Effects of gestational diabetes on fetal oxygen and glucose levels in vivo.

OBJECTIVE: Fetal hypoxia and acidemia have been reported in pregestational diabetic pregnancies in relation to poor glycaemic control, but it is still uncertain whether this is the case in apparently well-controlled gestational diabetes. POPULATION AND METHODS: Maternal arterial and umbilical venous and arterial blood samples were collected from 37 normal (N) and 38 pregnancies complicated by gestational diabetes (GDM) at the time of caesarean section. MAIN OUTCOME MEASURES: Respiratory gases, acid-base balance, lactate and glucose concentrations were measured. RESULTS: Both fetal and placental weights were significantly increased in GDM compared to N pregnancies, despite similar gestational age. Maternal biochemical parameters were similar in N and GDM but GDM fetuses were significantly more hypoxic (O2 saturation: N 63.2+/-13.9; GDM 53.8+/-14.6%, P<0.01; O2 content: N 5.5+/-1.4; GDM 4.8+/-1.2 mmol/l, P<0.05). Glucose (N 3.4+/-0.5, GDM 3.9+/-1.2 mmol/l, P<0.05) and lactate (N 1.32+/-0.49; GDM 1.64+/-0.75 mmol/l, P<0.05) concentrations were significantly increased in the umbilical vein in GDM compared to N fetuses. Placental histology was consistent with altered villous morphology. CONCLUSIONS: Our data indicate that fetuses from gestational diabetic mothers have increased umbilical glucose concentrations despite normal maternal glucose levels and a reduction in oxygen saturation and O2 content together with increased lactate concentration, reflecting altered fetal metabolism. These data suggest that 'good maternal metabolic control' achieved by currently used methods of monitoring glucose control is not sufficient to ensure a normal oxygenation status and metabolic milieu for the fetus in GDM pregnancies.

Flexible treatment of gestational diabetes modulated on ultrasound evaluation of intrauterine growth: a controlled randomized clinical trial.

OBJECTIVES: In order to prevent abnormalities of fetal growth still characterizing pregnancies complicated by Gestational Diabetes (GDM), in the present study we evaluated a therapeutic strategy for GDM based on ultrasound (US) measurement of fetal insulin-sensitive tissues. METHODS: All GDM women diagnosed before 28th week immediately started diet and self-monitoring of blood glucose; after 2 weeks they were randomized to conventional (C) or modified (M) management. In C the glycemic target (GT) was fixed at 90 fasting/120 post-prandial mg/dl; in M GT varied, according to US measurement of the Abdominal Circumference (AC) centile performed every 2 weeks: 80/100 if AC > or =75th, 100/140 if AC<75th. Therapy was tailored to mean fasting (FG) and postprandial glycemia (PPG). RESULTS: Globally, 229 women completed the study, 78 in C, 151 in M. Use of insulin was 16.7% in C, 30.4% in M (total groups), significantly more frequent in M than in C (59.7% vs 15.4%) when considering only women with AC > or =75th c. Mean metabolic data were similar in the 2 groups, but in M a tightly-optimized subgroup, resulting from the lowering of GT due to AC > or =75th, coexisted with a less-controlled one, whose higher GT was justified by AC<75th. Pregnancy outcome was better in M, with lower (p<0.05*) rate of LGA* (7.9% vs 17.9%), SGA (6.0% vs 9.0%) and Macrosomia* (3.3% vs 11.5%). CONCLUSIONS: Our data show the value of a flexible US-based approach to the treatment of GDM. This model does not necessarily involve a generalized aggressive treatment, allowing to concentrate therapeutical efforts on a small subgroup of women showing indirect US evidence of fetal hyperinsulinization. Such a selective approach allowed to obtain a near-normalization of fetal growth, with clear advantages on global pregnancy outcome.

Foetal and placental weights in relation to maternal characteristics in gestational diabetes.

An increased placental weight has been reported in pregnancies complicated with gestational diabetes (GDM). We have analysed foetal (F) and placental weight (P) and foetal length in 143 consecutive normal (N) and 132 GDM pregnancies in relation to type of treatment and to a number of maternal variables. All N pregnancies had a negative oral glucose challenge test at 24-28 weeks. GDM was diagnosed at 28-32 weeks by a 100-gm, 3-h oral glucose tolerance test (OGTT). Treatment was diet (D: n=82) or diet plus insulin (D+I: n=50) according to self-monitoring of blood glucose. A significant difference was observed between N and GDM pregnancies for maternal age (N=30.6+/-5.38 years; GDM=33.2+/-4.53 years; P< 0.001), pre-pregnancy weight (N=58.2+/-8.0 kg; GDM=63.0+/-12.9 kg; P< 0.001) and BMI (N= 21.9+/-2.63; GDM=24.4+/-4.71;P< 0.001). Foetal weight became significantly higher in the GDM group (N=3274.2+/-296.0 g; GDM=3287.1+/-474.1g; P< 0.05) once correction was made for the significant difference in gestational age between the two groups (N=39.4+/-1.17 weeks; GDM=38.8+/-1.39 weeks; P< 0.001). Significantly higher placental weights (N=561.87+/-91.0 g; GDM=592.2+/-115.8 g;P< 0.01) and significantly lower F/P weight ratios were found in GDM pregnancies (N=5.96+/-1.02; GDM=5.69+/-1.13; P< 0.05). In GDM pregnancies a significantly negative correlation was found between the OGTT response and weights of foetus and placentae at delivery, suggesting that both foetal and placental growth are affected by maternal insulin resistance.