Premium
Nasogastric feeding enhances nutritional status in paediatric liver disease but does not alter circulating levels of IGF‐I and IGF binding proteins
Author(s) -
Holt Richard,
Miell John,
Jones Jennifer,
MieliVergani Giorgina,
Baker Alastair
Publication year - 2000
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1046/j.1365-2265.2000.00934.x
Subject(s) - medicine , endocrinology , cirrhosis , failure to thrive , enteral administration , malnutrition , parenteral nutrition
OBJECTIVE Complications of childhood cirrhosis include abnormal growth and malnutrition, associated with abnormalities in circulating IGFs and IGFBPs. Controlled studies suggest that intensive enteral feeding enhances nutritional status. The aim was to ascertain whether nasogastric feeding improves nutritional status in clinical practice and to assess the effect of feeding on serum IGF‐I and IGFBPs. PATIENTS Thirty‐three children (median age 0.6 years) with biliary atresia and failure to thrive who were treated with nasogastric feeding. MEASUREMENTS Height, weight and triceps skin fold thickness were measured prior to feeding and regularly for 1 year or until feeding was stopped. Serum IGF‐I and IGFBPs were measured by immunoassay at the same intervals. RESULTS The median duration of feeding was 3.7 months. Twenty‐two stopped feeding after liver transplantation, while 10 stopped electively and 1 boy died. Before feeding, the children were losing weight and height centile. Triceps skin fold thickness, weight and height sd scores improved with feeding. Baseline serum IGF‐I and IGFBP‐3 were low, while IGFBP‐1 and IGFBP‐2 were raised. IGF‐I and IGFBP‐1 did not change with feeding. IGFBP‐2 fell and reached a nadir by 3 months, while IGFBP‐3 rose temporarily for 4–6 weeks. CONCLUSIONS Nasogastric feeding improves body composition in paediatric liver disease but circulating IGF‐I and IGFBPs remain abnormal and do not play a major role in mediating these changes. This does not exclude a paracrine or autocrine effect of IGF‐I.