Preeclampsia, being one of the leading causes of maternal and perinatal morbidity and mortality, has been the subject of extensive research since its description. Preeclampsia has been called the disease of theories due to the enigma surrounding its exact pathophysiology. Despite the absence of treatment that reverses the disease process once started, screening for preeclampsia and intrauterine growth restriction (IUGR) has been a major clinical and research issue since the disease was first reported. This review evaluates the current evidence for prediction and prevention of preeclampsia and IUGR using clinical tests, maternal serum markers, and uterine artery Doppler screening. In addition, we critically evaluate the evidence regarding the different therapeutic strategies for the prevention of preeclampsia and IUGR and the latest clinical recommendations for their use.
"Despite the improvements in the prediction of the disease , there is no treatment that reverses this pathology once it has begun. This is mainly explained by the fact that the different tests used to predict PE have a better performance after the first trimester of pregnancy, a period in which the intervention to decrease the prevalence of the disease has proved to be ineffective . This is why more research is needed to develop clinical tools that allow a prediction in even more early stages, or even before the patient gets pregnant. "
[Show abstract][Hide abstract] ABSTRACT: Preeclampsia (PE) is one of the main causes of maternal and fetal morbidity and mortality in the world, causing nearly 40% of births delivered before 35 weeks of gestation. PE begins with inadequate trophoblast invasion early in pregnancy, which produces an increase in oxidative stress contributing to the development of systemic endothelial dysfunction in the later phases of the disease, leading to the characteristic clinical manifestation of PE. Numerous methods have been used to predict the onset of PE with different degrees of efficiency. These methods have used fetal/placental and maternal markers in different stages of pregnancy. From an epidemiological point of view, many studies have shown that PE is a disease with a strong familiar predisposition, which also varies according to geographical, socioeconomic, and racial features, and this information can be used in the prediction process. Large amounts of research have shown a genetic association with a multifactorial polygenic inheritance in the development of this disease. Many biological candidate genes and polymorphisms have been examined in their relation with PE. We will discuss the most important of them, grouped by the different pathogenic mechanisms involved in PE.
Journal of pregnancy 01/2012; 2012:632732. DOI:10.1155/2012/632732
[Show abstract][Hide abstract] ABSTRACT: Die Vorhersage der intrauterinen Wachstumsrestriktion (IUGR) beruht auf Anamnese, Klinik und Doppler-Sonographie (DS) der
A.uterina (22–24SSW). Der positive Vorhersagewert der DS ist geringer als der negative (30 vs. 95%). Eine effektive Prävention
und Therapie ist nur im Einzelfall möglich. Die ambulante Überwachung erfolgt mittels Biometrie und DS der fetalen Gefäße
in 2-wöchigen Intervallen. Die schwergradige IUGR mit zunehmender rechtskardialer Belastung bei kindlicher Lebensfähigkeit
erfordert eine stationäre Überwachung. Bei enddiastolischem Nullfluss/Reverse-Flow (AREDF) in der A.umbilicalis erfolgt die
Entbindung per Sectio individuell ab 30+0SSW, bei AREDF im Ductus venosus und/oder pathologischem Kardiotokogramm auch früher.
Perinatale Morbidität und Mortalität sind erhöht und werden durch Gestationsalter sowie Schweregrad der IUGR bestimmt. Mittel-
und langfristig haben die Kinder ein erhöhtes Risiko für eine Zerebralparese, eine Beeinträchtigung der somatischen, sensorischen,
neuromotorischen und intellektuellen Entwicklung und ein metabolisches Syndrom.
The prediction of intrauterine growth restriction (IUGR) is based on medical history, clinical findings, and Doppler sonography
(DS) of the uterine arteries (22–24 weeks). The positive predictive value of DS is higher than the negative predictive value
(30% vs. 95%). Prevention and therapy are effective in single cases only. In outpatient care, sonographic biometry and DS
of fetal vessels are performed in biweekly intervals. Severe IUGR with increasing afterload of the right ventricle and fetal
viability requires intensive clinical surveillance. Absent or reversed end-diastolic flow (AREDF) in the umbilical artery
requires delivery by cesarean section after 30+0 weeks. Fetuses with AREDF in the ductus venosus and/or pathological cardiotocography
may need to be delivered earlier. Perinatal mortality and morbidity are increased and are dependent on gestational age and
the severity of IUGR. Children are at risk of cerebral palsy; growth reduction; impaired neurodevelopmental, sensory, and
cognitive functions; and metabolic syndrome.
Der Gynäkologe 11/2007; 40(12):983-999. DOI:10.1007/s00129-007-2083-7
[Show abstract][Hide abstract] ABSTRACT: Uteroplacental insufficiency leads to intrauterine growth retardation (IUGR) and adult onset insulin resistance in both humans and rats. IUGR rat liver is characterized by persistent changes in histone 3 lysine 9 and lysine 14 acetylation, which may induce postnatal changes in gene expression. We hypothesized that it would be possible to identify hepatic genes whose epigenetic characteristics and mRNA levels are altered due to IUGR using chromatin immunoprecipitation (ChIP) coupled with random primed differential display polymerase chain reaction (PCR). One of the isolated sequences identified contained exon 2 of the dual specificity phosphatase-5 gene (DUSP5). IUGR affected hepatic DUSP5 mRNA levels and exon 2 DNA methylation into adulthood in the rat. DUSP5 dephosphorylates Erk1 and Erk2 within the MAPK signaling cascade, which in turn affects serine 612 phosphorylation of insulin receptor substrate-1 (p612 IRS-1). In adult rat liver, IUGR increased Erk1/Erk2 phosphorylation and p612 IRS-1 phosphorylation. Increased serine phosphorylation of hepatic IRS-1 may contribute to the insulin resistance that characterizes these animals. We conclude that intrauterine growth retardation induced by uteroplacental insufficiency 1) affects the hepatic epigenetic characteristics and mRNA of the DUSP-5 and 2) increases hepatic insulin receptor substrate-1 phosphorylation at serine 612 in adult rats.
The FASEB Journal 11/2006; 20(12):2127-9. DOI:10.1096/fj.06-6179fje · 5.04 Impact Factor
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