Preeclampsia (PE) affects 5-8% of pregnant women, and it is the major cause of perinatal morbidity and mortality. It is defined as arterial hypertension in women after 20 weeks of gestation which cooccurs with proteinuria (300 mg/d) or as arterial hypertension which is accompanied by one of the following: renal failure, liver dysfunction, hematological or neurological abnormalities, intrauterine growth restriction, or uteroplacental insufficiency. Currently, pathophysiology of preeclampsia poses a considerable challenge for perinatology. Preeclampsia is characterized by excessive and progressive activation of the immune system along with an increase in proinflammatory cytokines and antiangiogenic factors in fetoplacental unit as well as in vascular endothelium in pregnant women. A single, major underlying mechanism of preeclampsia is yet to be identified. This paper discusses the current understanding of the mechanisms which underlie the development of the condition. Some significant factors responsible for PE development include oxidative stress, abnormal concentration and activity in mononuclear phagocytic system, altered levels of angiogenic and antiangiogenic factors, and impaired inflammatory response triggered by inflammasomes. Detailed understanding of pathophysiology of inflammatory process in PE can largely contribute to new, targeted anti-inflammatory therapies that may improve perinatal outcomes in PE patients.

Since first being identified in December 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) as an etiological agent behind Coronavirus disease 19 (COVID-19), has caused three waves of a global pandemic, with a fourth in progress. Despite its high percentage of asymptomatic and low-symptomatic courses of illness, the SARS-CoV-2 pandemic has claimed a higher death toll than the SARS-CoV and MERS-CoV epidemics because of its high infectivity when compared to the other coronaviruses. High COVID-19 mortality is associated with age and other coexisting morbidities, as well as healthcare quality. According to several studies, pregnant women are at a higher risk of severe COVID-19 infection and adverse pregnancy outcomes (caesarean delivery, pre-term birth, low birth weight, preeclampsia, ICU admission, and need for mechanical ventilation). In our review of recent literature, we focused on the effects of COVID-19 in pregnant women, emphasizing the subcellular pathophysiology of SARS-CoV-2. In this paper, we concentrate on the pathophysiology of sub-cellular changes in COVID-19 and endeavor to highlight the aspects that manifest in physiological pregnancy and potentially create a higher risk of SARS-CoV-2 infection and acute COVID-19 symptoms. Understanding how pregnancy-associated changes can cause a synergistic effect with COVID-19 may point us in the right direction for future prophylaxis and treatment for women undergoing COVID-19 during pregnancy.

Preeclampsia and intrauterine growth restriction are two separate disease entities that, according to numerous reports, share the same pathogenesis. In both, angiogenesis disorders and generalized inflammation are the dominant symptoms. In this study, we hypothesized that both diseases demonstrate the same profile in early preeclampsia, late preeclampsia, and intrauterine growth restriction patients, with the only difference being the degree of exacerbation of lesions. One hundred sixty-seven patients were enrolled in the study and divided into four groups: early preeclampsia, late preeclampsia, and intrauterine growth restriction groups, and one control group. Concentrations of the angiogenesis and inflammatory markers soluble fms-like tyrosine kinase receptor 1, placental growth factor, high-sensitivity C-reactive protein, and interleukin-6 were determined, and the behavior of these markers and correlations among them were studied. Higher concentrations of soluble fms-like tyrosine kinase receptor 1, high-sensitivity C-reactive protein, and interleukin-6 and a lower concentration of placental growth factor were observed in the study groups compared with the control group. No differences in concentrations of the studied markers were found among the study groups but significant correlations were observed. The higher values for the angiogenesis and inflammatory markers both in preeclampsia patients and patients with intrauterine growth restriction of placental origin compared with the control group suggest the existence of the same underlying disorders in the development of these pathologies. The observed mutual correlations for disordered angiogenesis and inflammatory markers are suggestive of a mutual relationship between these processes in the development of pathologies evolving secondary to placental ischemia. The same lesion profile was observed for both preeclampsia and ‘placental’ intrauterine growth restriction patients, which could be used in developing common diagnostic criteria for pregnant patients.

The last decade has seen an improved understanding of the cause of the development of pathologies such as gestational hypertension, preeclampsia, intrauterine growth restriction, intrauterine fetal death or placental abruption. Nowadays, we know that most conditions within this group share the same pathogenesis, the cause of which is placental ischemia. The following review is an attempt to propose a new method for prediction, diagnosis and--above all--appropriate monitoring of pregnant women and fetuses developing the ischemic placental syndrome with the use of tests that are new but yet widely available in clinical diagnosis. They are closely related to the condition's pathogenesis, therefore their elevated levels may predate clinical symptoms, and--most importantly--they correlate with syndrome aggravation and the occurrence of complications. Perhaps, the new look will allow us to improve perinatal results by reducing mortality and severe complications in pregnant women and fetal deaths resulting from sudden intrauterine fetal death or placental abruption.

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