Comparative study of sialic acid content in saliva between preeclampsia and normal gestation patients

Abstract

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.