11 research outputs found

    Plasma N-terminal propeptide of type III procollagen accurately predicts liver fibrosis severity in children with non-alcoholic fatty liver disease

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    Background & Aims We examined the diagnostic performance of plasma N‐terminal propeptide of type III procollagen (PIIINP) levels, aspartate aminotransferase to platelet ratio index (APRI) and Fibrosis‐4 (FIB‐4) score for predicting non‐alcoholic steatohepatitis (NASH) and liver fibrosis stage in children/adolescents with non‐alcoholic fatty liver disease (NAFLD). Methods We enrolled 204 children/adolescents with biopsy‐proven NAFLD at the "Bambino GesĂč" Children's Hospital. We measured plasma PIIINP levels using a commercially available enzyme‐linked immunosorbent assay kit and calculated APRI and FIB‐4 scores using standard methods. Results Children with NASH had higher plasma PIIINP levels, APRI and FIB‐4 scores compared with those without NASH (all P < .001). However, PIIINP levels had much better diagnostic performance and accuracy than APRI and FIB‐4 scores for predicting liver fibrosis stage. PIIINP levels correlated with the total NAFLD activity score (NAS) and its constituent components (P < .0001). The risk of either NASH or F ≄ 2 fibrosis progressively increased with increasing PIIINP levels (P < .0001), independent of age, gender, adiposity measures, insulin resistance, NAS score and the patatin‐like phospholipase domain‐containing protein‐3 rs738409 polymorphism. For every 3.6 ng/mL increase in PIIINP levels, the likelihood of having F ≄ 2 fibrosis increased by ~14‐fold (adjusted‐odds ratio 14.1, 95% CI 5.50‐35.8, P < .0001) after adjustment for the aforementioned risk factors. The area under the receiver operating characteristics curve was 0.921 (95% CI 0.87‐0.97) for F ≄ 2 fibrosis, and 0.993 (95% CI 0.98‐1.0) for F3 fibrosis respectively. Conclusions Unlike APRI and FIB‐4 scores, plasma PIIINP levels are a promising, non‐invasive biomarker for diagnosing liver fibrosis stage in children/adolescents with biopsy‐proven NAFLD

    Higher levels of plasma hyaluronic acid and N-terminal propeptide of type III procollagen are associated with lower kidney function in children with non-alcoholic fatty liver disease

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    Objective: hyaluronic acid (HA) and N-terminal propeptide of type III procollagen (PIIINP) are two non-invasive biomarkers of liver fibrosis in non-alcoholic fatty liver disease (NAFLD). We examined the relationships of plasma levels of HA and PIIINP with kidney function in children with NAFLD. Methods: plasma HA and PIIINP levels were measured using two commercially available enzyme32 linked immunosorbent assay kits in a cohort of 106 Caucasian overweight or obese children with biopsy-proven NAFLD. Glomerular filtration rate (eGFR) was estimated using the Bedside Schwartz equation. Genotyping for the patatin-like phospholipase domain-containing protein-3 (PNPLA3) rs738409 variant was performed using an allelic discrimination assay. Results: children with fibrosis F2 had significantly higher plasma PIIINP and HA levels than those with F0 or F1 fibrosis. Liver fibrosis was positively associated with plasma HA and PIIINP, as well as with the presence of the risk allele G of PNPLA3 rs738409 variant, and negatively with eGFR. Moreover, eGFR showed significant inverse associations with HA and PIIINP levels, as well as the presence of G of PNPLA3 rs738409, and liver fibrosis stage. Notably, our multivariable regression models showed that higher plasma PIIINP (standardized beta coefficient: -0.206, p=0.011) and HA levels (standardized beta coefficient: -0.531, p<0.0001) were associated with lower eGFR values, even after adjustment for age, sex, systolic blood pressure, PNPLA3 rs738409 genotype and any stage of liver fibrosis. Conclusions: higher levels of HA and PIIINP were associated with lower eGFR values in Caucasian children with biopsy-proven NAFLD, independently of PNPLA3 rs738409 genotype and other potential confounding factors

    ÎČ-Klotho gene variation is associated with liver damage in children with NAFLD

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    Nonalcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease in adults and children. Along with obesity, diabetes and insulin resistance, genetic factors strongly impact on NAFLD development and progression. Dysregulated bile acid metabolism and the fibroblast growth factor 19 (FGF19) pathway play a pivotal role in NAFLD pathogenesis. However, it remains to be defined the mechanism through which the FGF19 receptor system is associated with liver damage in NAFLD
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