Dear Colleagues,

Preeclampsia (PE) and other placental hypoperfusion-related conditions account for almost 6–10% of gestational complications and have become more and more prevalent in recent decades.

Throughout the years, the name of this condition has changed quite radically a number of times. Initially, it was referred to as toxemia of pregnancy, later as EPH gestosis that consisted of a triad of clinical symptoms, namely, edema proteinuria–hypertension. Attempts to redefine the problem have resulted in identifying two forms of preeclampsia: one with an early onset, developing before the end of the 34th week of pregnancy, and one with a late onset, developing after the 34th week of pregnancy. Some authors consider late preeclampsia to be a separate disease entity with a different pathogenesis. In some cases, fetal growth restriction (FGR) has the same etiology as preeclampsia, but its clinical manifestation pertains to the fetus. FGR often remains the only clinical symptom, while the mother demonstrates none.

Placental insufficiency affects perinatal outcome in newborns and has long-term effects in children. These both result from iatrogenic effects resulting in preterm labor such as changes in metabolism that are termed fetal programming. Chronic changes in the intrauterine environment affect the functions of the circulatory system, the central nervous system, alimentary, and many others, which are currently the subject of numerous studies.

A Special Issue will be devoted to the assessment of both the early and late consequences of delivering births from pregnancies complicated by preeclampsia and its impact on the condition, well-being, and development of newborns and children.

Dr. Sebastian Kwiatkowski
Guest Editor

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• Fetal programming 
• Intensive care unit—ICU 
• Organ function 
• Short–long-term results 
• Placental insufficiency 
• Small for gestational age (SGA) 
• Fetal growth restriction (FGR)