ABSTRACT
The morbidity and subsequent development of the infant of the diabetic mother is associated with hyperglycemia. Therefore, the goal of insulin therapy is to achieve and maintain normoglycemia before, during, and after all pregnancies complicated by diabetes. The fetal demise associated with pregnancy complicated by type 1 diabetes seems to arise from glucose extremes. Although controversial, the rate of complications in pregnancies of diabetic women has been tied to the metabolic control of maternal glucose. Perhaps the debate remains because some reports claim that neonatal complications occur in spite of excellent metabolic control, although they fail to measure postprandial glucose levels. Anti-insulin antibodies that cross the placenta may contribute to hyperinsulinemia in utero and thus potentiate the metabolic aberrations in the fetus. There are three situations in life in which rapid normalization of blood glucose levels increase the risk for deterioration of diabetic retinopathy: puberty, pregnancy, and rapid normalization of blood glucose levels.
