**1. Introduction**

268 From Preconception to Postpartum

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During pregnancy, mother's well-being affects directly the newborn development. Some maternal and placental complications, such as gestational diabetes, preeclampsia (PE), preterm delivery and intrauterine growth restriction (IUGR), may contribute to fetal growth deviations or fetal development modifications. Usually the newborn weight correlates positively with placenta weight, showing the interaction between the development of placenta and fetal growth.

Normal human pregnancy is associated with physiological blood changes, namely, neutrophilic leukocytosis, hyperlipidemia and procoagulant, hypofibrinolytic and inflammatory conditions. PE has been associated with an enhancement in these changes and with placental abnormalities, that may condition its perfusion and, therefore, feto-maternal transfer. The placental dysfunction, characterized by a disturbance in the angiogenic/antiangiogenic factors and in the hypoxia/placental reoxygenation process, seems to trigger a maternal endothelial dysfunction. To this maternal endothelial dysfunction may also contribute the oxidative stress, dyslipidemia and the inflammatory process which are present in maternal circulation.

PE is a maternal pathology involving placental modifications, which is also associated with fetal complications. Prematurity and IUGR, are the most representative complications. In this chapter we will address the impact of the maternal disturbances in the newborns from a normal and a preeclamptic (PEc) gestation. Indeed, there are several studies in literature about changes in maternal circulation, but few studies about fetal blood changes in the presence of PE. Moreover, these studies have shown controversial results. We intend to focus on neonatal consequences of PE, by assessing different biochemical and hematologic parameters in the umbilical cord blood. In this way, we will address the effect of some modifications usually observed in PEc women, such as, in lipid profile, in hematologic profile, inflammatory and antioxidant markers, angiogenic/anti-angiogenic factors and hemostatic disturbances, in umbilical cord blood.

Umbilical Cord Blood Changes in Neonates from a Preeclamptic Pregnancy 271

The risk of developing PE seems to be associated with some factors, such as nulliparity (about 2/3 of cases occur in the first pregnancy), multiple pregnancy, change of paternity, age over 40 years, family history of PE and eclampsia, body mass index (BMI) greater than 35 kg/m2, diabetes, disease prior to pregnancy (e.g., diabetes mellitus, hypertension, renal disease and thrombophilia) and hydatidiform mole (Duckitt & Harrington, 2005; Magnussen et al., 2007; Jim et al., 2010). According to Magnussen et al. (2007), there is an enhanced risk to develop PE, when cardiovascular risk factors, such as increased

Several studies associate smoking habits with a lower risk of developing PE (Magnussen et al., 2007; Wikström et al., 2010). However, maternal smoking is associated with various maternal and fetal complications (Kalle, 2001; Steyn et al., 2006), including placenta previa,

PE is the main maternal risk factor associated with low birth weight newborns and/or IUGR (Table 2). Intrauterine growth restriction and/or fetal death can occur in about 30% of PEc cases as a direct result of placental insufficiency (Jim et al., 2010). The neonatal complications risk is higher in cases of severe PE and eclampsia (Duley, 2009). IUGR is associated with a high rate of perinatal morbidity and mortality (Rizzo &

Several studies indicate that PE is associated with a higher incidence of newborns with low birth weight (Groom et al., 2007; Duley, 2009; Wu et al., 2009). In addition, there's an increased incidence of newborns with low birth weight in pregnant women who developed PE at an earlier stage of pregnancy, compared with those who later developed PE (Xiong & Fraser, 2004; Groom et al., 2007). Prematurity is the leading cause of perinatal morbidity and mortality (Goldenberg et al., 2008) and PE is often associated with preterm delivery (Sibai et al., 2005; Goldenberg et al., 2008; Duley, 2009; Wu et al., 2009). Some neonatal complications resulting from PEc pregnancy are described, and are associated with prematurity, including jaundice, respiratory distress, apnea, seizures, hypoglycaemia and prolonged

Long term chronic diseases ("fetal programming" or "fetal origins of disease in adult life")

According to Barker's theory, the origin of some adulthood chronic diseases such as cardiovascular diseases, hypertension and diabetes have their origin in intrauterine life (Barker & Bagby, 2005). This hypothesis, called "fetal programming" or "fetal origins of disease," suggests that the intrauterine environment in which the fetus develops may be the origin of diseases in adult life. Changes that may occur in intrauterine environment and that somehow could disrupt normal development of the fetus can trigger metabolic changes,

which may result in the development of long-term disorders (Barker, 2004).

triglycerides (TG), total cholesterol and LDLc, are present before pregnancy.

low birth weight, preterm birth, miscarriage and neonatal death.

hospitalization (Duley, 2009; Wu et al., 2009).

Intrauterine growth restriction (IUGR)

Table 2. Newborn complications in preeclampsia

**Newborn complications:** 

Prematurity Neurologic lesions Neonatal death

Arduini, 2009).

Disturbances in angiogenic/anti-angiogenic factors, in the lipid profile and an enhanced inflammatory response, in the fetal circulation, may cause a short-term effect, such as endothelial dysfunction. However, the impact of these modifications, that are known cardiovascular risk changes, in the future life of these newborn are still unknown and should be clarified. These neonates and their mothers should deserve, therefore, a closer clinical follow-up later in life. This issue will be also addressed in this chapter. cause hypertensive of
