Despite the significant worldwide success of fundamental and clinical medicine pre-eclampsy (PE) remains one of the key causes of both maternal and perinatal mortality; according to WHO data up to 2-8% of pregnancies are associated with pre-eclampsy [1].
Multiple factors contribute to PE etiology. Moreover, PE itself is a manifestation involving various body systems with a complex pathophysiologic background. PE mechanisms depend on various complex factors that require further investigation. At present, most authors consider endotheliosis the main pathologic element that triggers PE. Endotheliosis is a result of multiple processes, both single and acting in combination.
Recent studies were focused on placentation disorders theory resulting in angiogenesis impairments associated with endothelium dysfunction in particular blood vessels [2] – usually due to perfusion dysfunction in chorion villi with resulting in disorders of oxygenation and blood circulation. These processes contribute to release of multiple trophoblastic factors from placenta. These factors facilitate maternal inflammatory response that results in hypertension and proteinuria [3-4]. It is considered that placenta pre-eclampsy develops during the placentation process (gestation weeks 12-16). It can result in earlier and more severe disease, while maternal factors (maternal pre-eclampsy) result in later disease [5]. Placenta dysfunction results in placenta stress followed by manifestation of PE signs and [6].
Placenta-associated theory of pre-eclampsy pathogenesis is supported by study results, where placenta size, weight and location were evaluated as risk factors.
L’Abee C et. Al. studied maternal factors that influence placenta weight increase in association with body weight index (BWI) increase. They report placenta weight increase up to 3.6 g with each extra kg/m2 unit of maternal BWI [7]. J.M. Wallace studied placenta weight in 55105 pregnant patients subdivided into 3 groups according to weight: low placenta weight – lower third (mean weight 484 g), medium weight – medium third (mean weight 622 g) and high weight – upper third (mean weight 788 g). Authors concluded that lower weight of placenta is pre-eclampsy risk factor (P <0,001), while higher placenta weight is associated with a higher risk of cesarean section, prolonged gestation and higher foetal weight at birth (P <0,001).
No correlation of maternal BWI and placenta weight was reported. Authors consider both BWI disorders and placenta weight independent PE risk factors [8]. Prabhjot Kaur studied 100 placentas, with 75 cases associated with pre-eclampsy or pregnancy-associated hypertension (study group), while 25 cases were associated with normotension pregnancy (control group). Females of all ages were enrolled, gestation term was 35 weeks.
Significant decrease of placenta weight in study group was reported. Mean placenta weight decrease in study group was 375.95 ± 67.195 g, while in control group the corresponding level was 458.28 ± 42.13 g. Though various placenta weights were reported, no statistically significant difference has been detected [9].
M. J. Quinn reports association of vascular disorders and small size of placenta with early development of pre-eclampsy, while larger placenta sizes were reported during the third trimester of pregnancy [10]. In 2017 Johanne Dypvik et al conducted a population – based study evaluating females with two consequent pregnancies (n = 186859). Pre-eclampsy during the second pregnancy has been reported in 1.4% (2507/177149) of females who had no pre-eclampsy during the first pregnancy. females PE risk during the second pregnancy was associated with the lowest placenta weight during the first pregnancy (odds ratio (OR) 1.30, 95% CI 1.14-1.47).