• Pediatric Gastroenterology, Hepatology & Nutrition
• /
• v.13 no.1
• /
• pp.51-57
• /
• 2010

Purpose: It has been reported that children with hypopituitarism have features of metabolic syndrome, including obesity, impaired glucose tolerance, and dyslipidemia. The aim of this study was to investigate the clinical features and liver histology of pediatric non-alcoholic fatty liver disease (NAFLD) associated with hypopituitarism. Methods: We reviewed the clinical data of 11 children diagnosed with NAFLD among patients with hypopituitarism. Results: The mean age at the time of diagnosis of hypopituitarism was 10.4${\pm}$3.2 years, and the mean age at the time of diagnosis of NAFLD was 13.1${\pm}$2.7 years. A craniopharyngioma was the most common cause of pituitary dysfunction. At the time of diagnosis of NAFLD, 9 patients (82%) had a body mass index greater than the 85th percentile, 5 patients (45%) had elevated fasting blood glucose levels, and 9 patients (82%) had hypertriglyceridemia. The mean height SD score was significantly lower at the time of diagnosis of NAFLD than at the time of diagnosis of hypopituitarism. Of the six patients who were biopsied, one had cirrhosis, two had non-alcoholic steatohepatitis (NASH) with bridging fibrosis, two had NASH with mild portal fibrosis, and one had simple steatosis. Conclusion: Children with hypopituitarism are at risk of short stature, obesity, dyslipidemia, and NAFLD. The early diagnosis of NAFLD is important in children with hypopituitarism because advanced fibrosis is common.

• Pediatric Gastroenterology, Hepatology & Nutrition
• /
• v.10 no.2
• /
• pp.185-192
• /
• 2007

Purpose: This study was conducted to evaluate the role of adiponectin, leptin, and tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) in obese children, and to elucidatethe relationship between these adipokines and insulin resistance. Methods: A total of 61 obese children (M : F=42 : 19, mean age 11.2${\pm}$1.3 years) admitted to our facility between March 2004 and June 2005 were included in this study. Patients were divided into three groups based on their NAFLD status obese children without fatty liver (N=23); obese children with simple steatosis (N=20); and obese children with non-alcoholic steatohepatitis (NASH) (N=18). The serum levels of adiponectin, leptin, and TNF-${\alpha}$ were measured, and insulin resistance determined by homeostasis model assessment (HOMA-IR) was calculated to estimate insulin resistance. In addition, the VSR (visceralsubcutaneous fat ratio) was estimated using abdominal computed tomography. Results: There was no difference in serum TNF-${\alpha}$ and leptin levels observed between the 3 groups (22.13${\pm}$6.37 vs. 21.35${\pm}$6.95 vs. 25.17${\pm}$9.30; p=0.342 & 20.29${\pm}$8.57 vs. 16.42${\pm}$6.85 vs. 20.10${\pm}$7.86; p=0.330). However, the serum adiponectin level was significantly lower in children with non-alcoholic steatohepatitis (NASH) than in the other two groups (6.08${\pm}$1.38 in children without steatosis vs. 5.69${\pm}$0.79 in simple steatosis vs. 4.93${\pm}$1.75 in NASH; p=0.026). In addition, the VSR was significantly increased in the NASH group (0.31${\pm}$0.08 vs. 0.32${\pm}$0.11 vs. 0.47${\pm}$0.14; p=0.001), and HOMA-IR revealed a significant difference among the three groups (4.77${\pm}$3.67 vs. 6.89${\pm}$7.05 vs. 10.42${\pm}$6.73; p=0.000). However, there was no significant correlation observed between the adiponectin levels and the HOMA-IR or the VSR (r=-0.117; p=0.450 & r=-0.106; p=0.499). Conclusion: Insulin resistance may affect the development of hepatic steatosis and steatohepatitis in children, and the results of this study suggest that, of several adipokines evaluated, adiponectin is important in the progression of steatosis to steatohepatitis in obese children.

• Clinical and Experimental Pediatrics
• /
• v.49 no.10
• /
• pp.1037-1041
• /
• 2006

Purpose : The prevalence of obesity and nonalcoholic steatohepatitis(NASH) was increased in adolescents. This study was performed to observe the prevalence of elevated aminotransferase levels in adolescents and to assess the correlations between aminotransferase levels and obesity related parameters(body mass index, waist circumference, hip circumference, waist to hip ratio and insulin level). Methods : We obtained weight, height, waist circumference and hip circumference from 2,417 male and 1,219 female adolescents. Mean age was $15.7{\pm}0.7$ years old. We measured fasting insulin, aspartate aminotransferase(AST) and alanine aminotransferase(ALT). Obese and overweight were defined as body mass indices(BMI) of more than the 95th, and 85th-94th percentiles, respectively, for age and sex. Results : The number of adolescents with obesity is 324(8.9 percent). 414(11.4 percent) subjects belonged to the overweight group. The average ALT level of obese, overweight and control groups were significantly different(obese : $32.1{\pm}34.3U/L$, overweight : $19.6{\pm}13.6U/L$, control : $12.7{\pm}6.7U/L$, P<0.001). The average AST level was also different according to group(obese : $27.8{\pm}16.5U/L$, overweight : $22.8{\pm}8.6U/L$, control : $20.8{\pm}8.5U/L$, P<0.001). AST and ALT were correlated with anthropometric parameters and insulin level. After multiple regression analysis, waist circumference was the significant predictive value for AST(r=0.234, P<0.001). Waist circumference, BMI and insulin levels were significant predictive values for ALT(r=0.435, P<0.001). Conclusion : The prevalence of abnormal aminotransferase was higher in the obese and overweight groups than control group. Waist circumference was useful to predict abnormal aminotransferase levels.

• Pediatric Gastroenterology, Hepatology & Nutrition
• /
• v.15 no.1
• /
• pp.44-51
• /
• 2012

Purpose: Tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) polymorphism has been suggested to play an important role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) in obese adults, and known to be a mediator of insulin resistance. In this study, we evaluated the role of TNF-${\alpha}$ promoter polymorphisms and insulin resistance in the development of NAFLD in obese children. Methods: A total of 111 obese children (M:F=74:37; mean age, $11.1{\pm}2.0$ yrs) were included. The children were divided into 3 groups: controls (group I, n=61), children with simple steatosis (group II, n=17), and children with non-alcoholic steatohepatitis (group III, n=33). Serum TNF-${\alpha}$ levels, homeostasis model assessment of insulin resistance (HOMA-IR), and TNF-${\alpha}$ -308 and -238 polymorphisms were evaluated. Results: There were no differences in TNF-${\alpha}$ polymorphism at the -308 or the -238 loci between group I and group II + III ($p$=0.134 and $p$=0.133). The medians of HOMA-IR were significantly different between group I and group II + III ($p$=0.001), with significant difference between group II and group III ($p$=0.007). No difference was observed in the HOMA-IR among the genotypes at the -308 locus ($p$=0.061) or the -238 locus ($p$=0.207) in obese children. Conclusion: TNF-${\alpha}$ promoter polymorphisms at the -308 and -238 loci were not significantly associated with the development of NAFLD in children; nevertheless, insulin resistance remains a likely essential factor in the pathogenesis of NAFLD in obese children, especially in the progression to NASH.