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Abstract Ref Number = APCP26
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Detection of Persistent Hypoglycemia in Newborns
Francesco Chiarelli Department of Pediatrics, University of Chieti, Italy
Hypoglycemia is commonly detected after birth in healthy newborns, representing a progressive adaptation to postnatal life and the need of promptly available source of energetic fuel. Glucose, like oxygen, is of fundamental importance for any living being and it is the major energy source for the fetus and the neonate during gestation. The placenta ensures a steady supply of glucose to the fetus, while birth marks a sudden change in substrate delivery and a major change in metabolism. Hypoglycemia is one of the most common pathologies encountered in the neonatal intensive care unit and affects a wide range of neonates. A universal definition of neonatal hypoglycemia by using a standardized cutoff number remains so far controversial. Persistent hypoglycemia might be the consequence of vital prenatal mechanisms involved in fetal regulation of glucose metabolism. Infants present peculiarity in glucose metabolism that may harm a glucose-dependent tissue such as the brain. Nevertheless, signs and symptoms of hypoglycemia are often blurred and nonspecific. Etiology of persistent hypoglycemia includes several endocrine and metabolic disorders: hyperinsulinism, growth hormone and adrenal gland defects, IUGR/SGA or LGA newborns, maternal diabetes or inborn errors of metabolism. Preterm, small for gestational age (GA) and intra-uterine growth restricted neonates are especially vulnerable due to their lack of metabolic reserves and associated co-morbidities. Hence, an accurate clinical evaluation and laboratory tests may help to guide diagnosis when a seeming transient hypoglycemia persists despite appropriate treatment. Symptomatic hypoglycemia or persistent albeit asymptomatic hypoglycemia must be promptly treated, reaching a safer glucose target. Pancreatic β cells are functionally programmed to release insulin in response to changes in plasma glucose concentration. Insulin secretion is precisely regulated so that, under normal physiological conditions, fasting plasma glucose concentrations are kept within a narrow range of 3•5-5•5 mmol/L. In hyperinsulinaemic hypoglycaemia, insulin secretion becomes dysregulated (ie, uncoupled from glucose metabolism) so that insulin secretion persists in the presence of low plasma glucose concentrations. Hyperinsulinaemic hypoglycaemia is the most common cause of severe and persistent hypoglycaemia in neonates and children. At a molecular level, mutations in nine different genes can lead to the dysregulation of insulin secretion and cause this disorder. Rapid diagnosis and prompt management of hyperinsulinaemic hypoglycaemia is essential to avoid hypoglycaemic brain injury, especially in the vulnerable neonatal and childhood periods. Advances in the field of hyperinsulinaemic hypoglycaemia include use of rapid molecular genetic testing for the disease, application of novel imaging techniques (6-[fluoride-18]fluoro-levodopa [18F-DOPA] PET-CT and glucagon-like peptide 1 (GLP-1) receptor imaging), and development of novel medical treatments (eg, long-acting octreotide formulations, mTOR inhibitors, and GLP-1 receptor antagonists) and surgical therapies (eg, laparoscopic surgery).
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