Decrease of Pancreatic Somatostatin in Neonatal Nesidiobiastosis

The inappropriate insulin release that is characteristic of severe neonatal hypoglycemie and nesidiobiastosis was thought to be principally due to a marked proliferation of B-cells. A possible deficiency of somatostatin, one of the factors controlling insulin release, has only recently been considered. We report here a significant decrease of pancreatic somatostatin cells and somatostatin content in nesidiobiastosis, as compared with appropriate controls. Pancreatic tissue from five babies with severe hypoglycemie, hyperinsulinemia, and nesidiobiastosis was examined for insulin, somatostatin, and glucagon by immunocytochemistry and radioimmunpassay. There was a variable insulin cell hyperplasia among the nesidioblastotic specimens but no significant difference from controls was detected. In contrast, there was a consistent and highly significant ( P < 0.02) decrease (of more than 50%) of somatostatin cells (controls, 1.29 ± 0.22%; nesidiobiastosis, 0.53 ± 0.14%, mean ± SEM). Similarly, there was no significant alteration in insulin content, although a slight increase was found in non-microadenomatous areas of the diseased pancreata (controls, 42.3 ± 4.1; nesidiobiastosis, 58.6 ± 9.4 nmol/g wet weight of tissue, mean ± SEM). However, somatostatin content was almost 60% below control values (controls, 0.365 ± 0.038; nesidiobiastosis, 0.16 ± 0.039 nmol/g), a statistically significant difference ( P < 0.01). Thus, a marked reduction in the content of somatostatin was present in the pancreata of these infants with nesidiobiastosis, resulting in a distinct alteration of the normal pancreatic hormone balance.