Pre-eclampsia (PE) continues to be a leading cause of maternal and fetal mortality and morbidity. While substantial progress has been made in understanding the pathomechanisms of PE, the pathophysiology of the disease is still not fully understood. While the “two-stage model” of the development of PE is the most widely accepted theory, stating that the placenta is the main source of the disease, there are some other pathophysiological models of PE. Among these other theories, the one considering heart dysfunction as serving as the primary cause of PE seems to be gaining increasing prominence. In this review, we aim to elucidate these two divergent concepts concerning the development of PE. Despite some differences in their proposed pathomechanisms, both theories share vital pathophysiological elements in common. A central and critical component in both models is impaired placental perfusion, which appears to be a crucial phenomenon in PE. A comprehensive understanding of the different pathomechanisms involved in PE may be helpful in clinical practice, prompting a more individual approach to care of patients with PE.

The endothelium, which constitutes the inner layer of blood vessels and lymphatic structures, plays an important role in various physiological functions. Alterations in structure, integrity and function of the endothelial layer during pregnancy have been associated with numerous gestational complications, including clinically significant disorders, such as preeclampsia, fetal growth restriction, and diabetes. While numerous experimental studies have focused on establishing the role of endothelial dysfunction in pathophysiology of these gestational complications, their mechanisms remain unknown. Numerous biomarkers of endothelial dysfunction have been proposed, together with the mechanisms by which they relate to individual gestational complications. However, more studies are required to determine clinically relevant markers specific to a gestational complication of interest, as currently most of them present a significant overlap. Although the independent diagnostic value of such markers remains to be insufficient for implementation in standard clinical practice at the moment, inclusion of certain markers in predictive multifactorial models can improve their prognostic value. The future of the research in this field lies in the fine tuning of the clinical markers to be used, as well as identifying possible therapeutic techniques to prevent or reverse endothelial damage.

Objectives: The aims of our study were to assess the correlation between the amniotic fluid index (AFI) value and the frequency and type of fetal anomalies. Material and methods: The material included 94 patients at the third trimester of pregnancy, 60 with mild polyhydramnios, 19 with moderate one, and 15 with severe one. Polyhydramnios was diagnosed if AFI was > 24 cm. All patients were divided into three groups based on the value of AFI: 1) mild polyhydramnios with AFI between 24.1 and 29.9 cm, 2) moderate polyhydramnios with AFI between 30–34.9 cm, and 3) severe polyhydramnios with AFI ≥ 35 cm. Results: The incidence of fetal malformations correlated significantly with the degree of polyhydramnios and was the highest in patients with severe polyhydramnios (53.3%, p = 0.002). Congenital malformations of the gastrointestinal tract were the most frequent fetal anomalies in the whole group of patients (5.3%). Trisomy 18 was the most frequent aneuploidy found in women with polyhydramnios (2.1%). Conclusions: The incidence of fetal congenital anomalies significantly increases with the degree of polyhydramnios, being most frequent in severe one and rather rare in a mild one. Congenital malformations of the gastrointestinal tract were the most frequent anomalies in patients with polyhy­dramnios, especially in women with severe polyhydramnios. Objectives: The aims of our study were to assess the correlation between the amniotic fluid index (AFI) value and the frequency and type of fetal anomalies. Material and methods: The material included 94 patients at the third trimester of pregnancy, 60 with mild polyhydramnios, 19 with moderate one, and 15 with severe one. Polyhydramnios was diagnosed if AFI was > 24 cm. All patients were divided into three groups based on the value of AFI: 1) mild polyhydramnios with AFI between 24.1 and 29.9 cm, 2) moderate polyhydramnios with AFI between 30–34.9 cm, and 3) severe polyhydramnios with AFI ≥ 35 cm. Results: The incidence of fetal malformations correlated significantly with the degree of polyhydramnios and was the highest in patients with severe polyhydramnios (53.3%, p = 0.002). Congenital malformations of the gastrointestinal tract were the most frequent fetal anomalies in the whole group of patients (5.3%). Trisomy 18 was the most frequent aneuploidy found in women with polyhydramnios (2.1%). Conclusions: The incidence of fetal congenital anomalies significantly increases with the degree of polyhydramnios, being most frequent in severe one and rather rare in a mild one. Congenital malformations of the gastrointestinal tract were the most frequent anomalies in patients with polyhy­dramnios, especially in women with severe polyhydramnios.

With regard to differences in the clinical symptoms of preeclampsia (PE), the degree of endothelial dysfunction may differ between early and late-onset preeclampsia (EOP and LOP). The authors of this study examined it by assessing the endothelial injury level in women with EOP (20 patients) and LOP (20 patients) and in normotensive pregnant women (20 patients) in their late second and third trimesters of pregnancy, using the two markers—the serum concentration of hyaluronan (HA) and the serum level of soluble vascular cell adhesion molecule-1 (sVCAM-1). The serum concentrations of HA and sVCAM-1 did not differ significantly between the EOP and LOP patients. However, these were statistically higher than that of the control group participants (p < 0.05; p < 0.001). A significant correlation between the levels of HA and sVCAM-1 was found both in the entire group of patients with preeclampsia (p = 0.0277) and in women with late-onset disease (p = 0.0364), but not in the patients with early-onset preeclampsia (p = 0.331). The obtained results indicated a comparable level of endothelial injury in the two types of PE. The presence of a similar degree of endothelial injury in patients with EOP and LOP should create awareness among all clinicians about the possible fatal complications in both groups of patients with PE.

The most widely accepted theory for the development of preeclampsia is the “two-stage theory”. An imbalance between antiangiogenic and proangiogenic factors is considered the link between the two stages. Nowadays, an increasing amount of data is available on the use of measurements of serum...