• S Grasso and G D Roversi.
• J Perinat Med. 1987 Jan 1; 15 (1): 73-82.

AbstractIn this study the birth weights of 431 infants of diabetic mothers of the Milan series have been compared with the birth weights of infants of a control group. The averages and the centile distributions of weights of infants of gestational diabetic mothers (Class A) and of diabetic mothers without vascular complications (Classes B and C) did not differ substantially from those of control newborns (table I, figure 1). This confirms the clinical indication, based on the hyperglycemia-hyperinsulinism theory that fetal macrosomia can be prevented provided maternal metabolism is strictly controlled. In this series insulin was administered at the maximal tolerated dose (MTD), a therapeutic regimen that provides excellent metabolic control of the mother. In multiparae, the birth weights of the infants of the latest pregnancy were drastically lower than the birth weights of the infants in their previous pregnancies (without MTD insulin) (table II). Our results do not confirm the recent hypothesis that pregnant diabetics with strict metabolic control during pregnancy generally give birth to growth retarded infants. The MTD of insulin has also been administered to gestational diabetic mothers, and fetal macrosomia was prevented (table I, figure 1). This confirms the opinion of those who believe that a diet-regimen must be accompanied by insulin administration to correct the slight metabolic abnormality of these patients. As would be expected because of placental insufficiency, infants of patients with vascular complications, including those who have only calcifications of the pelvic vessels (White' Class E), were growth retarded (table I, figure 1). The risk of fetal growth retardation in Class E has not been remarked upon in the literature, since pathology of pelvic vessels is usually disregarded and the patients remain undifferentiated among Classes A-C. The possibility to prevent fetal macrosomia with a strict control of maternal diabetes has been questioned because of the lack of correlation between fetal macrosomia and the degree of maternal hyperglycemia and of fetal hyperinsulinism. We postulate that, if fetal hyperinsulinism causes hypoxia, as it does in experimental animals, the lack of correlation may be due to the fetal hyperinsulinism itself.

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