Disorders of glucose homeostasis The presence of neonatal hypoglycemia or hyperglycemia signals a failure of the normal transition from fetal to postnatal patterns of glucose homeostasis. Under normal conditions, glucose from maternal circulation is transported across the placenta via specific glucose transporters to be used by the fetus. The high fetal insulin : glucagon ratio suppresses glycogenolysis and gluconeogenesis and stimulates hepatic glycogen deposition during late gestation. At delivery, glucose delivery to the infant stops abruptly. Until an exogenous supply of substrate is provided, the infant must rely on hepatic glucose production to meet metabolic needs. Both glycogenolysis and gluconeogenesis contribute to glucose homeostasis during the first few days of extrauterine life. However, hepatic glucose production via these two pathways requires availability of glycogenand gluconeogenic precursors, appropriate levels and activity of hepaticenzymes necessary for glycogenolysis and gluconeogenesis, and anormalendocrine response. The absence of any of these components may result in neonatal hypoglycemia or hyperglycemia. Hypoglycemia Incidence and clinical presentation The reported incidence of neonatal hypoglycemia varies depending on the population studied, the method used for glucose measurement, and the definition of hypoglycemia used. In appropriate-for-gestational-age (AGA) term infants the incidence ranges from 5%-30%,1-4but may be as high as 50% in preterm infants,5, 6and 70% in small-for-gestational-age (SGA) infants.7-10Clinical signs of hypoglycemia are nonspecific and may include lethargy, jitteriness, poor feeding, seizures, and temperature disturbances. The frequency of observation of the most common findings is listed in Table 31.1.
|Original language||English (US)|
|Title of host publication||Neonatal Nutrition and Metabolism, Second Edition|
|Publisher||Cambridge University Press|
|Number of pages||12|
|ISBN (Print)||9780511544712, 0521824559, 9780521824552|
|Publication status||Published - Jan 1 2006|
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