Hyperinsulinemic Hypoglycemia of the Neonate Associated with Persistent Fetal Histology and Function of the Pancreas

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Abstract
Early in development, the fetal pancreas is characterized by the presence of two distinct generations of endocrine cells and a B-Cell mass that is unresponsive to acute changes in circulating glucose levels. Near the end of intrauterine development, the normal pancreas has "matured" and contains a single generation of endocrine cells and B-Cells that are responsive to changes in glucose concentrations. Recent microscopic examination of resected pancreatic tissue from an infant with hyperinsulinemic hypoglycermia revealed a combination of all three of the currently accepted findings in this neonatal condition: hyperplasia, adenomatosis, and nesidioblastosis. These observations prompted the following hypothesis: When compared to the usual histology of the developing pancreas, nesidioblastosis may be interpreted as an abnormal continuation of normal proliferation of endocrine cells; hyperplasia may be a specific overproduction of the Secondary Islands of Langerhans; and adenomatosis may be an abnormal continuation or overgrowth of the Primary Island of Langerhans. Such extrapolation suggests that infants with hyperinsulinemic hypoglycemia may represent a failure in the normal histological and functional maturation of the endocrine portion of the fetal pancreas.