A longitudinal study comparing growth in diabetic pregnancies with growth in normal gestations: I. The fetal weight.

Diabetes mellitus is associated with fetal growth acceleration and retardation. These aberrations in fetal growth seem to be influenced by a variety of factors including vascular disease, glycemic control, hypertension and smoking. In order to characterize fetal growth under the above conditions, longitudinal sonographic evaluations were performed in 52 pregnant, insulin-dependent diabetic women with the usual monitoring of the patients' metabolic control. Regression analyses revealed that vascular disease and glycemic conditions were the most important influences for growth, with manifestation beyond the second trimester. With stringent glucose control (mean whole blood less than or equal to 100 mg/dl) in the absence of vasculopathy (white classes A, B, C), fetal growth was similar to that in normal pregnancies. In the presence of vasculopathy (white classes D and FR), growth was reduced, especially when near-normal glycemic levels were achieved. Conversely, in poorly controlled diabetic women, enhanced fetal growth were observed in patients with and without vasculopathy. No aberrations in fetal growth were observed, however, before the third trimester. The findings of our study demonstrate that vasculopathy and glycemia are dominant and independent regulators of fetal growth. However, their influences are not manifested in growth changes before the third trimester.

Sonographic assessment of growth of the fetal head in diabetic pregnancies compared with normal gestations.

A longitudinal ultrasound study was conducted in 45 insulin-dependent diabetic patients who maintained good glycemic control (mean plasma glucose less than 120 mg/dl) throughout most of their pregnancy in order to assess growth of the fetal head in the presence of euglycemia. Patients with and without vasculopathy were found to be comparable with regard to their glycemic control, medical and obstetric complications, as well as incremental growth and the velocity of growth of the fetal biparietal diameter (BPD). When compared with the control group, the velocity of growth of the BPD was not significantly different throughout pregnancy. However, the actual increment in BPD growth remained less than that of the control fetuses, especially during the second trimester when a significant statistical difference was found. Possible explanations may include delayed ovulation, reduced growth velocity in the first trimester, or constitutionally smaller embryos among the diabetic group. The pattern of BPD growth among diabetics was best described by a third degree polynomial regression equation. These results demonstrate that in well-controlled diabetics, although the increment in BPD was less than controls, the growth pattern of the fetal BPD was similar among the White classes B to FR, and the velocity of growth of the BPD was similar among diabetics and nondiabetics.