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.
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- Alexander D. P., Britton H. G., Nixon D. A. Further observations on the administration of anti-insulin serum to lambs in the perinatal period. Biol Neonate. 1971;19(4):451–458. doi: 10.1159/000240437. [DOI] [PubMed] [Google Scholar]
- Asplund K. Dynamics of insulin release from the foetal and neonatal rat pancreas. Eur J Clin Invest. 1973 Jul;3(4):338–344. doi: 10.1111/j.1365-2362.1973.tb00360.x. [DOI] [PubMed] [Google Scholar]
- Bucha V., Taylor R. E., Berger R., Haury E. W. Geomagnetic Intensity: Changes during the Past 3000 Years in the Western Hemisphere. Science. 1970 Apr 3;168(3927):111–114. doi: 10.1126/science.168.3927.111. [DOI] [PubMed] [Google Scholar]
- Crowder W. L., Maclaren N. K., Gutberlet R. L., Frost J. L., Mason G. R., Cornblath M. Neonatal pancreatic beta-cell hyperplasia: report of a case with failure of diazoxide and benefit of early subtotal pancreatectomy. Pediatrics. 1976 Jun;57(6):897–900. [PubMed] [Google Scholar]
- FERNER H. The A- and B-cells of the pancreatic islets as sources of the antagonistic hormones glucagon and insulin; the shift of the AB-relation in diabetes mellitus. Am J Dig Dis. 1953 Oct;20(10):301–306. doi: 10.1007/BF02895538. [DOI] [PubMed] [Google Scholar]
- Fonkalsrud E. W., Trout H. H., 3rd, LaFranchi S., Dakake C. Idiopathic hypoglycemia in infancy. Surgical management. Arch Surg. 1974 Jun;108(6):801–804. doi: 10.1001/archsurg.1974.01350300043012. [DOI] [PubMed] [Google Scholar]
- Gabbe S. G., Quilligan E. J. Fetal carbohydrate metabolism: its clinical importance. Am J Obstet Gynecol. 1977 Jan 1;127(1):92–103. doi: 10.1016/0002-9378(77)90321-0. [DOI] [PubMed] [Google Scholar]
- Hamilton J. P., Baker L., Kaye R., Koop C. E. Subtotal pancreatectomy in the management of severe persistant idiopathic hypoglycemia in children. Pediatrics. 1967 Jan;39(1):49–58. [PubMed] [Google Scholar]
- Heitz P. U., Klöppel G., Häcki W. H., Polak J. M., Pearse A. G. Nesidioblastosis: the pathologic basis of persistent hyperinsulinemic hypoglycemia in infants. Morphologic and quantitative analysis of seven cases based on specific immunostaining and electron microscopy. Diabetes. 1977 Jul;26(7):632–642. doi: 10.2337/diab.26.7.632. [DOI] [PubMed] [Google Scholar]
- LIU H. M., POTTER E. L. Development of the human pancreas. Arch Pathol. 1962 Nov;74:439–452. [PubMed] [Google Scholar]