Journal of obstetrics and women's diseases

BACKGROUND: Pelvic floor pathology is a leading cause of gynecological disease, affecting many women of all ages and negatively impacting their quality of life. Despite numerous scientific publications and constantly evolving approaches to diagnosis and treatment, many questions remain open, and the need to improve early diagnosis and prevention methods continues to be an urgent task. The need to implement innovative analytical tools based on mathematical predictive models underscores the critical importance of in-depth study of the risk factors that influence the development of pelvic floor dysfunction.

AIM: Based on the analysis of the anatomical and functional characteristics of the female pelvic floor, the aim of this study was to develop a prognostic model for assessing the risk of developing pelvic dysfunctions in women.

METHODS: A single-center case-control study was conducted. In Group 1, patients reported the onset of pelvic floor dysfunction symptoms within the past 12 months; in Group 2, there were no complaints associated with pelvic dysfunction. Inclusion criteria were age above 18 years or older, Caucasian ethnicity, and signed informed consent. Pregnant women, recent postpartum women (less than 24 months), and those with acute gynecological conditions or genital malformations were excluded. Anatomical and functional characteristics were evaluated using the Pelvic Organ Prolapse Quantification System (POP-Q) and PERFECT systems, alongside pelvic floor ultrasound measurements. Binary logistic regression was utilized to develop a predictive model, validated by ROC curve analysis.

RESULTS: The study involved 218 women: 115 patients in Group 1 and 103 patients in Group 2. The most significant predictors for pelvic floor dysfunction included pelvic floor muscle contraction strength (p = 0.012), difference in urethral inclination α-angle at rest and during the Valsalva maneuver (p = 0.016), height of the perineal tendon center (p = 0.017), number of pelvic muscle contraction repetitions when assessed using the PERFECT system (p = 0.019), thickness of musculus puborectalis (p = 0.030), thickness of musculus bulbospongiosus (p = 0.030), pelvic floor muscle endurance (p = 0.039), and asymmetry index of musculi bulbospongiosus (p = 0.046). The model demonstrated high predictive accuracy (AUC 0.870; sensitivity 78.3%, specificity 82.5%).

CONCLUSION: The created model for assessing the risk of developing pelvic floor dysfunction has high prognostic characteristics. A key advantage of the created model is its universality in relation to the age of patients, which allows assessing the risk of pelvic dysfunction in women at different age periods. Using the created model for assessing the probability of developing pelvic dysfunction in women will enable timely correction of any identified pathology.

BACKGROUND: Early-onset preeclampsia in multifetal pregnancy is a major clinical challenge associated with high maternal and perinatal morbidity and mortality. Its pathogenesis is complex and is thought to arise from interactions between genetic susceptibility and environmental factors, with oxidative stress representing a key mechanistic component. Although the genetic basis of oxidative stress has been investigated in a number of domestic and international research centers, comprehensive studies that integrate the epistatic interactions between genes and their relationship to oxidative status in patients with multifetal pregnancy remain scarce.

AIM: The aim of this study was to assess the frequency of polymorphic variants in genes involved in hemostasis and folate metabolism, identify significant epistatic interactions, and evaluate oxidative status markers in patients with multifetal pregnancy complicated by early-onset preeclampsia.

METHODS: This single-center case-control study included patients with multifetal pregnancy, with or without preeclampsia. Genotyping of 12 single nucleotide variants in hemostasis related genes (F2, F5, F7, F13, FGB, ITGA2, ITGB3, SERPINE1) and folate cycle genes (MTHFR, MTRR, MTR) was performed using real-time polymerase chain reaction. Oxidative status was assessed by total antioxidant capacity, lipid peroxidation index (PerOx), and the integral oxidative stress index (OxyStat). Epistasis was explored using the generalized multifactor dimensionality reduction (GMDR) method.

RESULTS: The study included 157 women (main group: 38 women with early-onset preeclampsia; control group: 119 women without preeclampsia). The carriage of minor alleles in the SERPINE1 −6755G>4G, ITGA2 807C>T, and MTRR 66A>G gene variants was associated with an increased risk of early-onset preeclampsia in multifetal pregnancy. The GMDR method identified significant epistatic interactions; the most predictive three-locus model (ITGA2 + SERPINE1 + MTRR genes) achieved a balanced accuracy of 0.8902 with a sensitivity of 97.5%. Patients with preeclampsia exhibited a marked oxidative imbalance, with a 4.2-fold decrease in total antioxidant capacity and nearly 3-fold increases in PerOx and OxyStat compared to control values. The carriage of the SERPINE1 4G allele and the ITGA2 T allele was associated with more pronounced impairment of oxidative status.

CONCLUSION: The data obtained support a plausible pathogenic link between genetic susceptibility and oxidative stress in early-onset preeclampsia in multifetal pregnancy. Unfavorable genotype combinations in the SERPINE1, ITGA2, and MTRR genes may confer a high genetic risk that, in the context of multifetal gestation, is realized through hypercoagulability, endothelial dysfunction, and placental ischemia-reperfusion, culminating in severe oxidative stress and clinical manifestation of preeclampsia. The results substantiate the rationale for a comprehensive risk stratification approach integrating genetic testing and oxidative status assessment.

BACKGROUND: Late intrauterine fetal death is the dominant cause of perinatal mortality in developed economies. Despite progress in reducing neonatal mortality, the incidence of stillbirths has stagnated over the past decades. Morphological examination of the placenta, which provides a wealth of diagnostic information, has the potential of in-depth insight into the pathophysiological mechanisms that underlie adverse pregnancy outcomes, including late intrauterine fetal death.

AIM: The aim of this study was to assess the relationship between different types of placental inflammation and fetal death before 28 weeks of gestation.

METHODS: This case-control study included patients with intrauterine fetal death at 22⁺⁰–27⁺⁶ weeks of gestation (main group) and with a live birth (control group). Morphological examination of the placentas was performed using the standard technique of formalin fixation, alcohol dehydration, and paraffin embedding. Sections approximately 6–8 µm thick were prepared for hematoxylin and eosin staining. For morphological examination, 12 placental samples were prepared (material was collected from the central, paracentral, and peripheral zones, with 4 samples from each zone). Inflammatory changes were determined, expressed as characteristic cellular infiltration of various placental structures, namely, the chorionic plate, basal and parietal decidua, amnion, and villous stroma.

RESULTS: The study included 97 patients, of which 36 women formed the main group and 61 women formed the control group. Inflammation of any localization was 2.4 times more common in the group with late intrauterine fetal death compared to the control group (p = 0.004). Chorioamnionitis, intervillitis, and villitis were 3.7 (p = 0.001), 2.75 (p = 0.003), and 4.5 times (p = 0.02) more common in the stillbirth group, respectively. In the group of women who delivered a live infant, placental inflammation was more often associated with the presence of pathogens than in the group with late intrauterine fetal death (p = 0.003). In patients with stillbirth, the presence of microorganisms in bacterial cultures from the cervical canal was associated with three or more microorganisms in quantities greater than 10⁵ CFU/ml. The leading microorganisms were Staphylococcus aureus, Escherichia coli, Acinetobacter Baumannii, Enterococcus faecalis, Staphylococcus haemolyticus, and Proteus vulgaris. Inflammatory reactions, with the exception of funisitis, were observed more frequently in the placentas of women in the main group.

CONCLUSION: The increased frequency of inflammatory placental lesions in stillbirths suggests that inflammation may play a key role in the etiology of intrauterine fetal death before 28 weeks of gestation.

BACKGROUND: Alcohol consumption during pregnancy has a negative impact on the expectant mother’s body and the fetus, especially in early gestation. Even in small doses, ethanol promotes lipid peroxidation, which is a major pathogenic mechanism for the onset of carbonyl and oxidative stresses. To date, the parameters of these metabolic stresses and their impact in the first trimester of pregnancy remain poorly understood.

AIM: The aim of this study was to evaluate the individual parameters of oxidative and carbonyl stresses in the blood plasma of women in the first trimester of pregnancy and their correlation with phosphatidylethanol level as a marker of alcohol consumption.

METHODS: This case-control study included women in the first trimester of pregnancy. To identify the fact and amount of alcohol consumption, plasma levels of phosphatidylethanol 16:0/18:1 were determined by high-performance liquid chromatography–mass spectrometry. Depending on the marker concentration, groups of women were identified: Group 1, ≤8 ng/ml (non-drinkers, control); Group 2, 8–45 ng/ml (women who consumed less than 1 dose over the past 28 days); and Group 3, ≥45 ng/ml (women who consumed more than 1 dose over the past 28 days). To assess oxidative and carbonyl stress parameters, plasma levels of lipid peroxidation products, advanced oxidation protein products, and oxidative DNA modifications were determined by spectrophotometric and immunoassay methods.

RESULTS: The study included 167 women (n = 63 in Group 1, n = 68 in Group 2, and n = 36 in Group 3). The levels of ketodienes and conjugated trienes in Groups 2 and 3 of women were higher than in the control group (p = 0.001 and p = 0.003, respectively). In Group 2, the levels of advanced oxidation protein products and oxidative DNA modifications were lower than in the control group (p <  0.001 and p <  0.001, respectively) and Group 3 (p = 0.014 and p <  0.001, respectively). ROC analysis showed the diagnostic significance of ketodienes and conjugated trienes (p <  0.001), advanced oxidation protein products (p = 0.057), and 8-OH-deoxyguanosine (p <  0.001) for Group 2 of pregnant women, and only ketodienes and conjugated trienes for Group 3 (p = 0,002). When analyzing pregnant women who consumed alcohol, informative were the levels of advanced oxidation protein products (p = 0,009) and 8-OH-deoxyguanosine (p <  0,001).

CONCLUSION: The consumption of alcohol by pregnant women, even in small doses, affects free radical homeostasis, which can contribute to metabolic disorders in the mother-placenta-fetus system. The use of ROC analysis revealed that oxidative and carbonyl stress parameters are sensitive markers of alcohol consumption in the first trimester of pregnancy.

The female reproductive tract microbiota plays a key role in maintaining women’s health, including the reproductive function. Contemporary research refutes the notion of sterility in the upper reproductive tract and proves the existence of unique microbial communities in the vagina, cervical canal, endometrium, fallopian tubes, and ovaries. An imbalance in this ecosystem — dysbiosis — is characterized by a decrease in lactobacilli (especially Lactobacillus crispatus) and an increase in opportunistic pathogens (Gardnerella, Prevotella, Atopobium). This condition is associated with a wide range of pathologies, such as chronic endometritis, infertility, pregnancy loss, pelvic inflammatory disease, and endometriosis, as well as the persistence of human papillomavirus and the progression of cervical neoplasia. Dysbiosis triggers a local inflammatory response, creating unfavorable conditions for embryo implantation and pregnancy progression. The diagnosis of microbiota disorders is currently undergoing significant changes. Traditional methods (microscopy, culture) are increasingly being replaced by high-precision molecular genetic technologies, such as 16S ribosomal RNA gene sequencing and metagenomic analysis, which allow for a detailed characterization of the taxonomic and functional potential of the microbiota. Modern approaches to correcting dysbiosis include not only etiotropic antibiotic therapy but also strategies for restoring a normal microbial balance using probiotics, synbiotics, phage therapy, postbiotics, and promising methods such as vaginal microbiota transplantation. Thus, comprehensive assessment and targeted modulation of the female reproductive tract microbiota open new avenues for personalized and targeted therapy of gynecological diseases and improving reproductive outcomes.

Despite their rarity, trophoblastic tumors are an important obstetric problem due to the high risk of severe complications in both the mother and fetus. Trophoblastic disease, including its benign and malignant manifestations, most often affects young women at an age when their social life is most active and their reproductive function is at its peak. This circumstance underscores the importance and urgency of finding effective treatments for this pathology, as well as preserving the reproductive health of patients. Hydatidiform mole is a benign variant of trophoblastic disease. In addition, it poses a serious threat in early pregnancy, as it can be asymptomatic in the first two months of gestation, which in turn creates significant difficulties for its timely diagnosis. The article describes a rare clinical case of pregnancy and delivery of a healthy live fetus with a partial hydatidiform mole, as well as the features of pregnancy and postpartum management. The patient’s pregnancy was accompanied by ovarian hyperstimulation, threatened miscarriage, and premature labor, with bilateral giant theca lutein cysts being formed. The cysts form in the ovaries due to high levels of human chorionic gonadotropin and prolactin. The pregnancy outcome was favorable.