Polycystic ovary syndrome (PCOS) is the most frequent endocrinopathy during women’s reproductive age. PCOS is a heterogeneous disorder featuring specific cardiometabolic properties. The association between the presence of metabolic disorders and PCOS supports the claim that the regulation of glycemic status is very important in these patients. There is a wide range of therapeutic options (including those treating diabetes mellitus type 2) with potential advantages available for the management of PCOS. Sodium–glucose cotransporter type 2 inhibitors (SGLT-2is) improve glucose metabolism, reduce fat tissue, lower blood pressure, reduce oxidative stress and inflammation, and protect the cardiovascular system. Currently, the use of SGLT-2is is not widespread in PCOS therapy, although these drugs represent a promising new therapeutic approach. Therefore, it is necessary to initiate further study in order to determine more effective therapies for PCOS and investigate the effect of SGLT-2is, both as a monotherapy and in combination with other drugs. It is necessary to understand the mechanisms underlying SGLT-2is in PCOS and their effects on long-term complications, especially since the gold standard treatment for PCOS, such as metformin and oral contraceptives, do not have long-term cardioprotective effects. The effects of SGLT-2is seem to involve cardiac protection, while diminishing endocrine and reproductive abnormalities in PCOS. In the current narrative review, we examine the most recent clinical evidence and discuss the potential applications of SGLT-2is for PCOS therapy.

Background and Objectives: Polycystic ovary syndrome (PCOS) is a frequent multifactorial endocrinopathy affecting women in the reproductive period, often associated with infertility and metabolic disorders. The use of animal models helps to better understand etiopathogenesis, enabling the examination of the effects of certain drugs in order to discover the best possible therapeutic approach. We tried to investigate the additional effect of estradiol-valerate (EV) and high-fat diet (HFD) in female rats to explore PCOS-related alterations with special focus on oxidative stress. Materials and Methods: Animals were divided into three groups: control group (CTRL, n = 6), estradiol-valerate group (EV, n = 6), and estradiol-valerate group on HFD (EV + HFD, n = 6). PCOS was induced by single subcutaneous injection of long-acting EV in a dose of 4 mg/per rat. We tried to improve the metabolic characteristics of the PCOS animal model by adding HFD, so the CTRL and EV group had a regular diet, while the EV + HFD group had HFD during the induction period of 60 days. Results: We observed alterations of anthropometric parameters and hormonal disturbances, along with estrus cycle impairment reassembly to obese-type PCOS phenotype. Moreover, glucose metabolism was impaired after addition of HFD to EV protocol, contrary to EV administered alone. Histological analysis confirmed more numerous cystic follicles after the combination of EV and HFD protocol. The alterations of oxidative stress markers could be related to and serve as the mechanistic base for development of PCOS-related endocrine, reproductive, and metabolic properties. Conclusions: The additive effect of EV and HFD was obvious in the majority of the parameters observed. Our study strongly demonstrated metabolic as well as reproductive properties of PCOS in rats.

The inflammatory processes that occur at the maternal–fetal interface are considered one of the factors that are responsible for preterm birth. The pro-inflammatory roles of the Gal-3-induced activation of NLRP3 inflammasome and the consecutive production of IL-1β have been described in several acute and chronic inflammatory diseases, but the role of this inflammatory axis in parturition has not been studied. The aim of this study was to analyze the protein expression of Gal-3, NLRP3, and IL-1β in the decidua, villi, and fetal membranes, and to analyze their mutual correlation and correlation with the clinical parameters of inflammation in preterm birth (PTB) and term birth (TB). The study included 40 women that underwent a preterm birth (gestational age of 25.0–36.6) and histological chorioamnionitis (PTB) and control subjects, 22 women that underwent a term birth (gestational age of 37.0–41.6) without histological chorioamnionitis (TB). An analysis of the tissue sections that were stained with anti- Gal-3, -NLRP3, and -IL-1β antibodies was assessed by three independent investigators. The expression levels of Gal-3 and IL-1β were significantly higher (p < 0.001) in the decidua, villi, and fetal membranes in the PTB group when they compared to those of the TB group, while there was no difference in the expression of NLRP3. A further analysis revealed that there was no correlation between the protein expression of NLRP3 and the expression of Gal-3 and IL-1β, but there was a correlation between the expression of Gal-3 and IL-1β in decidua (R = 0.401; p = 0.008), villi (R = 0.301; p = 0.042) and the fetal membranes (R = 0.428; p = 0.002) in both of the groups, PTB and TB. In addition, the expression of Gal-3 and IL-1β in decidua and the fetal membranes was in correlation with the parameters of inflammation in the maternal and fetal blood (C-reactive protein, leukocyte number, and fibrinogen). The strong correlation between the expression of Gal-3 and IL-1β in the placental and fetal tissues during labor indicates that Gal-3 may participate in the regulation of the inflammatory processes in the placenta, leading to increased production of IL-1β, a cytokine that plays the main role in both term and preterm birth.

Background: The impact of the SARS-CoV-2 viral infection during pregnancy on the fetus can be direct—transmitted through the placenta—and indirect—creating unfavorable conditions for the development of the fetus because of inflammation, micro-thrombosis, and hypercoagulation. Our study aimed to determine the types and frequency of pathohistological changes in placental tissue in SARS-CoV-2-positive pregnant women and to examine the possible role of oxidative stress in the prognosis of the delivery and its maternal and fetal complications. Methods: This prospective clinical study included 50 pregnant women divided into two groups, SARS-CoV-2 positive (COVID-19 group) and SARS-CoV-2 negative (control group), from who we collected demographic, clinical, obstetric, biochemical and pathologic data. Data about the newborn characteristics were also collected, which included anamnestic, clinical, and biochemical data. Results: The values of the superoxide anion radical and index of lipid peroxidation were significantly different in mothers concerning the presence of the SARS-CoV-2 infection, while the levels of the nitric oxide, index of lipid peroxidation, reduced glutathione, and superoxide dismutase were significantly different in the newborns depending on the SARS-CoV-2 infection. Newborn characteristics were similar between groups except for concentrations of IgM antibody. The incidence of pathohistological changes of the FVM type in the COVID-19 group of pregnant women was 46%, while in the control group, the incidence was 18%. Conclusions: This study confirmed the significant impact of the SARS-CoV-2 viral infection on maternal and fetal biochemical parameters and oxidative stress-mediated placental dysfunction. Future studies should be performed with more participants and follow-up neonatal development.

Introduction: Leiomyosarcoma (LMS), together with smooth muscle tumors of uncertain malignant potential (STUMP) and benign leiomyomas, belongs to a heterogeneous group of uterine neoplasms. According to the World Health Organization, tumors originating from uterine smooth muscle fibers are the second most frequent tumors. It is challenging to distinguish between STUMP and LMS because of an overlap of symptoms, lack of a precise definition, and unequivocal information obtained using imaging diagnostic methods. Following myomectomy or hysterectomy with laparoscopic or laparotomy surgery and a definitive histological diagnosis of STUMP, the course of treatment is determined by the need to preserve fertility. In 2014, the U.S. Food and Drug Administration published an alert that unprotected laparoscopic morcellation is correlated with a 3-fold higher likelihood of dissemination of malignant cells and disease progression. Unprotected morcellation was independently associated with a higher risk of disease recurrence after demolition or conservative surgery, with a relative risk of 2.94.Conclusion: Hematoperitoneum resulting from the spontaneous rupture of a uterine tumor is a rare gynecological emergency, with very few cases reported in the last decade.

SARS-CoV-2 has an affinity for binding to the human Angiotensin-converting enzyme 2 (ACE2) receptor through cleavage and conformational changes at the S1–S2 boundary and the receptor binding domain of the spike protein, which is also the most variable part of SARS-CoV-2. This study aimed to investigate the expression of Angiotensin-converting enzyme 2 (ACE2), spike protein, and CD68+ markers in placental tissue to demonstrate a possible correlation with the level of systemic oxidative stress biomarkers in patients who were infected with SARS-CoV-2 during pregnancy. A prospective clinical cohort study was designed to investigate the presence of CD68+ macrophages, ACE2, and spike proteins in placental tissue using immunohistochemical methods and to compare these results with oxidative stress from our previous study. Spike and CD68+ macrophages’ immunoreactivity were more pronounced in the placental tissue of patients from the SARS-CoV-2 group. Placental tissue spike protein and CD68+ immunoreactivity correlate with maternal and fetal Thiobarbituric Acid Reactive (TBARS) levels. This study has confirmed that spike protein expression in placental tissue is associated with the newborn’s stay in intensive neonatal care. Therefore, immunoreactivity analysis for the Spike antigen is important in detecting newborns at risk of early neonatal complications.