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A project set up to provide the first systematically collected population health data for women in Northern Cyprus has received a number of generous donations. This support will enable researchers to better understand health and illness patterns, as well as the personal, social and economic burden of disease, in this relatively isolated region.
Adverse drug reactions that arise from the use of medicinal products outside the terms of the marketing authorisation.
BACKGROUND: New European (EU) pharmacovigilance (PV) legislation, introduced in 2012, widened the scope of an Adverse Drug Reactions (ADR) definition so that it also includes noxious and unintended response to a medicinal product arising from the use outside the terms of the marketing authorisation (MA), whereby the use outside the MA also includes off-label use, overdose, misuse, abuse and medication errors (MEs). OBJECTIVES: To explore the ADRs arising from the use outside the terms of the MA reports in the Croatian pharmacovigilance database. METHODS: A retrospective, observational study of the HALMED PV database was undertaken before and after the implementation of the new legislation in Croatia. The outcome measure included ADRs arising from the use of the products outside the terms of the MA. An assessment was performed based on the information provided in a reference document, an SmPC, using predefined criteria. RESULTS: Among 679 ADRs included in the analysis, 162 (23,9%) ADR reports were related to the use outside of the MA, 370 (54,5%) were related to the use within the MA and 147 (21,6%) were adjudged as not-assessable. Our study demonstrated a significant increase in the number of ADRs arising from the use outside the terms of the MA after the implementation of the new legislation (P = 0,039), primarily due to a notable increase in the number of overdose reports received by the poisoning centre, while the number of ADRs caused by MEs did not change significantly (p = 0,672). CONCLUSION: This study elucidated partial implementation of the new EU PV legislation and the need for instilling proper education for patients and HCPs, improving reporting systems and strengthening collaboration between relevant stakeholders.
A method to isolate syncytiotrophoblast-derived medium-large extracellular vesicle small RNA from maternal plasma.
Syncytiotrophoblast-derived extracellular vesicles (STB-EVs) have an important role in placental research: both as mediators of feto-maternal signalling and as liquid biopsies reflecting placental health. Recent evidence highlights the importance of STB-EV RNA. Isolation of STB-EV RNA from maternal blood is therefore an important challenge. We describe a novel technique where we first separate medium-large particles from plasma using centrifugation then use a highly specific bead-bound antibody to placental alkaline phosphatase to separate STB-EVs from other similar-sized particles. We demonstrate the yield and size profile of small RNA obtained from plasma STB-EVs. We present data confirming isolation of placenta-derived micro RNA from maternal plasma using this method. The technique has been successfully applied to validate novel RNA discoveries from placental perfusion models. We propose it could offer new insights through transcriptomic analyses, providing a syncytiotrophoblast-specific signal from maternal blood.
Neuropilin-1 is uniquely expressed on small syncytiotrophoblast extracellular vesicles but not on medium/large vesicles from preeclampsia and normal placentae.
UNLABELLED: Preeclampsia (PE) is a multisystem progressive hypertensive disorder unique to human pregnancy. The placenta is fundamental to its pathogenesis and releases placental factors as well as extracellular vesicles (small and medium/large syncytiotrophoblast extracellular vesicles (STB-EVs)) as a response to syncytiotrophoblast stress such as tissue factor and plasminogen activator inhibitors 1. Neuropilin 1 (NRP-1) is an anti-angiogenic factor involved in development, angiogenesis, arteriogenesis, and vascular permeability. NRP-1 acts as a co-receptor for growth factors such as vascular endothelial growth factor (VEGF), placenta growth factor (PLGF), and epidermal growth factor (EGF). Given the documented pro and anti-angiogenic roles of STB-EVs, we hypothesized that 1) STB-EVs might express NRP-1; and 2) the expression of NRP-1 might differ between normal and preeclampsia STB-EVs. METHODS: We isolated STB-EVs (both small and medium/large) from PE and NP placentae using the physiologic ex vivo dual lobe perfusion model. The enriched STB-EVs were characterized by Western blot, transmission electron microscopy (TEM), and nanoparticle tracking analysis (NTA) according to the international society of extracellular vesicles (ISEV) guidelines. We assessed for NRP-1 expression with Western blot (placenta and STB-EVs) and immunohistochemistry (placenta). We performed co-expression analysis for placenta alkaline phosphatase (PLAP - a known STB-EV marker) and NRP-1 with immunoprecipitation followed by Western blot. RESULTS: We confirmed NRP-1 expression in NP and PE placenta. We showed that NRP-1 Expression was limited to small syncytiotrophoblast membrane extracellular vesicles (S STB-EVs) but not medium/large STB-EVs and that NRP-1 is co-expressed with PLAP. CONCLUSION: Neuropilin-1 is uniquely expressed on small syncytiotrophoblast extracellular vesicles but not on medium/large vesicles from preeclampsia and normal placentae.
Syncytiotrophoblast Extracellular Vesicles From Late-Onset Preeclampsia Placentae Suppress Pro-Inflammatory Immune Response in THP-1 Macrophages
Syncytiotrophoblast derived Extracellular Vesicles (STBEV) from normal pregnancy (NP) have previously been shown to interact with circulating monocytes and B cells and induce pro-inflammatory cytokine release. Early-onset preeclampsia (EOPE) is associated with an exacerbated inflammatory response, yet there is little data regarding late-onset PE (LOPE) and immune function. Here, using a macrophage/monocyte cell line THP-1, we investigated the inflammatory potential of STBEV, comprising medium/large-STBEV (>200nm) and small-STBEV (<200nm), isolated from LOPE (n=6) and normal (NP) (n=6) placentae via dual-lobe ex-vivo placental perfusion and differential centrifugation. THP-1 cells bound and internalised STBEV isolated from NP and LOPE placentae, as revealed by flow cytometry, confocal microscopy, and ELISA. STBEV-treated THP-1 cells were examined for cytokine gene expression by RT-qPCR and the cell culture media examined for secreted cytokines/chemokines. As expected, NP medium/large-STBEV significantly upregulated the transcriptional expression of TNF-α, IL-10, IL-6, IL-12, IL-8 and TGF-β compared to PE medium/large-STBEV. However, there was no significant difference in the small STBEV population between the two groups, although in general, NP small STBEVs slightly upregulated the same cytokines. In contrast, LOPE STBEV (medium and large) did not induce pro-inflammatory responses by differentiated THP-1 macrophages. This decreased effect of LOPE STBEV was echoed in cytokine/chemokine release. Our results appear to suggest that STBEV from LOPE placentae do not have a major immune-modulatory effect on macrophages. In contrast, NP STBEV caused THP-1 cells to release pro-inflammatory cytokines. Thus, syncytiotrophoblast extracellular vesicles from LOPE dampen immune functions of THP-1 macrophages, suggesting an alternative mechanism leading to the pro-inflammatory environment observed in LOPE.
Syncytiotrophoblast‐derived extracellular vesicles carry apolipoprotein‐E and affect lipid synthesis of liver cells in vitro
AbstractIn normal pregnancy, hepatic metabolism adaptation occurs with an increase in lipid biosynthesis. Placental shedding of syncytiotrophoblast‐derived extracellular vesicles (STBEVs) into the maternal circulation constitutes a major signalling mechanism between foetus and mother. We investigated whether STBEVs from normal pregnant women might target liver cells in vitro and induce changes in lipid synthesis. This study was performed at the Nuffield Department of Women's & Reproductive Health, Oxford, UK. STBEVs were obtained by dual‐lobe placental perfusion from 11 normal pregnancies at term. Medium/large and small STBEVs were collected by ultracentrifugation at 10,000g and 150,000g, respectively. STBEVs were analysed by Western blot analysis and flow cytometry for co‐expression of apolipoprotein‐E (apoE) and placental alkaline phosphatase (PLAP). The uptake of STBEVs by liver cells and the effect on lipid metabolism was evaluated using a hepatocarcinoma cell line (HepG2 cells). Data were analysed by one‐way ANOVA and Student's t test. We demonstrated that: (a) STBEVs carry apoE; (b) HepG2 cells take up STBEVs through an apoE‐LDL receptor interaction; (c) STBEV incorporation into HepG2 cells resulted in (i) increased cholesterol release (ELISA); (ii) increased expression of the genes SQLE and FDPS (microarray) involved in cholesterol biosynthesis; (iii) downregulation of the CLOCK gene (microarray and PCR), involved in the circadian negative control of lipid synthesis in liver cells. In conclusion, the placenta may orchestrate the metabolic adaptation of the maternal liver through release of apoE‐positive STBEVs, by increasing lipid synthesis in a circadian‐independent fashion, meeting the nutritional needs of the growing foetus.
Placental Vesicles Carry Active Endothelial Nitric Oxide Synthase and Their Activity is Reduced in Preeclampsia
Preeclampsia, a multisystem hypertensive disorder of pregnancy, is associated with increased systemic vascular resistance. Placentae from patients with preeclampsia have reduced levels of endothelial nitric oxide synthase (eNOS) and, thus, less nitric oxide (NO). Syncytiotrophoblast extracellular vesicles (STBEV), comprising microvesicles (STBMV) and exosomes, carry signals from the syncytiotrophoblast to the mother. We hypothesized that STBEV-bound eNOS (STBEV-eNOS), capable of producing NO, are released into the maternal circulation. Dual-lobe ex vivo placental perfusion and differential centrifugation was used to isolate STBEV from preeclampsia (n=8) and normal pregnancies (NP; n=11). Plasma samples of gestational age–matched preeclampsia and NP (n=6) were used to isolate circulating STBMV. STBEV expressed placental alkaline phosphatase, confirming placental origin. STBEV coexpressed eNOS, but not inducible nitric oxide synthase, confirmed using Western blot, flow cytometry, and immunodepletion. STBEV-eNOS produced NO, which was significantly inhibited by N G -nitro- l -arginine methyl ester (eNOS inhibitor; P <0.05) but not by N -(3-(aminomethyl) bezyl) acetamidine) (inducible nitric oxide synthase inhibitor). STBEV-eNOS catalytic activity was confirmed by visualizing eNOS dimerization. STBEV-eNOS was more abundant in uterine vein compared with peripheral blood, indicating placental origin. STBEV isolated from preeclampsia-perfused placentae had lower levels of STBEV-eNOS (STBMV; P <0.05) and overall lower NO activity (STBMV, not significant; syncytiotrophoblast extracellular exosomes, P <0.05) compared with those from NP. Circulating plasma STBMV from preeclampsia women had lower STBEV-eNOS expression compared with that from NP women ( P <0.01). This is the first observation of functional eNOS expressed on STBEV from NP and preeclampsia placentae, as well as in plasma. The lower STBEV-eNOS NO production seen in preeclampsia may contribute to the decreased NO bioavailability in this disease.
Placental extracellular vesicles express active dipeptidyl peptidase IV; levels are increased in gestational diabetes mellitus
ABSTRACTGestational diabetes mellitus (GDM) is the most common metabolic disorder in pregnancy and is characterized by insulin resistance and decreased circulating glucagon‐like peptide‐1 (GLP‐1). GDM resolves rapidly after delivery implicating the placenta in the disease. This study examines the biological functions that cause this pathology. The placenta releases syncytiotrophoblast‐derived extracellular vesicles (STB‐EVs) into the maternal circulation, which is enhanced in GDM. Dipeptidyl peptidase IV (DPPIV) is known to play a role in type 2 diabetes by breaking down GLP‐1, which in turn regulates glucose‐dependent insulin secretion. STB‐EVs from control and GDM women were analysed. We show that normal human placenta releases DPPIV‐positive STB‐EVs and that they are higher in uterine than paired peripheral blood, confirming placental origin. DPPIV‐bound STB‐EVs from normal perfused placentae are dose dependently inhibited with vildagliptin. DPPIV‐bound STB‐EVs from perfused placentae are able to breakdown GLP‐1 in vitro. STB‐EVs from GDM perfused placentae show greater DPPIV activity. Importantly, DPPIV‐bound STB‐EVs increase eightfold in the circulation of women with GDM. This is the first report of STB‐EVs carrying a biologically active molecule that has the potential to regulate maternal insulin secretion.
Protein Profiling of Placental Extracellular Vesicles in Gestational Diabetes Mellitus
Throughout pregnancy, some degree of insulin resistance is necessary to divert glucose towards the developing foetus. In gestational diabetes mellitus (GDM), insulin resistance is exacerbated in combination with insulin deficiency, causing new-onset maternal hyperglycaemia. The rapid reversal of insulin resistance following delivery strongly implicates the placenta in GDM pathogenesis. In this case–control study, we investigated the proteomic cargo of human syncytiotrophoblast-derived extracellular vesicles (STBEVs), which facilitate maternal–fetal signalling during pregnancy, in a UK-based cohort comprising patients with a gestational age of 38–40 weeks. Medium/large (m/l) and small (s) STBEVs were isolated from GDM (n = 4) and normal (n = 5) placentae using ex vivo dual-lobe perfusion and subjected to mass spectrometry. Bioinformatics were used to identify differentially carried proteins and mechanistic pathways. In m/lSTBEVs, 56 proteins were differently expressed while in sSTBEVs, no proteins reached statistical difference. Differences were also observed in the proteomic cargo between m/lSTBEVs and sSTBEVs, indicating that the two subtypes of STBEVs may have divergent modes of action and downstream effects. In silico functional enrichment analysis of differentially expressed proteins in m/lSTBEVs from GDM and normal pregnancy found positive regulation of cytoskeleton organisation as the most significantly enriched biological process. This work presents the first comparison of two populations of STBEVs’ protein cargos (m/l and sSTBEVs) from GDM and normal pregnancy isolated using placenta perfusion. Further investigation of differentially expressed proteins may contribute to an understanding of GDM pathogenesis and the development of novel diagnostic and therapeutic tools.
Placental small extracellular vesicles from normal pregnancy and gestational diabetes increase insulin gene transcription and content in β cells
Abstract Insulin secretion increases progressively during pregnancy to maintain normal maternal blood glucose levels. The placenta plays a crucial role in this process by releasing hormones and extracellular vesicles into the maternal circulation, which drive significant changes in pregnancy physiology. Placental extracellular vesicles, which are detectable in the plasma of pregnant women, have been shown to signal peripheral tissues and contribute to pregnancy-related conditions. While studies using murine models have demonstrated that extracellular vesicles can modulate insulin secretion in pancreatic islets, it remains unclear whether these effects translate to human biology. Understanding how placental signals enhance insulin synthesis and secretion from β cells could be pivotal in developing new therapies for diabetes. In our study, we isolated placental small extracellular vesicles from human placentae and utilised the human β cell line, EndoC-βH3, to investigate their effects on β-cell function in vitro. Our results indicate that human β cells internalise placental small extracellular vesicles, leading to enhanced insulin gene expression and increased insulin content within the β cells. Moreover, these vesicles up-regulated the expression of Annexin A1, a protein known to increase insulin content. This up-regulation of Annexin A1 holds promise as a potential mechanism by which placental small extracellular vesicles enhance insulin biosynthesis.
In vivo evidence of significant placental growth factor release by normal pregnancy placentas
AbstractPlacental growth factor (PlGF) is an angiogenic factor identified in the maternal circulation, and a key biomarker for the diagnosis and management of placental disorders. Furthermore, enhancing the PlGF pathway is regarded as a promising therapy for preeclampsia. The source of PlGF is still controversial with some believing it to be placental in origin while others refute this. To explore the source of PlGF, we undertook a prospective study enrolling normal pregnant women undergoing elective caesarean section. The level of PlGF was estimated in 17 paired serum samples from the uterine vein (ipsilateral or contralateral to the placental insertion) during caesarean section and from a peripheral vein on the same day and second day post-partum. PlGF levels were higher in the uterine than in the peripheral vein with a median difference of 52.2 (IQR 20.1–85.8) pg/mL p = 0.0006. The difference when the sampled uterine vein was ipsilateral to the placenta was 54.8 (IQR 37.1–88.4) pg/mL (n = 11) and 23.7 (IQR −11; 70.5) pg/mL (n = 6) when the sample was contralateral. Moreover, PlGF levels fell by 83% on day 1–2 post-partum. Our findings strongly support the primary source of PlGF to be placental. These findings will be of value in designing target therapies such as PlGF overexpression, to cure placental disorders during pregnancy.
Genome-wide association study meta-analysis provides insights into the etiology of heart failure and its subtypes.
Heart failure (HF) is a major contributor to global morbidity and mortality. While distinct clinical subtypes, defined by etiology and left ventricular ejection fraction, are well recognized, their genetic determinants remain inadequately understood. In this study, we report a genome-wide association study of HF and its subtypes in a sample of 1.9 million individuals. A total of 153,174 individuals had HF, of whom 44,012 had a nonischemic etiology (ni-HF). A subset of patients with ni-HF were stratified based on left ventricular systolic function, where data were available, identifying 5,406 individuals with reduced ejection fraction and 3,841 with preserved ejection fraction. We identify 66 genetic loci associated with HF and its subtypes, 37 of which have not previously been reported. Using functionally informed gene prioritization methods, we predict effector genes for each identified locus, and map these to etiologic disease clusters through phenome-wide association analysis, network analysis and colocalization. Through heritability enrichment analysis, we highlight the role of extracardiac tissues in disease etiology. We then examine the differential associations of upstream risk factors with HF subtypes using Mendelian randomization. These findings extend our understanding of the mechanisms underlying HF etiology and may inform future approaches to prevention and treatment.
The mHealth clinical decision-making tools for maternal and perinatal health care in Sub-Saharan Africa: A systematic review
Introduction mobile Health (mHealth) refers to use of mobile wireless technologies for health. The potential for mHealth to enhance healthcare delivery is supported by near-universal availability of mobile phones and their expanding coverage in low- and middle-income countries. This systematic review analyses the available evidence on mHealth clinical decision-making tools in maternal and perinatal health, and whether they lead to improved maternal and perinatal health outcomes in Sub-Saharan Africa (SSA). Methods Eligibility criteria: Studies conducted in SSA describing mHealth tools piloted or used for clinical decision-making in maternal or perinatal healthcare. Exclusion criteria included mHealth tools used outside of maternal and perinatal healthcare, publications lacking sufficient detail (where information couldn’t be obtained through contacting authors), articles where tools were used on a laptop or desktop computer, and articles not published in English. Data sources: PubMed, CINAHL, EMBASE, Global Health, and Web of Science were searched for relevant articles following a predetermined search strategy with no date restrictions. A limited grey literature search was conducted. Risk of bias: We assessed the quality of included studies using the Cochrane Risk of bias 2 tool, Newcastle- Ottawa scale and COREQ. This comprehensive approach ensured a rigorous evaluation of bias and validity in our systematic review. Data extraction and synthesis: Two independent reviewers screened articles and extracted data. Results 1119 records were screened, and 36 articles met the inclusion criteria. Fifteen mHealth tools were identified across 11 SSA countries. Conclusion mHealth tools for clinical decision-making in maternal and perinatal care were found to be feasible, usable, and acceptable. They demonstrated adequate user satisfaction, and some demonstrated improvement of pregnancy outcomes. However, technologies lack scalability, with only one scaled up nationally, and few tools interacted with existing health information systems or had plans for sustainability. This review will help establish best practice for developing and scaling up mHealth clinical decision-making tools, helping to improve maternal and perinatal healthcare in SSA.
Measurement, determinants and outcomes of maternal care satisfaction in Nigeria: a systematic review
IntroductionMaternal mortality rates are unacceptably high in Nigeria. Understanding women’s satisfaction with the maternity health system is fundamental, as perceived quality of care is a determinant of service utilisation and improved birth outcomes.ObjectivesThis systematic review aims to explore patients’ satisfaction with maternal healthcare in Nigeria, examining the measurement, determinants, and outcomes of satisfaction.DesignA systematic review following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines.Data sourcesSearches were conducted in Embase, Maternity and Infant Care, Global Health, Ovid, Africa Journals Online, Cochrane Central Register of Controlled Trials, MEDLINE, Web of Science, Cumulative Index to Nursing and Allied Health Literature (CINAHL), Scopus and Google Scholar, alongside citation searches of relevant studies.Eligibility criteriaOriginal studies assessing patient satisfaction with maternal health services in Nigeria were included. There were no restrictions on study design types. Studies were excluded if they did not clearly define how satisfaction was measured or did not focus on the maternal health service domains under review (ie, antenatal, delivery, and/or postnatal care).Data extraction and synthesisKey information relevant to this study was extracted into an Excel spreadsheet and narratively synthesised. The Quality Assessment for Diverse Studies tool was used to appraise the quality of the selected literature.ResultsMaternal care satisfaction (MCS) ratings are high in Nigeria, but this may either indicate genuine positive experiences or be influenced by measurement-related biases. Several factors determine women’s satisfaction with maternity services. Key factors influencing MCS in Nigeria are positive client-provider relationships, a favourable hospital environment with easy accessibility and affordable care costs. While our study demonstrated a correlation between MCS and socioeconomic and demographic factors, there is no complete consensus within the literature about this correlation. Furthermore, patient satisfaction was associated with women’s future health-seeking behaviour and willingness to recommend care to others.ConclusionUnderstanding the multifaceted nature of MCS determinants and outcomes can better equip us to provide the support and care that mothers need to thrive. The findings from this study can inform policy, improve health responsiveness and ensure that women are provided with satisfactory and patient-centred maternity care, hence leading to a decline in poor pregnancy outcomes in Nigeria. It also highlights the need for robust methodologies that accurately measure women’s experiences, which is essential for enhancing the quality of maternal health services.PROSPERO registration numberA protocol was developed for this study and published on PROSPERO, the International Prospective Register of Systematic Reviews (CRD42023414771).
PatchCTG: A Patch Cardiotocography Transformer for Antepartum Fetal Health Monitoring
Antepartum Cardiotocography (CTG) is a biomedical sensing technology widely used for fetal health monitoring. While the visual interpretation of CTG traces is highly subjective, with the inter-observer agreement as low as 29% and a false positive rate of approximately 60%, the Dawes–Redman system provides an automated approach to fetal well-being assessments. However, it is primarily designed to rule out adverse outcomes rather than detect them, resulting in a high specificity (90.7%) but low sensitivity (18.2%) in identifying fetal distress. This paper introduces PatchCTG, an AI-enabled biomedical time series transformer for CTG analysis. It employs patch-based tokenisation, instance normalisation, and channel-independent processing to capture essential local and global temporal dependencies within CTG signals. PatchCTG was evaluated on the Oxford Maternity (OXMAT) dataset, which comprises over 20,000 high-quality CTG traces from diverse clinical outcomes, after applying the inclusion and exclusion criteria. With extensive hyperparameter optimisation, PatchCTG achieved an AUC of 0.77, with a specificity of 88% and sensitivity of 57% at Youden’s index threshold, demonstrating its adaptability to various clinical needs. Its robust performance across varying temporal thresholds highlights its potential for both real-time and retrospective analysis in sensor-driven fetal monitoring. Testing across varying temporal thresholds showcased it robust predictive performance, particularly with finetuning on data closer to delivery, achieving a sensitivity of 52% and specificity of 88% for near-delivery cases. These findings suggest the potential of PatchCTG to enhance clinical decision-making in antepartum care by providing a sensor-based, AI-driven, objective tool for reliable fetal health assessment.
FIGO position statement on postpartum intrauterine devices (PPIUD)
AbstractPostpartum contraception is a critical intervention to address the unmet need for family planning, which affects over 218 million women globally, predominantly in low‐ and middle‐income countries (LMICs). Immediate postpartum family planning (PPFP) offers a unique opportunity to provide contraception during a crucial health‐seeking encounter, particularly given the rise in institutional births worldwide. Short inter‐pregnancy intervals are associated with increased maternal and neonatal morbidity and mortality, making timely postpartum contraception essential. The postpartum intrauterine device (PPIUD), a long‐acting reversible contraceptive (LARC), is a highly cost‐effective, non‐hormonal method with a low failure rate. It can be safely inserted immediately after vaginal or cesarean delivery, offering women a reliable and accessible option. However, successful implementation of PPIUD services requires overcoming barriers such as fragmented health services, provider bias, sociocultural misconceptions, and supply chain challenges. FIGO advocates for integrating PPFP, including PPIUD, into routine maternity care and emphasizes task sharing, community engagement, and comprehensive counseling as critical strategies. By incorporating postpartum contraception into standard maternal care, particularly in LMICs, health systems can improve maternal and child health outcomes, advance Sustainable Development Goals (SDGs), and empower women to make informed reproductive choices.
Review: The potential role of placental extracellular vesicles in blood-brain barrier disruption and neuroinflammation in preeclampsia
Preeclampsia is a complex pregnancy disorder characterized by hypertension and multisystem organ damage, notably affecting the liver, kidneys, and brain. Eclampsia, a severe form of preeclampsia, is marked by the sudden onset of generalized tonic-clonic seizures. Brain complications, including eclampsia, are responsible for 60–70 % of preeclampsia-related maternal deaths, particularly in low-income regions. Despite the significant impact of brain complications in preeclampsia, their underlying pathophysiology remains unclear. Evidence suggests that brain edema in preeclampsia and eclampsia results from disruption of the blood-brain barrier (BBB). Although direct analysis of the BBB is challenging, in vitro studies indicate that plasma from women with preeclampsia can compromise the BBB, with the specific circulating factors involved still unidentified. Among the potential culprits, recent findings highlight placental-derived small extracellular vesicles (PDsEVs) as key players in BBB disruption observed in preeclampsia. This review examines the role of PDsEVs in the pathophysiology of brain edema associated with preeclampsia, emphasizing areas for future research, including neuroinflammation and neuron dysfunction. Additionally, we discuss the protective role of magnesium sulfate in these processes.