Hypoglycemia in the neonate.

After a brief history of the development of neonatal hypoglycemia, this review emphasizes the current approach to the anticipation, diagnosis, and management of the neonate with a low plasma glucose concentration. Current techniques for studying the neurophysiological and endocrine-metabolic effects of significant hypoglycemia provide new approaches for establishing relevant definitions of significant hypoglycemia, its prognosis, and pathogenesis. The inadequacy of glucose oxidase strips for screening, the definition of high-risk infants, new definitions for low plasma glucose concentrations, and their treatment are presented as well as the ability of the neonate to respond to significantly low glucose values.

Controversies regarding definition of neonatal hypoglycemia: suggested operational thresholds.

The definition of clinically significant hypoglycemia remains one of the most confused and contentious issues in contemporary neonatology. In this article, some of the reasons for these contentions are discussed. Pragmatic recommendations for operational thresholds, ie, blood glucose levels at which clinical interventions should be considered, are offered in light of current knowledge to aid health care providers in neonatal medicine.

Neonatal hypoglycemia 30 years later: does it injure the brain? Historical summary and present challenges.

Since 1911, blood sugars have been measured in newborn infants. Significant neonatal hypoglycemia was first reported in 1937. In 1959, the report of transient symptomatic neonatal hypoglycemia generated worldwide reports.

An international symposium on neonatal hypoglycemia: thirty years later. Does it injure the neonatal brain?

A discussion of neonatal hypoglycemia was held on 18 November 1995 as a satellite symposium of the 40th Annual Meeting of Japan Society for Premature and Newborn Medicine and continued in closed session of 19 November to address neonatal hypoglycemia in the 21st century. This represented a 30-year follow-up of a discussion of carbohydrate and energy metabolism in the newborn held in Tokyo on 10 November 1965. This follow-up was prompted by the incredible advances in clinical care in perinatal medicine and in basic knowledge in the neurosciences, neonatal physiology and metabolism that have occurred in Japan and around the world throughout these 3 decades.

Hypoglycemia in the neonate.

After a brief history of the development of neonatal hypoglycemia, this review emphasizes the current approach to the anticipation, diagnosis, and management of the neonate with a low plasma glucose concentration. Both transient and recurrent or persistent hypoglycemia are discussed. Current techniques for studying the neurophysiologic and endocrine-metabolic effects of significant hypoglycemia provide new approaches for establishing relevant definitions of significant hypoglycemia, its prognosis, and pathogenesis.

Familial hyperproinsulinemia due to a proposed defect in conversion of proinsulin to insulin.

Familial hyperproinsulinemia is a genetic disorder characterized by elevated plasma levels of proinsulin-like material. In two previously described kindreds this has been shown to be due to a structural abnormality in the proinsulin molecule. We have identified a third family with hyperproinsulinemia in which there appeared to be a different defect.

The use of the plasma epinephrine response in the diagnosis of idiopathic postprandial syndrome.

Patients with idiopathic postprandial syndrome (IPS) report recurrent postprandial episodes that resemble the clinical manifestations of hypoglycemia. In an effort to find objective criteria for diagnosis of IPS, we studied a group of patients with IPS and controls during an oral glucose tolerance test. Patients with IPS had a significantly lower mean glucose nadir and higher hypoglycemic index than controls.

Neonatal 'brain damage'-an analysis of 250 claims.

Advances in perinatal care have resulted in decreased neonatal mortality. Increasingly, damage in survivors has been attributed to alleged negligence. We analyzed the 250 claims (1957 to 1982) from one major insurance company for factors to characterize high-risk pregnancies and then to distinguish preventable from nonpreventable causes within the group.

Segmental hyperlucent defects in the liver.

When lucent defects in the liver have a segmental configuration, they may be on an ischemic basis and related to decreased vascular perfusion. Portal venous inflow, by virtue of its low pressure, is particularly susceptible to diversion by focal intrahepatic masses, intravenous thrombi, or external compression. Innovative operative techniques for tumor enucleation may also result in lucent defects that can be confused with, or conceal, pathology.

Influence of glycogen on liver density: computed tomography from a metabolic perspective.

The liver is a metabolically active organ with a radiographic density that can be modified by its glycogen and fat content. In rhesus monkeys an increase in liver glycogen induced by glucose loading was accompanied by an increase in attenuation values on computed tomography and a decrease in total liver fat. Conversely, fasting depleted glycogen, increased fat, and decreased liver attenuation.

Insulin receptors in the developing fetal lung.

Fetal lung insulin receptor numbers and affinities were studied in rat pregnancies from 15 to 22 days gestation. Insulin receptor binding capacities were found to increase six-fold from approximately 100 fmoles insulin bound/mg lung DNA at 15 days gestation to approximately 600 fmoles bound/mg DNA at 22 days gestation. However, the affinity constants of the receptors were unchanged during this same period (high affinity, 1.

Computed tomography of the liver and kidneys in glycogen storage disease.

Glycogen, in concentrations encountered in von Gierke's disease, has computed tomography (CT) attenuation coefficients in the 50 to 70 Hounsfield unit (HU: 1,000 scale) range and accounts for the increased density of the liver. However, in eight patients with Type I glycogen storage disease, simultaneous hepatic infiltration with fat and glycogen led to a range of liver CT densities from 13 to 80 HU. Fatty infiltration may facilitate the demonstration of hepatic tumors in older patients with this disease.

Increased 125I-insulin receptor binding to erythrocytes of hypoglycemic infants and children.

The measurement of 125I-insulin specific binding to erythrocytes obtained from seven infants and children with various hypoglycemic syndromes showed a significant increase in six patients with recurrent, documented, symptomatic hypoglycemia (percent specific 125I-insulin binding 9 to 14 versus 6.1 +/- 1.4% mean +/- 2 S.

Reciprocal regulation of glucose and glutamine utilization by cultured human diploid fibroblasts.

Human diploid fibroblasts utilize both glucose and glutamine as energy sources. The utilization of glutamine by fibroblasts is regulated by glucose, and vice versa. This conclusion is supported by the following observations: (1) essentially identical growth rates were observed in Eagle's minimum essential medium (MEM)3 in which the glucose concentration was either 5.

Effect of L-alanine infusion on gluconeogenesis and ketogenesis in the rat in vivo.

1. In 48 h-starved 6-week-old rats the 14C incorporation in vivo into blood glucose from a constant-specific-radioactivity pool of circulating [14c]actateconfirmed that lactate is the preferred gluconeogenic substrate. 2.

Hypoketonaemic effect of L-alamine. Specific decrease in blood concentrations of 3-hydroxybutyrate in the rat.

1. The injection of L-alanine (50-100 mg/kg) into 35-day-old rats that had been starveed for 48 h increased blood L-alanine concentration to values observed in fed animals and lowered the blood concentration of 3-hydroxybutyrate within 2 min. 2.

Effects of starvation and development on mitochondrial acetoacetyl-coenzyme A thiolase of rat liver.

The activity of the putative ketogenic beta-oxoacyl-CoA thiolase from mitochondria of rat liver increases with starvation, during neonatal life, and after the injection of glucagon. These changes are associated with alteration in ketonaemia. The changes in activities of this species of thiolase are not associated with significant alterations in the apparent affinity (Km) for the ketogenic substrate, acetyl-CoA.