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Unique brain anomalies in an infant of a diabetic mother
B G Kousseff1, C Villaveces, C R Martinez
1Department of Pediatrics, University of South Florida, Tampa.
An offspring of a class F diabetic primigravida with marginal control during the first 8 weeks of the gestation had a level II sonogram at 23 weeks. It showed polyhydramnios and "hydrocephaly." Macrosomia, right hydroureter, megacystis and premature birth corroborated the diagnostic impression of diabetic embryopathy. At age 3 years, the child functions within the moderate range of mental retardation. Angiography, choanogram, CT and MRI scans showed unique CNS abnormalities that appeared secondary to a hamartomatous growth within the left cerebral hemisphere. Such anomaly, most likely a part of the phenotype of the diabetic embryopathy, implies a growth disturbance secondary to dysregulated paracrine growth factors (somatomedins, nerve growth factor, panregulin and/or their receptors in this case). It also indicates a possibility of interaction between two dysregulated major growth mechanisms; the endocrine in the mother considered responsible for the overall phenotype of the diabetic embryopathy/fetopathy and the paracrine fine tuning mechanism in the embryo incriminated by the hamartomatous over/undergrowth.
An offspring of a class F diabetic primigravida with marginal control during the first 8 weeks of the gestation had a level II sonogram at 23 weeks. It showed polyhydramnios and "hydrocephaly." Macrosomia, right hydroureter, megacystis and premature birth corroborated the diagnostic impression of diabetic embryopathy. At age 3 years, the child functions within the moderate range of mental retardation. Angiography, choanogram, CT and MRI scans showed unique CNS abnormalities that appeared secondary to a hamartomatous growth within the left cerebral hemisphere. Such anomaly, most likely a part of the phenotype of the diabetic embryopathy, implies a growth disturbance secondary to dysregulated paracrine growth factors (somatomedins, nerve growth factor, panregulin and/or their receptors in this case). It also indicates a possibility of interaction between two dysregulated major growth mechanisms; the endocrine in the mother considered responsible for the overall phenotype of the diabetic embryopathy/fetopathy and the paracrine fine tuning mechanism in the embryo incriminated by the hamartomatous over/undergrowth.