Cho and colleagues (2016), analyzed more than 3000 Korean women who underwent a 50-g OGTT and found that neonates born to women with a screening result :200 mg/dL were 84 times more likely to have hypoglycemia than those born to women with a result < 140 mg/dL. he risk of neonatal hypoglycemia correlates with umbilical cord C-peptide levels. But, importantly, the risk also rises with birthweight, independent of a maternal diabetes diagnosis (Mitanchez, 2014).
Maternal Obesity. In women with gestational diabetes, maternal body mass index (BMI) is an independent and more substantial risk factor for fetal macrosomia than is glucose intolerance (Ehrenberg, 2004; Mission, 2013). Stuebe and associates (2012) completed a secondary analysis of women with either untreated mild gestational diabetes or normal glucose tolerance testing results. They found that higher BMI levels were associated with rising birthweight, regardless of glucose levels. In one analysis of more than 600,000 pregnant women, gestational diabetes, compared with obesity or gestational weight gain, contributed the least to the population-attributable fraction of LGA neonates (Kim, 2014). he highest fraction of LGA neonates was attributable to maternal obesity plus excessive gestational weight gain. Similarly, Egan and colleagues (2014) found that excessive gestational weight gain is common in women with gestational diabetes and confers an additive risk for fetal macrosomia. Weight distribution also seems to playra role because the risk of gestational diabetes is greater with maternal truncal obesity. Suresh and colleagues (2012) veriied that increased maternal abdominal subcutaneous fat thickness as measured by sonography at 18 to 22 weeks' gestation correlated with BMI and was a better predictor of gestational diabetes.
Women with gestational diabetes can be divided into two functional classes using fasting glucose levels. Pharmacological methods are usually recommended if diet modiication does not consistently maintain the fasting plasma glucose levels <95 mg/dL or the 2-hour postprandial plasma glucose < 120 mg/dL (American College of Obstetricians and Gynecologists, 2017 a). Whether pharmacological treatment should be used in women with lesser degrees of fasting hyperglycemia is unclear. here have been no controlled trials to identiy ideal glucose targets for fetal risk prevention. On the other hand, the HAPO study (2008) did demonstrate increased fetal risk at glucose levels below the threshold used for diagnosis of diabetes. The Fifth International Workshop Conference recommended that fasting capillary glucose levels be kept ;95 mg/ dL (Metzger, 2007).
In a systematic review, Hartling and colleagues (2013) concluded that treating gestational diabetes resulted in a signiicantly lower incidence of preeclampsia, shoulder dystocia, and macrosomia. For example, the calculated risk ratio was 0.50 for delivering a newborn >4000 g ater treatment. These investigators caution that the attributed risk for these outcomes is low, especially when glucose values are only moderately elevated. Importantly, they were unable to demonstrate an efect on neonatal hypoglycemia or on future metabolic outcomes in the ofspring.