Content area
Full Text
Journal of Perinatology (2014) 34, 247248
& 2014 Nature America, Inc. All rights reserved 0743-8346/14 http://www.nature.com/jp
Web End =www.nature.com/jp
LETTERS TO THE EDITOR
Transient hyperinsulinemia may be responsible from electrolyte abnormalities of refeeding syndrome seen in very low birth weight infants with intrauterine growth-restriction
Journal of Perinatology (2014) 34, 247; doi:http://dx.doi.org/10.1038/jp.2013.181
Web End =10.1038/jp.2013.181
We read with great interest the article by Ross et al.,1 in which they report the incidence of refeeding syndrome, dened by the presence of hypophosphatemia, in very low birth weight (VLBW) infants with intrauterine growth restriction (IUGR) born to mothers with preeclampsia. They reported high incidence of refeeding syndrome and suggested that its occurrence, in addition to associated hypokalemia, hypomagnesemia and hyperglycemia, in IUGR VLBW infants is consistent with refeeding syndrome. However, IUGR infants are prone to hyperinsulinemic state,2,3 and insulin transfers extracellular electrolytes into the intracellular compartment, as a consequence of which, increased transfer of phosphate from the extracellular into the intracellular compartment causes hypophosphatemia.4 Simmons et al.3 reported that newborn rats with IUGR caused by uterine placenta insufciency developed mild fasting hyperglycemia, hyperinsulinemia and high insulin resistance index. Therefore, we think that electrolyte abnormalities (for example, hypophosphatemia, hypokalemia and hypomagnesemia) seen in refeeding syndrome of VLBW infants with IUGR may be due...