Hyperinsulinemic Hypoglycemia of the Neonate Associated with Persistent Fetal Histology and Function of the Pancreas
Hyperinsulinemic Hypoglycemia of the Neonate Associated with Persistent Fetal Histology and Function of the Pancreas
复制标题
新生儿高胰岛素性低血糖与持续胎儿胰腺组织学和功能相关
DOI:
10.1097/00000658-198002000-00009
复制
发表时间:
1980
影响因子:
9
通讯作者:
J. Haller
中科院分区:
文献类型:
--
作者:
D. Shermeta;G. Mendelsohn;J. Haller
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.