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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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate if measurements of MMP-2, MMP-9, TIMP-1 and TIMP-2 have clinical applicability as markers of liver fibrosis and to assess the effect of long-term lamivudine treatment on liver fibrosis in children with chronic hepatitis B (chB). Material and methods: The observation was carried out on 41 children with biopsy proven chB (HBe/+/, HBVDNA/+/) who were nonresponders to previous IFNα therapy. Lamivudine was administered in the group of 29 children (3 mg/kg/day, maximum 100 mg/daily). The serum concentration of examined markers was measured with ELISA before and after 24 months of therapy. ROC analysis was used to calculate the power of the assays to detect advanced liver fibrosis (score >2 according to Batts&Ludwig). Results: Serum TIMP-1 and TIMP-2 levels were significantly higher and MMP-9 lower in children with chB compared to controls. There was a significant positive correlation between serum MMP-2 and negative correlation between MMP-9 level and the stage of liver fibrosis. The ability of serum MMP-9 to differentiate children with mild fibrosis from those with advanced fibrosis was significant (AUC=0.75; p=0.03). Other serum markers did not allow a useful prediction. 2-year lamivudine treatment did not improve histological fibrosis but it caused significant decrease of serum TIMP-2 (p=0.01) and increase of MMP-9 level (p=0.00005). Conclusions: MMP-9 is a better serum fibrosis marker than MMP-2, TIMP-1 and TIMP-2 to diagnose children with advanced liver fibrosis. The significant decrease of TIMP-2 and increase of MMP-9 level during therapy suggest antifibrotic effect of lamivudine in children with chB. [ABSTRACT FROM AUTHOR]