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ABSTRACT: Malnutrition is a treatable complication in children with end-stage liver disease (ESLD). Biliary atresia and other cholestatic disorders are the most frequent cause of ESLD in children. No single variable provides adequate information about nutrition status, yet effective nutrition support is the one intervention known to improve pre- and posttransplant outcomes. A proactive approach consisting of screening anthropometry interpreted using appropriate growth references, recognition of clinical manifestations associated with micronutrient deficiency, and timely aggressive nutrition support is of a paramount importance to maximize anabolism and optimize outcomes. This article presents the principles of nutrition assessment, intervention, and monitoring in children with ESLD.
Nutrition in Clinical Practice 03/2013; · 1.59 Impact Factor
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Pediatric Transplantation 05/2011; 15(3):344-6. · 1.48 Impact Factor
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Journal of pediatric gastroenterology and nutrition 05/2009; 48(4):495-7. · 2.18 Impact Factor
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Journal of Pediatric Gastroenterology and Nutrition 10/2005; 41(3):363,365. · 2.30 Impact Factor
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Journal of Pediatric Gastroenterology and Nutrition 08/2005; 41(3):363,365. · 2.30 Impact Factor
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ABSTRACT: The acquired or perinatal form of biliary atresia is a Th1 fibro-inflammatory disease affecting both the extrahepatic and intrahepatic bile ducts. Osteopontin (OPN) is a Th1 cytokine implicated in several fibro-inflammatory and autoimmune diseases. We examined the expression of OPN in acquired biliary atresia in comparison to normal liver and several pediatric cholestatic liver diseases. We also assessed OPN expression by cultured human bile duct epithelial cells. We found that liver OPN mRNA and protein expression were significantly increased in biliary atresia versus normal and other cholestatic diseases. OPN expression in biliary atresia was localized to epithelium of proliferating biliary structures (ductules and/or ducts) and bile plugs contained therein. No portal biliary OPN expression could be demonstrated in normal liver, syndromic biliary atresia, biliary obstruction not due to biliary atresia, and idiopathic neonatal hepatitis. OPN expression by human bile duct epithelial cells in culture was responsive to IL-2 and TNF-alpha. Our results demonstrate an up-regulation of OPN expression by interlobular biliary epithelium in biliary atresia, which correlates with biliary proliferation and portal fibrosis. These findings suggest a role for OPN in the pathogenesis of biliary atresia.
Pediatric Research 07/2005; 57(6):837-44. · 2.70 Impact Factor
