Abstract

The definition of neonatal hypoglycemia is controversial. Operational thresholds of blood glucose values at which intervention should be considered have been proposed. IDM and GDM infants frequently exhibit a pronounced drop of plasma glucose immediately after birth. This exaggerated physiological decline of glucose is transient and is seldom accompanied by suppressed lipolysis or clinical symptoms. It is generally attributed to hyperinsulinism elicited by maternal hyperglycemia. Alternative substrates for CNS i.e. lactate and astrocyte glycogen may explain lack of symptoms. Similarly low glucose values later on may cause clinical symptoms. Glucose production rates vary from attenuated to normal likely reflecting differences in maternal glycemic control. The HAPO study of around 25,000 non-diabetic pregnancies revealed strong associations between glucose values (75g OGTT) and increased fetal size and hyperinsulinemia at birth - findings adding strong support to the maternal hyperglycemia - fetal hypinsulinism theory. Mothers with the highest fasting glucose had infants with the highest frequency of clinical neonatal hypoglycaemia (4,6%).

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