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Aim: Poor glucose control is associated with adverse outcomes in pregnancies with pre-existing diabetes. However, strict glucose control increases the risk of severe hypoglycaemia, particularly in the first trimester. Therefore, we aimed to investigate whether less tight glucose control in the first trimester determines adverse outcomes or can be compensated for by good control in late pregnancy., Methods: Retrospective data were collected from 517 singleton pregnancies complicated by pre-existing diabetes delivering between 2010 and 2017. Three hundred and thirty-six pregnancies fulfilled the inclusion criteria of having available HbA 1c values either pre-conception or in the first trimester (65% type 1 diabetes, 35% type 2 diabetes)., Results: Higher HbA 1c values in the first trimester were associated with increasing rates of large for gestational age (LGA) neonates, preterm delivery or neonatal intensive care unit admissions. Multiple regression analysis demonstrated third trimester HbA 1c , type 1 diabetes, multiparity and excess weight gain, but not first trimester HbA 1c , to be independently predictive for LGA. Pre-eclampsia and third trimester HbA 1c increased the risk for preterm delivery. If HbA 1c was ≤ 42 mmol/mol (6.0%) in the third trimester, rates of adverse outcomes were not significantly higher even if HbA 1c targets of ≤ 48 mmol/mol (6.5%) had not been met in the first trimester. Good first trimester glucose control did not modify the rates of adverse outcomes if HbA 1c was > 42 mmol/mol (6.0%) in the third trimester., Conclusions: Less tight glycaemic control, for example due to high frequency of severe hypoglycaemia in the first trimester, does not lead to increased adverse neonatal events if followed by tight control in the third trimester. Besides glycaemic control, excess weight gain is a modifiable predictor of adverse outcome., (© 2020 Diabetes UK.)

Aims: To compare glycaemic control, maternal and neonatal outcomes in pregnancies with Type 1 diabetes, managed either by continuous subcutaneous insulin infusion, multiple daily insulin injection or switch from multiple daily insulin injection (MDI) to continuous subcutaneous insulin infusion (CSII) in early pregnancy., Research Design and Methods: Data from 339 singleton pregnancies were retrospectively reviewed. HbA 1c values were measured preconception and in each trimester. In a secondary analysis, use of CSII pre-pregnancy was compared with initiation of CSII during pregnancy., Results: MDI was used in 140 pregnancies (41.3%) and CSII was used in 199 (58.7%), including 34 pregnancies (10.0%) during which the women switched to CSII. In pregnancies during which CSII was used duration of diabetes [median (interquartile range) 16.0 (8.0-23.0) years vs 11.0 (5.5-17.5) years; P<0.001] was longer, and the Institute of Medicine recommendations for appropriate weight gain were exceeded more often (64.8% vs. 50.8%; P=0.01). CSII use and pre-pregnancy BMI were independent predictors of excess weight gain. There was no difference in glucose control, but CSII was associated with higher birth weight [median (interquartile range) 3720 (3365-4100) g vs 3360 (3365-4100) g; P<0.001] and higher large-for-gestational-age (LGA) rate (44.7% vs. 33.6%; P=0.04) than MDI. HbA 1c concentration in the third trimester and excess weight gain were predictive of LGA infants [odds ratio 2.33 (95% CI 1.54-3.51); P<0.001 and 1.89 (95% CI 1.02-3.51); P=0.04]. In pregnancies where CSII therapy was initiated in the first trimester and in those with pre-pregnancy use, similar glucose control and outcome was achieved., Conclusions: There was no advantage of CSII with respect to glycaemic control and neonatal outcomes. The rate of LGA neonates was higher in the CSII group, possibly mediated by excess maternal weight gain, which was more frequent than in women treated with MDI., (© 2019 Diabetes UK.)

Aims: To evaluate the potential contribution of maternal glucose and lipids to fetal metabolic variables and growth in pregnancies with normal glucose tolerance in comparison with pregnancies with well-controlled gestational diabetes previously reported by us., Methods: In 190 pregnancies with normal oral glucose tolerance tests (controls), insulin, glucose and lipid components were determined in maternal and arterial cord blood serum. Birthweight and neonatal fat mass were obtained after delivery. Values were adjusted for maternal pre-pregnancy BMI, Caesarean section and gestational age. Measurements were compared with those of gestational diabetes previously reported., Results: Maternal serum glucose, triacylglycerol, free fatty acid and cholesterol levels did not differ between control pregnancies and those with gestational diabetes, whereas insulin, homeostasis model assessment and glycerol values were significantly lower in the former (2.6 vs. 5.6 μmol/l and 176 vs. 193 μmol/l, respectively). In contrast, cord blood glucose and free fatty acids were significantly lower in control pregnancies than in those with gestational diabetes (3.9 vs. 4.4 mmol/l and 80.7 vs. 137 μmol/l, respectively); the same was valid for insulin (0.03 vs. 0.05 nmol/l) and homeostasis model assessment (1.0 vs. 1.87). In control pregnancies, maternal serum glucose, free fatty acids and glycerol correlated with those in cord blood, but not with neonatal weight and fat mass, as seen for free fatty acids in those with gestational diabetes. The negative correlation between cord blood triacylglycerols and neonatal weight or fat mass previously reported in gestational diabetes could not be confirmed in control pregnancies, where all fetal lipids showed a positive correlation to neonatal anthropometrics., Conclusion: In normal pregnancies, in contrast to those with gestational diabetes, maternal lipids do not influence neonatal weight. Similar levels of maternal lipids in pregnancies with gestational diabetes and control pregnancies, but higher free fatty acids in the cord blood of those with gestational diabetes, indicate their enhanced placental transport and/or enhanced lipolysis as a result of decreased fetal insulin responsiveness., (© 2011 The Authors. Diabetic Medicine © 2011 Diabetes UK.)