Title: Fetal Risks of Maternal Diabetes
Volume: 3
Issue: 3
Author(s): Mikko Loukovaara, Sture Andersson, Vedran Stefanovic and Kari Teramo
Affiliation:
Keywords:
Diabetes mellitus, fetal hypoxia, fibroblast growth factor-2, insulin-like growth factor, leptin, macrosomia
Abstract: Diabetes mellitus is a growing problem globally. Similarly, the number of diabetic pregnancies can be expected to grow. Maternal diabetes increases the risk for congenital malformations, respiratory distress syndrome, and metabolic derangements in the newborn. Maternal diabetes also appears to predispose the offspring to the development of type 2 diabetes. Macrosomia, i.e. excessive growth of the fetus, is probably the most essential problem in diabetic pregnancies in the perinatal period. Macrosomia increases the risk for chronic fetal hypoxia, which may explain the increased occurrence of stillbirth in diabetic pregnancies during the third trimester. In addition, macrosomia increases the risk for shoulder dystocia, which can result in brachial plexus injury and permanent impairment of the function of the arm. The biochemical mechanisms by which maternal diabetes stimulates fetal growth are complex. According to a classical hypothesis, maternal hyperglycemia causes hyperglycemia in the fetus. This increases the secretion of insulin, which acts as the primary anabolic hormone of fetal growth. Moreover, the insulin-like growth factor system, fibroblast growth factor-2 and leptin may play a role in the regulation of intrauterine growth. The risks associated with maternal diabetes emphasize close pregnancy surveillance especially during the third trimester.
