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 g lucose and glycated haemoglobin (HbAlc) and infant size at birth in pr egestational diabetes. Design Longitudinal study from 6 to 14 weeks ge station. Women were treated intensively with insulin, aiming at normog lycaemia but avoiding hypoglycaemia. Blood glucose was determined six times daily, HbAlc every four weeks. Individual mean fasting and postp randial glucose levels were calculated for three-week periods of gesta tion. Birthweight > 2 SD or within +/- 2 SD for gestational age and ge nder was classified as large (LGA) or appropriate (AGA), respectively. Birthweight ratio was calculated as the ratio of birthweight to norma l mean birthweight after correction for gestational age and gender. Pa rticipants One hundred and thirteen consecutive pregnant women with pr egestational diabetes and their newborn infants. Results Perinatal mor tality was nil, the rates of spontaneous preterm delivery (8.9%) and s evere 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 s ignificantly and independently associated with pre-pregnancy bodyweigh t (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). HbAlc correlated with glucose levels but was unrelated to birthweight ratio. The fasting glucose lev el between weeks 30 and 32 was significantly interrelated with the fas ting glucose level from each of the six preceding three-week periods. Conclusion Near normoglycaemia cannot be obtained in all patients, pre sumably due to intrinsic differences in glucoregulatory ability betwee n individuals. The incidence of LGA infants was unexpectedly high. The modest abnormality in glycaemic control in mothers with LGA infants c ould only partly explain fetal oversize, suggesting that other factors must be implicated to explain fetal growth acceleration.