肥胖儿童非酒精性脂肪肝炎发病状况及机制探讨

Nonalcoholic steatohepatitis in obese children:the prevalence and possible mechanism

目的：观察不同程度肥胖儿童非酒精性脂肪肝炎（NASH）的发病状况，探讨其可能的发病机制。方法：123例体质指数（BMI）≥23的7～16岁的单纯性肥胖儿童，按BMI不同分为3组：BMI≥30组34例；25≤BMI〈30组57例；23≤BMI〈25组32例。分别检测肝脏（B超），血转氨酶、甘油三酯、胆固醇、血尿酸，以及空腹血糖／空腹血胰岛素（FGIR）比值。对其中24例怀疑合并良性黑棘皮病的患儿行皮肤病理活检，分析NASH与良性黑棘皮病的关系。结果：123例患儿中B超发现肝脂肪病变的有99例（80．49％），诊断为NASH的54例（43．90％）。BMI≥30组脂肪肝炎和良性黑棘皮病的发生率及FGIR〈7者均明显高于其他两组（P〈0．01）。在54例NASH患儿中20例伴良性黑棘皮病（37．04％），其发生高脂血症、胰岛素抵抗的概率及BMI值均明显高于24例不伴脂肪肝的肥胖儿童。经相关分析，ALT和AST与BMI、血胆固醇、血甘油三酯、FGIR有相关性（rs=0．413、0．290、0．379、-0．477，P〈0．01；rs=0．359、0．349、0．348、-0．369，P〈0．01）。结论：BMI≥30是肥胖儿童发生NASH的高危因素。NASH患儿中良性黑棘皮病发生率高，其严重的脂代谢紊乱及胰岛素抵抗可能是参与NASH发病的主要机制。

Objective： To investigate the prevalence of nonalcoholic steatohepatitis （NASH） in obese children and its possible mechanism, Methods： Three subgroups were classified according to their body mass index （BMI） in 123 obese children with BMI over 23 aged 7 to 16：34 cases with BMI≥30 group;57 cases with 25≤BMI（30 group; 32 cases with 23≤BMI（25 group. Ultrasonographic and biochemical parameters including serum alanine aminotransferase （ALT）, serum aspartate aminotransferase （AST）, serum cholesterol, serum triglyceride, serum uric acid and free glucose to free insulin ratio （FGIR） were assayed. Twenty four children suspected as benign acanthosis nigricans underwent skin biopsy and its association with nonalcoholic Fifty-four children diagnosed as NASH showed significantly higher incidence of hyperlipidemia, insulin resistance and higher body mass index as compared with 24 subjects without fatty liver changes. In 54 NASH children, 20 （37. 04%） had benign acanthosis nigricans. By bivariate analysis,ALT and AST were correlated well with BMI,cholesterol,triglyceride and FGIR （rs= 0.413, 0.290, 0.379, -0.477, P〈0.01; rs= 0.359, 0.349, 0.348, -0.369, P〈0.01）. Conclusion： There is a high prevalence of nonalcoholic steatohepatitis in simple obese children and high incidence of benign acanthosis nigricans in NASH subjects. BMI≥30 is a high risk factor of being NASH. Severe disturbance of lipid metabolism and insulin resistance may be involved in the mechanism of NASH.