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Abstract：
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.
OBJECTIVE: 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 and 21 pediatric cases without hepatic steatosis. All specimens were stained by Beclin1 and LC3A antibodies. According to final diagnosis obtained from Pediatric Hepatology department, patients were divided into two groups: chronic liver disease (CLD) group that included 45 cases and inborn error of metabolism (IEM) group that included 36 cases.
RESULTS: higher beclin1 expression was significantly correlated with higher stages of fibrosis and distorted liver architecture in CLD group, (P=0.043) for both. The control group showed higher positivity, percentage, as well as the median values of the H score of LC3A expression than did the CLD group or the IEM group (P=0.055, 0.001, and 0.008, respectively). Higher positivity of LC3A was significantly associated with higher stages of fibrosis and distorted liver architecture in the studied IEM group (P=0.021) for both.
CONCLUSIONS: Varying intensity grades of LC3A and Beclin 1 immunohistochemical expression demonstrate the variation of autophagy at different phases of pediatric hepatic steatosis and varied disease etiology.
OBJECTIVE: 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 and 21 pediatric cases without hepatic steatosis. All specimens were stained by Beclin1 and LC3A antibodies. According to final diagnosis obtained from Pediatric Hepatology department, patients were divided into two groups: chronic liver disease (CLD) group that included 45 cases and inborn error of metabolism (IEM) group that included 36 cases.
RESULTS: higher beclin1 expression was significantly correlated with higher stages of fibrosis and distorted liver architecture in CLD group, (P=0.043) for both. The control group showed higher positivity, percentage, as well as the median values of the H score of LC3A expression than did the CLD group or the IEM group (P=0.055, 0.001, and 0.008, respectively). Higher positivity of LC3A was significantly associated with higher stages of fibrosis and distorted liver architecture in the studied IEM group (P=0.021) for both.
CONCLUSIONS: Varying intensity grades of LC3A and Beclin 1 immunohistochemical expression demonstrate the variation of autophagy at different phases of pediatric hepatic steatosis and varied disease etiology.
摘要：
肝脏脂肪变性已成为全球儿童慢性肝病的最常见原因。脂质吞噬已被认为是影响脂肪变性发展和进展的途径。
目的：本研究旨在评估Beclin1和LC3A在伴有脂肪变性的小儿肝组织中的免疫组织化学表达，并将其表达与临床病理参数相关联。
方法：本研究包括81例埃及儿童肝性脂肪变性患者和21例无肝性脂肪变性患者。所有标本均用Beclin1和LC3A抗体染色。根据从小儿肝病科获得的最终诊断，将患者分为两组：慢性肝病（CLD）组45例，先天性代谢异常（IEM）组36例。
结果：在CLD组中，较高的beclin1表达与较高的纤维化分期和肝脏结构扭曲显著相关，（P=0.043）。对照组表现出更高的阳性，百分比,以及LC3A表达的H评分中位数高于CLD组或IEM组(分别为P=0.055,0.001和0.008).在所研究的IEM组（P=0.021）中，较高的LC3A阳性与较高的纤维化分期和扭曲的肝脏结构显着相关。
结论：LC3A和Beclin1免疫组织化学表达的不同强度等级表明自噬在小儿肝脂肪变性的不同阶段和不同的疾病病因中存在差异。
目的：本研究旨在评估Beclin1和LC3A在伴有脂肪变性的小儿肝组织中的免疫组织化学表达，并将其表达与临床病理参数相关联。
方法：本研究包括81例埃及儿童肝性脂肪变性患者和21例无肝性脂肪变性患者。所有标本均用Beclin1和LC3A抗体染色。根据从小儿肝病科获得的最终诊断，将患者分为两组：慢性肝病（CLD）组45例，先天性代谢异常（IEM）组36例。
结果：在CLD组中，较高的beclin1表达与较高的纤维化分期和肝脏结构扭曲显著相关，（P=0.043）。对照组表现出更高的阳性，百分比,以及LC3A表达的H评分中位数高于CLD组或IEM组(分别为P=0.055,0.001和0.008).在所研究的IEM组（P=0.021）中，较高的LC3A阳性与较高的纤维化分期和扭曲的肝脏结构显着相关。
结论：LC3A和Beclin1免疫组织化学表达的不同强度等级表明自噬在小儿肝脂肪变性的不同阶段和不同的疾病病因中存在差异。
