Serum concentration of adiponectin, leptin and resistin in obese children with non-alcoholic fatty liver disease.

PURPOSE: Obesity, insulin resistance and dyslipidemia are the most significant risk factors of non-alcoholic fatty liver disease (NAFLD) but the role of adipokines in patomechanism of this disease is not clear. The aim of the study was to evaluate the serum levels of leptin, adiponectin and resistin in obese children with NAFLD. MATERIAL/METHODS: The fasting serum levels of adipokines were determined in 44 consecutive obese children with suspected liver disease and in 24 lean controls. The degree of the ultrasound liver steatosis was graded according to Saverymuttu. RESULTS: The fatty liver was confirmed in 33 children by ultrasonography (16 of them also showed an increased ALT activity). The serum leptin level was significantly higher and adiponectin level was lower in the obese children with NAFLD when compared to controls. Only adiponectin correlated with homeostasis model assessment of insulin resistance (HOMA-IR). Significant negative correlations were found between the ultrasonographic grades of liver steatosis and adiponectin and resistin levels. Serum adiponectin and resistin levels were lower in children with an advanced liver steatosis (grade 3, n=10) compared to patients with a mild steatosis (grade 1-2, n=23). The ability of serum adiponectin and resistin to differentiate children with an advanced liver steatosis from those with mild steatosis was significant. CONCLUSIONS: These data suggest a role of both adiponectin and resistin in the pathogenesis of NAFLD in obese children and confirm the association between adiponectin and insulin resistance. Adiponectin and resistin may be suitable serum markers in predicting an advanced liver steatosis in children with NAFLD.

Serum level of YKL-40 does not predict advanced liver fibrosis in children with chronic hepatitis B.

PURPOSE: The aim of the study was to evaluate the serum concentration of YKL-40 (human cartilage glycoprotein-39) in the assessment of fibrosis stage in children compared to biopsy and prior to antiviral treatment for chronic hepatitis B. MATERIAL AND METHODS: We determined serum level of YKL-40 (METRA, EIA kit, Quidel Corporation, San Diego, USA) after an overnight fast in 63 children (age range 4-17 years, mean 10 years) with biopsy-verified chronic HBeAg-positive hepatitis B. Fibrosis stage and inflammation grade were assessed in a blinded fashion according to Ishak et al. We defined advanced liver fibrosis as a score >2. Receiver operating characteristics (ROC) analysis was used to calculate the power of the assay to detect advanced liver fibrosis (AccuROC, Canada). RESULTS: Serum concentration of YKL-40 was significantly higher in patients with chronic hepatitis B compared to controls (n=16) (38.5 +/- 19.2 vs 27.9 +/- 8.75 ng/mL; p = 0.032). The ability of serum YKL-40 to differentiate children with advanced liver fibrosis (n=31; 49.2%) from those with mild fibrosis was not significant (AUC = 0.387 +/- 0.072, p = 0.12). This marker was not a good predictor of histologic inflammation either. CONCLUSION: Serum level of YKL-40 does not predict advanced liver fibrosis in children with chronic hepatitis B.

Exocrine pancreatic function in biliary tract pathology treated with the endoscopic methods.

PURPOSE: Incidence of pancreatic exocrine insufficiency in biliary pathology is estimated for about 30%. The objective was to assess pancreatic exocrine function in biliary tract pathology (cholelithiasis, strictures) before and after endoscopic treatment. PATIENTS AND METHODS: Twenty-eight patients with choledocholithiasis and its complications (19F/9M; aging 31-90 years, median: 69 years) were evaluated. Fecal elastase 1 concentration was measured using ELISA, before, early, and 6-8 weeks after endoscopic treatment. The inflammatory response of pancreas to the treatment was also assessed. RESULTS: Initial fecal elastase 1 concentration in patients (median 454 microg/g) was not significantly different as compared to the control (median 357 microg/g). Nine patients (32%) had low fecal elastase 1 concentration (below 250 microg/g) and out of them 6 had the concentration below 200 microg/g, suggesting impairment of exocrine pancreatic function. Endoscopic treatment was successful in 82% of patients. Pancreatic inflammatory response was noted only in one patient. After 6-8 weeks fecal elastase 1 concentration in the whole group of patients did not significantly change in comparison to the initial level. However, out of 9 patients with initially low fecal elastase 1 concentration (median 191 microg/g) at least in 6 pancreatic function improved (median 310 microg/g), P < 0.001. CONCLUSION: One third of the patients with biliary pathology had a low fecal elastase 1 concentrations, suggesting pancreatic dysfunction. In at least 2/3 of these patients successful endoscopic treatment of biliary pathology resulted in the significant increase of fecal elastase 1 concentration. Therefore, an additional positive effect of such treatment in some patients, could be an improvement of the exocrine pancreatic dysfunction.