4.2 Article

Changes in fetal intracranial anatomy during maternal pregestational and gestational diabetes

Journal

JOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH
Volume 49, Issue 2, Pages 587-596

Publisher

WILEY
DOI: 10.1111/jog.15502

Keywords

fetal biometry; fetal brain; gestational diabetes; pregestational diabetes

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The study evaluated the changes in fetal intracranial structures in pregnant women with pregestational DM and GDM. It found that maternal hyperglycemia was significantly associated with an increase in the widths of fetal PLV, CSP, and CM, as well as a decrease in fetal TCD.
AimTo evaluate the changes in fetal intracranial structures in pregnant women with pregestational diabetes mellitus (DM) and gestational diabetes mellitus (GDM). MethodsThe study was conducted prospectively with patients who were grouped as pregestational DM (n = 110), GDM (n = 110), and control (n = 110). Fetal ultrasonographic measurements of widths of posterior lateral ventricles (PLV), cavum septum pellucidi (CSP), cisterna magna (CM), thalamus and transcerebellar diameter (TCD) were recorded and compared. ResultsFetal PLV, CSP, and CM widths were higher in pregestational DM and GDM groups than in control group, and also higher in pregestational DM group compared to GDM group (p < 0.001). Fetal TCD in the PGDM group was found to be less than both control and GDM groups (p < 0.001). No difference was found between three groups in terms of fetal thalamus size (p = 0.801). Fetal PLV, CSP, and CM values were positively correlated with maternal hyperglycemia, fetal abdominal circumference (AC), and deepest vertical pocket of amniotic fluid (DVP) (p < 0.001). Fetal TCD was negatively correlated with HbA1c and DVP (p = 0.002, p = 0.38, respectively). The optimal cut-off points to identify pregestational DM and GDM were 5.55 and 5.83 mm for PLV, 5.83 and 6.32 mm for CSP, and 7.26 and 6.62 mm for CM. ConclusionMaternal hyperglycemia was significantly associated with an increase in the widths of fetal PLV, CSP, and CM and a decrease in fetal TCD.

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