Hyperinsulinemia has prominent role in refeeding syndrome pathophysiology.

We appreciate the comments by Hakan et al.1 regarding the potential pathogenesis of the severe hypophosphatemia and additional electrolyte dyscrasias in the intrauterine growth-restriction (IUGR) population. We agree that the most likely mechanism for the reported electrolyte abnormalities is a transient hyperinsulinemia. Increased release of insulin in response to the carbohydrate load with refeeding a chronically malnourished patient has been implicated as the key trigger for many of the electrolyte disturbances seen with refeeding syndrome.2, 3