Objective: To investigate the placental and umbilical cord histopathology in intrauterine growth restriction (IUGR) and their relation to second-trimester maternal hematological parameters. Materials and Methods: Patients were selected for the IUGR group based on estimated fetal weight below the 10th percentile. Patients were recruited into the control group randomly. Patients were followed up with ultrasound, and blood samples were taken between the 20th and 24th gestational weeks. After delivery and formalin fixation, weight and volume of the placenta were recorded and histologic samples were processed. Results: Maternal platelet count strongly correlates with placental weight (r = 0.766). On the other hand, neonatal weight correlates with placental volume (r = 0.572) rather than with placental weight (r = 0.469). Umbilical arterial lumen cross-sectional area correlates with birth weight (r = 0.338). Conclusions: Maternal hematological parameters do not seem to affect neonatal outcome. Our main findings are the correlation of maternal platelet count with placental weight, the correlation of placental volume with birth weight being stronger than the correlation of placental weight with birth weight, and the correlation of umbilical artery lumen cross-sectional area with neonatal weight. Mild histopathologic alterations might occur in normal pregnancies; however, sufficient fetal nutrition can be maintained. This compensatory function of the placenta seems to be insufficient when two or more pathologies are present, which is characteristic for IUGR.

Purpose: Plasmapheresis in pregnancy adversely affects maternal hemodynamics, however there are studies suggesting it to reduce pregnancy loss in immunological diseases when medication is more harmful to the fetus. The overall optimal plasmapheresis treatment protocol remains unknown. Materials and methods: A pregnant with neuromyelitis optica was followed up after receiving six volumes of fresh frozen plasma via plasmapheresis. Results: The placenta compensated the hemodynamic change until the 33rd week of gestation, resulting a small for gestational age, otherwise healthy girl. Conclusions: More research is needed on plasma exchange during pregnancy because in our observation placental circulation can adapt to the change in blood pressure.

Introduction: The prevalence of intrauterine growth restriction is 4-5000/100,000 births, and they give the majority of perinatal morbidity. Aim: The aim of the authors was to compare the pathomorphologic data and vasoreactivity of umbilical vessels and placenta of small for date newborns to that of the normal pregnancies. Method: Samples of the umbilical cord and placenta were divided into case and control groups. Two 10 cm long segments were cut of the umbilical cord at placental insertion. Tissue bath experiment was performed on umbilical vessels and pathomorphologic data were collected according to the Royal College of Pathologists' protocol. Results: After the development of basal tone, oxytocin and desmopressin did not enhance the vascular contraction, but the pathomorphological and ultrasonographic data were significantly different in the two groups. Conclusions: The results indicate that umbilical vessels might not have oxytocin or vasopressin receptors. The pathomorphologic and flowmetric differences could be the causes of small birth weight.

Candida species are common colonizers of the female genital tract during pregnancy, whereas proven intra-amniotic Candida infection is rare. Candida albicans predominates among reported isolates in about 90%, and other Candida species, especially Candida glabrata (Nakaseomyces glabratus), and C. tropicalis, C. parapsilosis, C. krusei, C. famata and C. kefyr as well have been reported in approximately 10%. The available epidemiological evidence does not support the hypothesis that uncomplicated vaginal Candida colonization or vulvovaginal candidiasis would be a major independent cause of preterm birth. In contrast, Candida chorioamnionitis is a rare, but potentially severe form of ascending infection associated with very early preterm labor, preterm premature rupture of membranes (PPROM), fetal inflammatory response and congenital or neonatal candidiasis. This scoping review examines the biological transition from vaginal colonization to dysbiosis, ascending infection and placental invasion, with special emphasis on virulence of Candida species. Lactobacillus species are part of the body’s primary defense mechanism against Candida overgrowth, especially in the gut and the vaginal tract. The relationship between Candida and other bacteria in our body has a complex characteristics. This study uncovers how a mixed bacterial and fungal infection inside the uterus (polymicrobial intra-amniotic infection) affects the placenta, why it is difficult to accurately identify it with current tests, and how antifungal treatments impact the health of the newborn. Current evidence suggests that Candida species should not be interpreted as either universally pathogenic organisms or irrelevant bystanders. Rather, its clinical significance is likely context-dependent and may reflect interactions between fungal burden, Candida strain, the bacterial microbiome, disruption of the maternal–fetal barrier and host inflammatory responses. Future research should shift from simple detection of organisms longitudinal multiomics characterization of the vaginal mycobiome, polymicrobial communities, placental invasion and fetal inflammatory response.

Galectins represent a family of proteins which are capable of specifically binding to beta-galactoside-containing sugar molecules, known as glycans. Galectins possess carbohydrate recognition domains (CRDs) that fundamentally determine their ability to bind to sugars. Galectin-14 (Gal-14) and galectin-16 (Gal-16) are members of the galectin family that is particularly associated with the placenta. The galectins in the placenta constitute a specialized subgroup functioning at the maternal–fetal interface. They are expressed primarily in the syncytiotrophoblasts. This trophoblast layer is in direct contact with maternal blood and plays a crucial role in the metabolic, hormonal and immunological interactions between the fetus and the pregnant woman. In order to prepare this structured narrative review, we conducted a structured literature search across the MEDLINE (PubMed), Embase, Cochrane Library and Web of Science Core Collection databases; the final search has been performed on 1 July 2026. The search strategy has combined the terms galectin-14/LGALS14 and galectin-16/LGALS16 with terms related to the placenta, trophoblast, pregnancy, placentation and pregnancy complications. Search results were imported into Mendeley Reference Manager to remove duplicates, and the reference lists of relevant review articles and studies were manually screened. Two reviewers (Z.K. and A.S.) independently screened the titles and abstracts and subsequently evaluated the potentially relevant full-text articles. The final evidence synthesis included primary studies that directly investigated the expression, function, regulation, or clinical associations of LGALS14 or LGALS16; secondary publications were used for background and contextual information. In experimental studies, galectin-14 has been linked to trophoblast migration and invasion—involving mechanisms such as the PI3K/Akt signaling pathway, MMP-9 and N-cadherin—as well as to the modulation of activated maternal immune cell function. Galectin-16 is structurally more distinct and exhibits reduced classical β-galactoside-binding capacity; it appears to be closely associated with trophoblast differentiation and syncytialization, presumably through intracellular protein interactions. Altered expression of placenta-specific galectins has been observed in preeclampsia and fetal growth restriction; however, the causal relationship remains unclear. Clinical evidence regarding their use as biomarkers is emerging at this time; therefore, neither galectin-14 nor galectin-16 can be currently considered as a validated, clinically applicable biomarker. Altogether, available evidence mandates further study of galectin-14 and galectin-16, as they may be important regulators of placental biology and potential biomarker candidates. However, their physiological functions and clinical utility have not yet been sufficiently confirmed; therefore, further prospective and functional studies are required. The strongest putative mechanistic link to the development of preeclampsia exists for galectin-14, primarily involving trophoblast migration and invasion as well as PI3K/Akt-related signaling pathways. In contrast, evidence in connection with the direct role of galectin-16 is limited at present.