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REVERSAL OF MALNUTRITION IN CHILDREN WITH CIRRHOSIS DESPITE CONTINUED IGF 1 DEFICIENCY

Insulin-like growth factor 1 (IGF 1), the mediator of growth hormone, is manufactured in the liver but its release may be depressed by malnutrition. To date, the relative contributions of liver disease and the associated malnutrition to the depressed IGF 1 levels found in chidren with cirrhosis is unclear. We have therefore assessed the relative importance of nutritional status by measuring circulating IGF 1 in a group of cirrhotic children before and after reversal of severe malnutrition by intensive enteral feeding. Ten children with malnutrition and cirrhosis (biliary atresia 6; other causes 4; median age 9m range 4m-8y) were studied before and after intensive feeding over 8 weeks. Energy intake was increased by 40% and dietary nitrogen by 33%.Nutritional status improved dramatically: pre-feed midarm circumference % of media 76.9, post 95.1 (p<0.001). As expected, serum IGF 1 concentrations were low before enteral nutrition (mean 2.95nmol/l, range 1-9.3; reference range for age band 6-40 nmol/1, 95% confidence limits). However, despite correction of malnutrition, IGF 1 concentrations remained depressed (mean 4.7nmol/l, range 1-12; p<0.05).These data strongly suggest that the severity of the liver disease is a more important determinant of IGF1 deficiency than the associated malnutrition.