TY - JOUR
T1 - Diabetes during pregnancy
T2 - A maternal disease complicating the course of pregnancy with long-term deleterious effects on the offspring. a clinical review
AU - Ornoy, Asher
AU - Becker, Maria
AU - Weinstein-Fudim, Liza
AU - Ergaz, Zivanit
N1 - Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2021/3/2
Y1 - 2021/3/2
N2 - In spite of the huge progress in the treatment of diabetes mellitus, we are still in the situ-ation that both pregestational (PGDM) and gestational diabetes (GDM) impose an additional risk to the embryo, fetus, and course of pregnancy. PGDM may increase the rate of congenital malfor-mations, especially cardiac, nervous system, musculoskeletal system, and limbs. PGDM may in-terfere with fetal growth, often causing macrosomia, but in the presence of severe maternal com-plications, especially nephropathy, it may inhibit fetal growth. PGDM may also induce a variety of perinatal complications such as stillbirth and perinatal death, cardiomyopathy, respiratory mor-bidity, and perinatal asphyxia. GDM that generally develops in the second half of pregnancy induces similar but generally less severe complications. Their severity is higher with earlier onset of GDM and inversely correlated with the degree of glycemic control. Early initiation of GDM might even cause some increase in the rate of congenital malformations. Both PGDM and GDM may cause various motor and behavioral neurodevelopmental problems, including an increased incidence of attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). Most complications are reduced in incidence and severity with the improvement in diabetic con-trol. Mechanisms of diabetic-induced damage in pregnancy are related to maternal and fetal hy-perglycemia, enhanced oxidative stress, epigenetic changes, and other, less defined, pathogenic mechanisms.
AB - In spite of the huge progress in the treatment of diabetes mellitus, we are still in the situ-ation that both pregestational (PGDM) and gestational diabetes (GDM) impose an additional risk to the embryo, fetus, and course of pregnancy. PGDM may increase the rate of congenital malfor-mations, especially cardiac, nervous system, musculoskeletal system, and limbs. PGDM may in-terfere with fetal growth, often causing macrosomia, but in the presence of severe maternal com-plications, especially nephropathy, it may inhibit fetal growth. PGDM may also induce a variety of perinatal complications such as stillbirth and perinatal death, cardiomyopathy, respiratory mor-bidity, and perinatal asphyxia. GDM that generally develops in the second half of pregnancy induces similar but generally less severe complications. Their severity is higher with earlier onset of GDM and inversely correlated with the degree of glycemic control. Early initiation of GDM might even cause some increase in the rate of congenital malformations. Both PGDM and GDM may cause various motor and behavioral neurodevelopmental problems, including an increased incidence of attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). Most complications are reduced in incidence and severity with the improvement in diabetic con-trol. Mechanisms of diabetic-induced damage in pregnancy are related to maternal and fetal hy-perglycemia, enhanced oxidative stress, epigenetic changes, and other, less defined, pathogenic mechanisms.
KW - Anomalies
KW - Diabetic control
KW - Gestational diabetes
KW - Growth disturb-ances
KW - Neurodevelopmental problems
KW - Perinatal complications
KW - Pregestational diabetes
KW - Pregnancy
UR - http://www.scopus.com/inward/record.url?scp=85102415865&partnerID=8YFLogxK
U2 - 10.3390/ijms22062965
DO - 10.3390/ijms22062965
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C2 - 33803995
AN - SCOPUS:85102415865
SN - 1661-6596
VL - 22
SP - 1
EP - 38
JO - International Journal of Molecular Sciences
JF - International Journal of Molecular Sciences
IS - 6
M1 - 2965
ER -