Abstract Objective: To provide a contemporary synthesis of maternal, obstetric, and neonatal outcomes associated with active tuberculosis (TB) during pregnancy and identify clinically relevant factors linked to poorer prognosis. Methods: A systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 Statement and prospectively registered in PROSPERO. PubMed and Scopus were searched from database inception to June 30, 2026. Observational studies evaluating maternal, obstetric, and neonatal outcomes among pregnant women with active TB were included. Methodological quality was assessed using the Newcastle-Ottawa Scale. Due to substantial clinical and methodological heterogeneity, findings were synthesized narratively following the Synthesis Without Meta-analysis guidelines. Results: Twelve observational studies met the inclusion criteria. Active maternal TB was consistently associated with adverse obstetric and neonatal outcomes, including preterm birth, low birth weight, small-for-gestational-age status, stillbirth, miscarriage, and neonatal mortality. Women who developed TB following in vitro fertilization and embryo transfer (IVF-ET) experienced more severe disease and worse pregnancy outcomes than those who conceived naturally. Among studies evaluating drug-resistant TB, maternal treatment outcomes were generally favorable with newer or repurposed regimens, although adverse pregnancy and infant outcomes remained a concern. Conclusion: Active TB during pregnancy is consistently associated with adverse maternal, obstetric, and neonatal outcomes, with the greatest burden observed among women with severe or disseminated disease, human immunodeficiency virus co-infection, drug-resistant TB, or TB following IVF-ET. Early detection, rapid diagnostic testing, timely and effective treatment, and multidisciplinary care are essential for reducing preventable maternal and neonatal morbidity. Further prospective, multicenter studies are needed to strengthen the evidence base and inform pregnancy-specific clinical guidelines. Registration: PROSPERO; CRD420261426021
Abstract. Obstetric shock has traditionally been conceptualized within the framework of hemorrhage and macrocirculatory collapse. However, clinical deterioration may occur despite preserved blood pressure and cardiac output, indicating that disturbances in tissue perfusion and cellular metabolism can precede overt hemodynamic instability. This narrative review synthesizes current evidence examining the contributions of microcirculatory dysfunction, endothelial glycocalyx injury, mitochondrial impairment, immune–metabolic dysregulation, and placental signaling to the development and progression of obstetric shock beyond conventional hemodynamic paradigms. A literature review was conducted using PubMed/MEDLINE and PubMed Central, focusing on studies in obstetrics, critical care, endothelial biology, microcirculatory physiology, and mitochondrial function, with articles selected for their mechanistic, translational, and clinical relevance. Available evidence suggests that disruption of the microcirculation, endothelial injury, and impaired cellular energy metabolism may interact to produce tissue hypoperfusion despite preserved systemic hemodynamics, a phenomenon described as hemodynamic incoherence. These mechanisms may contribute to diverse clinical phenotypes, including normotensive hypoperfusion, endothelial dysfunction–associated shock, microthrombotic states, and impaired cellular oxygen utilization. Although much of the supporting evidence derives from studies of preeclampsia, sepsis, and non-obstetric critical illness rather than obstetric shock itself, these findings provide biologically plausible mechanistic insights that may improve understanding of unexplained maternal deterioration. Emerging physiologic monitoring techniques may facilitate earlier recognition of occult tissue hypoperfusion, although their validation and routine clinical application in obstetric practice remain limited. Overall, obstetric shock should be considered a heterogeneous syndrome that extends beyond hemorrhage alone, and an integrated framework incorporating microvascular, endothelial, metabolic, and placental processes may improve understanding of its pathophysiology while informing future diagnostic and therapeutic research. Further obstetric-specific studies are required to validate these concepts and define their clinical implications.
Abstract Objective: To investigate the role of decidual methyl-CpG-binding protein 2 ( MeCP2 ) expression in the pathogenesis of preeclampsia by comparing preeclamptic patients with normotensive pregnant controls, and to elucidate the underlying mechanisms through which this epigenetic regulator exerts its effects. Methods: Differentially expressed genes in the decidua of patients with preeclampsia were analyzed using single-cell sequencing. Target molecule expression was validated using western blotting, qPCR, and immunohistochemistry. Furthermore, the expression levels of DNA methyltransferase-related genes and decidualization markers were examined, and DNA 5-hydroxymethylcytosine (5-hmC) methylation levels were detected by enzyme-linked immunosorbent assay. To investigate the roles of decidualization and MeCP2 in preeclampsia, an in vitro model using human endometrial stromal cells (hESCs) was established. Decidualization was then induced, and MeCP2 was knocked down and the effects assessed. RNA sequencing was also used to analyze the effect of MeCP2 in hESCs. Results: MeCP2 expression was decreased in the decidua of patients with preeclampsia, accompanied by features indicative of decidualization defects. Aberrant DNA methylation levels, along with altered expression of DNA methyltransferase-related genes, were observed in the pre-eclamptic decidua, alongside an upregulation of DNA 5-hmC methylation levels. These findings suggest that an association exists between aberrant DNA methylation and impaired decidualization in preeclampsia. Further investigation revealed that the knockdown of MeCP2 in human endometrial stromal cells (hESCs) resulted in reduced decidualization capacity. Conclusion: In the preclamptic decidua, decreased expression of MeCP2 and aberrant DNA methylation are associated with defects in decidualization. Using an in vitro ESC model, MeCP2 was found to be associated with the decidualization process, wherein its knockdown resulted in characteristics of decidualization impairment.
