| dc.description | Preeclampsia (PE) is a serious pregnancy-related disorder. At least two basic
symptoms, hypertension (blood pressure >140/90 mmHg) and, typically, proteinuria [1]
which is commonly associated with edema and, on occasion, end-organ damage or liver
anomalies, define PE. Untreated PE may develop into the potentially deadly condition of
eclampsia [2]. PE is relieved only upon delivery [1].
Eclampsia is the occurrence of seizures in preeclamptic women [2], causing significant
rates of morbidity and mortality to both the mother and the perinatal baby. PE often
begins after the twentieth week of pregnancy, although it can be either early-onset
(before 34 weeks) or late-onset (after 34 weeks) [3].
Numerous risk factors have been linked to PE development. For example, high risk
factors include previous pregnancies with PE, particularly those that began at or before
34 weeks; highly multiparous, chronic blood pressure, type 1 or type 2 diabetes, kidney
illness, and autoimmune disease. Nulliparity, obesity, a BMI>30, a family history of PE
(mother, sister), age >35 years, low sociodemographic level, and a long intergenic
period >10 years are examples of moderate influencing variables [1–3].
Worldwide, the incidence of PE varies from 3% to 7% [4], and eclampsia, is one of the
main causes of maternal and newborn mortality [4,5]. Pregnant women with PE may
also die from uncontrolled hypertension, or systemic inflammation. The risk of death in
later life from cardiovascular and neurologic disease is also increased for women having
suffered PE [4]. Moreover, eclampsia develops in roughly 0.8% of pregnancies in
women with hypertension [6]. The estimated stillbirth rate for PE is 0.21% [7], making it
a significant risk factor on intrauterine fetal viability. Furthermore, 15% of all premature
births are caused by women having a cesarian delivery in order to avoid the harmful
effects of neglected PE [8].
In the human placenta, fetal trophoblast cells are in relatively close proximity to
maternal blood. Fetal cells are obviously half identical to those of the mother and half
alien; therefore, in the human placenta, fetal trophoblasts are particularly susceptible to
immunological assault at the fetal-maternal interface [9]. Numerous immune-protective
mechanisms have developed to offer this protection, creating a delicate biological
balance that allows the coexistence of the trophoblasts in close contact with the
maternal immune system; however, this is prone to imbalances and potential fatal
consequences for both mother and fetus. | |
