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Our purpose was to investigate the relationship between fetal pancreatic beta-cell function and fetal acidemia and macrosomia in pregnancies complicated by maternal diabetes mellitus.A cross-sectional study at the Harris Birthright Research Centre for Fetal Medicine, London, was performed. In 32 pregnancies complicated by maternal diabetes mellitus cordocentesis was performed at 36 to 39 weeks' gestation for the measurement of umbilical venous blood pH, PO2, PCO2, lactate, and glucose concentration; plasma insulin immunoreactivity; and insulin/glucose ratio. A reference range for plasma insulin and insulin/glucose ratio was constructed by studying fetal blood samples from 80 women who did not have diabetes mellitus.Mean umbilical venous blood pH was significantly lower and plasma insulin immunoreactivity and insulin/glucose ratio were significantly higher than the appropriate normal mean for gestation. There were significant associations between (1) maternal and fetal blood glucose concentrations (r = 0.95, p0.0001), (2) fetal blood glucose and plasma insulin immunoreactivity (r = 0.57, p0.01), (3) fetal plasma insulin immunoreactivity and blood pH (r = -0.39, p0.05), and (4) fetal insulin/glucose ratio and degree of macrosomia (r = 0.76, p0.0001).Fetal pancreatic beta-cell hyperplasia is implicated in the pathogenesis of both fetal acidemia and macrosomia.

Objective To determine whether computer assisted fetal heart rate analysis or the biophysical profile score can provide noninvasive prediction of fetal acidaemia. Design Cross sectional study. Setting Harris Birthright Research Centre for Fetal Medicine, King's College Hospital School of Medicine, London. Subjects Forty-one women with pregnancies complicated by diabetes mellitus. Interventions Fetal heart rate (FHR) monitoring with computer assisted analysis, biophysical profile score (BPS) and cordocentesis for measurement of umbilical venous blood glucose concentration and blood gases, up to 24 h before delivery at 27 to 39 weeks gestation. Results The mean umbilical venous blood pH was significantly lower than the normal mean for gestation, and was below the 5th centile in 18 pregnancies, including all six cases where the mother had nephropathy and hypertension. The mean pO2 was not significantly different from the normal mean for gestation. There were significant associations between fetal acidaemia and both the BPS (r= 0.46, P

Objective: Our purpose was to investigate placental and fetal circulation in pregnancies complicated by maternal diabetes mellitus and to relate any changes to fetal blood pH, P O 2 , and hematocrit. Study design: Doppler measurements of both uterine arteries, one umbilical artery, the fetal descending thoracic aorta, and one fetal middle cerebral artery were performed in 65 well-controlled diabetic pregnancies in a cross-sectional study at the Harris Birthright Research Centre for Fetal Medicine, London. In 41 cases cordocentesis was also performed for the measurement of umbilical venous blood pH, P O 2 , and hematocrit. Results: The mean umbilical venous blood pH was significantly lower and the hematocrit significantly higher than the appropriate normal mean for gestation. However, the Doppler indices of the placental and fetal circulations were essentially normal, except in some of the cases complicated by preeclampsia or intrauterine growth retardation. Conclusions: Maternal diabetes mellitus is not associated with abnormalities in Doppler indexes of the placental or fetal circulations.

Objective: Our purpose was to investigate the relationship between fetal plasma erythropoietin concentration and measures of short-term and long-term glycemic control and fetal oxygenation in pregnancies complicated by maternal diabetes mellitus. Study Design: A cross-sectional study was performed at The Harris Birthright Research Centre for Fetal Medicine, London. Cordocentesis was performed in 31 diabetic pregnancies for the measurement of umbilical venous blood pH, Po 2 , Pco 2 , lactate and glucose concentration, erythroblast count, hemoglobin, and plasma erythropoietin concentrations. Results: The mean pH was significantly lower and the Pco 2 , lactate, erythropoietin, hemoglobin, and erythroblast counts were significantly higher than the appropriate normal mean for gestation. There were significant associations betwen (1) fetal erythropoietin and erythroblast count, (2) fetal erythroblast count and hemoglobin, (3) fetal hemoglobin and maternal glycosylated hemoglobin, and (4) maternal glucose and fetal glucose, pH, and lactate. Conclusions: We postulate that maternal hyperglycemia causes fetal hyperglycemia and acidemia. Increased erythropoietin may be caused by tissue hypoxia or hyperinsulinemia. The increase in fetal hemoglobin may be the consequence of increased erythropoiesis, mediated by either erythropoietin or hyperinsulinemia.

OBJECTIVES: Our objectives were to determine in pregnancies complicated by diabetic nephropathy (1) if impedance to flow in the uterine and umbilical arteries is normal and (2) if these fetuses are hypoxemic and acidemic and if they have decreased fetal heart rate variation and Doppler blood flow redistribution. STUDY DESIGN: In a cross-sectional study at the Harris Birthright Research Centre for Fetal Medicine, London, serial assessment of fetal heart rate variation and Doppler velocimetry of the placental and fetal circulations was undertaken in six pregnancies complicated by diabetic nephropathy. In all cases cordocentesis was performed within 24 hours before delivery for the measurement of umbilical venous blood gases. RESULTS: Cordocentesis demonstrated these fetuses to be hypoxemic and acidemic. The fetal heart rate variation was decreased; however, impedance to flow in the uterine artery was normal, and increased impedance to flow in the umbilical artery with evidence of blood flow redistribution was observed in only one case. CONCLUSIONS: Fetal hypoxemia and acidemia in pregnancies complicated by diabetic nephropathy is not a consequence of impaired placental perfusion, and the degree of metabolic derangement may be obscured by the apparent normal growth and failure of these fetuses to demonstrate blood flow redistribution.