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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fetal growth restriction is the second leading cause of perinatal morbidity and mortality, behind prematurity, and is present in 5-12% of all pregnancies in the general population. Often confused with children constitutionally small for gestational age, those who had not achieved their potential for fetal growth and therefore having true growth restriction can be identified using customized growth curves. The point is to accurately identify fetuses with slowing growth or cessation of growth reflecting a pathological process, because these are at risk of death in utero or chronic fetal hypoxia with a significant impact on brain development. The kinetics of growth and prenatal markers of fetal growth restriction will influence the decision to extract the fetus and the gestational age at birth, as well as other factors involved in the neurodevelopmental outcome. Cognitive deficits and executive, motor, and behavioral dysfunctions described in the short term seem to persist together with greater risk of metabolic syndrome in adulthood. Decisions of fetal extraction by C-section continue to be debated until new epidemiological data will be available on large cohorts monitored over the long term using accurate neurocognitive tools. Understanding the effects of fetal growth restriction on the structure and function of the developing brain is essential for improving the relevance of fetal extraction decisions, perinatal care, and early evaluation of treatments for the prevention of neurodevelopmental disorders.
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PMID:[Intrauterine growth retardation and the developing brain]. 2389 Jul 31

It is now recognized that the quality of the fetal environment during early development is important in programming cardiovascular health and disease in later life. Fetal hypoxia is one of the most common consequences of complicated pregnancies worldwide. However, in contrast to the extensive research effort on pregnancy affected by maternal nutrition or maternal stress, the contribution of pregnancy affected by fetal chronic hypoxia to developmental programming is only recently becoming delineated and established. This review discusses the increasing body of evidence supporting the programming of cardiac susceptibility to ischaemia and reperfusion (I/R) injury, of endothelial dysfunction in peripheral resistance circulations, and of indices of the metabolic syndrome in adult offspring of hypoxic pregnancy. An additional focus of the review is the identification of plausible mechanisms and the implementation of maternal and early life interventions to protect against adverse programming.
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PMID:Developmental programming of cardiovascular disease by prenatal hypoxia. 2497 Jul 26