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The uncertainty of the etiology and underlying mechanisms of the pathophysiology of this disease makes causal structuring and primary prevention of preeclampsia impossible, making it difficult to control morbidity and mortality, both maternal and perinatal. From the many theories on preeclampsia, the disease can be classified into Placental preeclampsia, maternal preeclampsia, and Vascular Disorders of Pregnancy (VDP). Increased inflammatory response to placental factors, excessive inflammatory response to placental factors, and primary vascular disorders are the basis of distinction and also the basis of pathophysiology among the three forms of preeclampsia.

Background. Preeclampsia is a frequent complication of pregnancy. The literature data and the results of our own studies indicate the development of morphofunctional changes in the kidneys, ureters and bladder of fetuses and newborns that developed under maternal preeclampsia, in particular, sclerotic processes in these organs, morphogenesis of which is currently unknown. The purpose of the study was to search for the signs of epithelial-mesenchymal transition in the kidneys, ureters and bladder of fetuses and newborns, which developed under the conditions of maternal preeclampsia, and to evaluate its role in the development of sclerotic changes in these organs. Materials and methods. Study materials were the tissues of the kidneys, ureters and bladder of full-term fetuses and newborns. All materials were divided into the following groups: I — fetuses and newborns from mo­thers with physiological pregnancy; II — fetuses and newborns from mothers, whose pregnancy was complicated by mild preeclampsia; III — fetuses and newborns from mothers, whose pregnancy was complicated by moderate preeclampsia; IV — fetuses and newborns from mothers, whose pregnancy was complicated by severe preeclampsia. An immunohistochemical study was performed with monoclonal antibodies to vimentin, smooth muscle actin, desmin, cytokeratins 18 and 19. Results. A comprehensive analysis of the immunohistochemical reactions with monoclonal antibodies to vimentin, smooth muscle actin, desmin, cytokeratins 18 and 19 allowed to reveal in the kidneys, ureters and bladder of fetuses and newborns developed under the conditions of maternal preeclampsia of varying severity the signs of epithelial-mesenchymal transition, which increased with the increasing age of the child, aggravation of maternal preeclampsia. Epithelial-mesenchymal transition was characterized by increased expression of vimentin, smooth muscle actin, desmin and decreased expression of cytokeratins 18 and 19. Conclusions. In the kidneys, ureters and bladder of fetuses and newborns from mothers, whose pregnancy was complicated by preeclampsia of varying severity, the sclerotic changes are caused by the process of epithelial-mesenchymal transition, which becomes more significant from fetus to newborn and with the increasing severity of maternal preeclampsia. Chronic intrauterine hypoxia and activation of the macrophage system in these organs may influence the pathogenesis of epithelial-mesenchymal transition in the kidneys, ureters and bladder of fetuses and newborns developing under maternal preeclampsia.

Background: Possible impact of maternal hypertension and preeclampsia on neonatal respiratory disorders was unknown. We investigated the association of maternal hypertension and preeclampsia with neonatal respiratory disorders in preterm and full-term newborns.Method: In this study, we used a large Chinese population-based study which includes 185,687 singleton livebirths with gestational weeks between 28 and 42 weeks. The "exposure" was maternal hypertension and preeclampsia. The outcome was neonatal respiratory disorders including neonatal respiratory distress syndrome (NRDS), pneumonia and low Apgar scores. Logistic regression was used to examine the association between the maternal hypertensive disorders and the risk for neonatal respiratory disorders. We further evaluated the association in preterm and full-term infants.Results: As a result, the incidence of neonatal RDS, pneumonia, and low Apgar score in hypertensive group was higher than that in normotensive group. Preeclampsia was associated with RDS [(adjusted relative risk (aRR): 1.85, 95% confidence interval (CI): 1.22-3.05)]. Both maternal hypertension and preeclampsia increased risks for neonatal pneumonia (aRR: 1.79, 95%CI: 1.48-2.17; aRR: 1.81, 95%CI: 1.36-2.40, respectively), for low Apgar score at 1 min (aRR: 1.20, 95%CI: 1.13-1.27; aRR: 1.53, 95%CI: 1.41-1.67, respectively), and for low Apgar score at 5 min (aRR: 1.30, 95%CI: 1.17-1.45; aRR: 1.70, 95%CI: 1.46-1.99, respectively). The risk for neonatal respiratory disorders increased with severity of maternal hypertension. The observed associations were present in both full-term and preterm birth.Conclusion: Maternal hypertension and preeclampsia are risk factors for neonatal respiratory disorders in full-term and preterm newborns. [ABSTRACT FROM AUTHOR]

Aim: To investigate growth and neurodevelopment outcome of very low birth weight (VLBW) infants delivered by preeclamptic mothers. Methods: A cohort including all VLBW infants delivered between December 2003 and May 2005 was followed up to 12 and 18 months corrected age (CA). Exclusion criteria: death before 1 year corrected age, major malformations, deafness and blindness. Weight, length and head circumference were plotted on NCHS curves. Bayley Scales were performed at 12 and 18 months CA. Results: 40 infants in preeclamptic and 46 in control groups were studied. Birth weight and gestational age were 1148 g ± 236 and 1195 g ± 240, and 31.3 weeks ± 1 and 30.6 weeks ± 2 for preeclamptic and control groups, respectively. At 12 and 18 months, CA, weight for age (Z score) was significantly higher in control than in preeclamptic. PDI scores were higher in preeclamptic than in controls at 18 months CA. Conclusions: Catch-up of body weight did not occur in the first 18 months CA in preeclamptic infants. Neurodevelopment outcome was better in infants delivered by preeclamptic mothers than in controls at 18 months CA. [ABSTRACT FROM AUTHOR]

The ischemia in children affected by perinatal stroke has long been thought to be driven by nonhematologic maternal and perinatal events. New information from clinical studies, however, tells us that plasma-phase risk factors, such as factor V Leiden, elevated lipoprotein (a), and mutations in MTHFR, may be important in the pathogenesis of perinatal stroke, if not always in the risk of recurrence. With regard to stroke recurrence, this risk is only about 2% according to the largest follow-up study to date, and certainly less than 5%. Nonetheless, when strokes do recur, they tend to be associated with the presence of plasma-phase risk factors in the affected child, suggesting that a small percentage of children with a first perinatal stroke may benefit from anticoagulation therapy, both to prevent stroke recurrence as well as occurence of a second, non-CNS thrombotic event. Counselling of parents with regard to subsequent pregnancies should always include medical management of systemic maternal disorders, such as diabetes, persistently elevated antiphospholipid antibodies, and inherited maternal hypercoagulability states. [Copyright &y& Elsevier]