HISTOCHEMICAL, CLINICAL, AND IN-VITRO BETA-CELL RESPONSES IN A NEONATE WITH PERSISTENT HYPERINSULINEMIC HYPOGLYCEMIA OF INFANCY

When treatment with diazoxide and somatostatin for persistent hyperins ulinaemic hypoglycaemia of infancy failed, subtotal pancreatectomy was performed on a neonate on day 41. The pancreatic tissue was saved and used for immunohistochemical and cell culture studies. The initial im munohistochemistry of beta cells for insulin was negative, using a 1 i n 200 dilution of insulin antiserum, but positive results were obtaine d with an increased concentration of the antiserum. The insulin to som atostatin cell ratio in islets of Langerhans was about 1:1, with no so matostatin cells outside the islets. Glucose stimulated insulin secret ion in a concentration dependent manner in vitro. Isobutyl methyl xant hine doubled insulin secretion, but lithium had no effect. The glucose stimulated insulin secretion was inhibited by somatostatin, epinephri ne, and in the absence of Ca2+. In view of the normal in vitro respons es of beta cells to various secretory analogues, the lack of responsiv eness to somatostatin analogue before pancreatectomy may not have been due to deficiency or resistance to somatostatin, but to beta cell hyp erplasia overwhelming the paracrine regulatory mechanism(s).