background and Objectives: Hepatic steatosis has become the most common cause of chronic liver disease among children worldwide. Lipophagy has been considered as a pathway affecting steatosis development and progression. This study aimed to evaluate the immunohistochemical expression of Beclin1 and LC3A in pediatric hepatic tissues with steatosis and to correlate their expression with clinicopathological parameters. Methods This study included 81 Egyptian pediatric patients with hepatic steatosis. Also, 21 pediatric cases without hepatic steatosis were included. All specimens were stained by Beclin1 and LC3A antibodies. Results Higher beclin1 expression was significantly correlated with higher stages of fibrosis and distorted liver architecture in chronic liver diseases group, (P = 0.043) for both. The higher positivity, percentage and median values of H score of LC3A expression were seen in control group rather than in chronic liver disease group or the inborn error of metabolism group (P = 0.055, 0.001, 0.008 respectively). Higher positivity of LC3A was significantly associated with higher stages of fibrosis and distorted liver architecture in the studied inborn error of metabolism group (P = 0.021) for both. Conclusions Fluctuation of autophagy at different stages of pediatric hepatic steatosis and different disease etiology proved by different intensity grades of Beclin 1 and LC3A immunohistochemical expression.