Fetal size at birth in relation to quality of blood glucose control in pregnancies complicated by pregestational diabetes mellitus.

OBJECTIVE

To determine the relation between maternal levels of blood glucose and glycated haemoglobin (HbA1c) and infant size at birth in pregestational diabetes.

DESIGN

Longitudinal study from 6 to 14 weeks gestation. Women were treated intensively with insulin, aiming at normoglycaemia but avoiding hypoglycaemia. Blood glucose was determined six times daily, HbA1c every four weeks. Individual mean fasting and postprandial glucose levels were calculated for three-week periods of gestation. Birthweight > 2 SD or within +/- 2 SD for gestational age and gender was classified as large (LGA) or appropriate (AGA), respectively. Birthweight ratio was calculated as the ratio of birthweight to normal mean birthweight after correction for gestational age and gender.

PARTICIPANTS

One hundred and thirteen consecutive pregnant women with pregestational diabetes and their newborn infants.

RESULTS

Perinatal mortality was nil, the rates of spontaneous preterm delivery (8.9%) and severe maternal hypoglycaemia (4.4%) were low. Mothers with LGA infants (26%) had a significantly higher fasting glucose between weeks 27 and 32 than mothers of AGA infants (P < 0.01). Relative birthweight was significantly and independently associated with pre-pregnancy bodyweight (r = 0.24, P < 0.05) and fasting glucose at weeks 27 to 29 (r = 0.27, P < 0.01) but together could only explain 12.3% of the variation in birthweight (mult. r = 0.35, P < 0.01). HbA1c correlated with glucose levels but was unrelated to birthweight ratio. The fasting glucose level between weeks 30 and 32 was significantly interrelated with the fasting glucose level from each of the six preceding three-week periods.

CONCLUSION

Near normoglycaemia cannot be obtained in all patients, presumably due to intrinsic differences in glucoregulatory ability between individuals. The incidence of LGA infants was unexpectedly high. The modest abnormality in glycaemic control in mothers with LGA infants could only partly explain fetal oversize, suggesting that other factors must be implicated to explain fetal growth acceleration.