Open AccessHyperinsulinemic Hypoglycemia of the Neonate Associated with Persistent Fetal Histology and Function of the Pancreas
Author(s) -
Dennis W. Shermeta,
Geoffrey Mendelsohn,
Julia A. Haller
Publication year - 1980
Publication title -
annals of surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.153
H-Index - 309
eISSN - 1528-1140
pISSN - 0003-4932
DOI - 10.1097/00000658-198002000-00009
Subject(s) - nesidioblastosis , hyperinsulinemic hypoglycemia , medicine , pancreas , endocrine system , enteroendocrine cell , hypoglycemia , endocrinology , hyperplasia , fetus , histology , insulin , hormone , pregnancy , insulinoma , biology , genetics
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.