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Preeclampsia (PE) is a multifactorial pregnancy disorder characterized by hypertension and proteinuria, posing significant risks to both maternal and fetal health. Despite extensive research, its complex pathophysiology remains incompletely understood. This narrative review aims to elucidate the intricate mechanisms contributing to PE, focusing on abnormal placentation, maternal systemic response, oxidative stress, inflammation, and genetic and epigenetic factors. This review synthesizes findings from recent studies, clinical trials, and meta-analyses, highlighting key molecular and cellular pathways involved in PE. The review integrates data on oxidative stress biomarkers, angiogenic factors, immune interactions, and mitochondrial dysfunction. PE is initiated by poor placentation due to inadequate trophoblast invasion and improper spiral artery remodeling, leading to placental hypoxia. This triggers the release of anti-angiogenic factors such as soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng), causing widespread endothelial dysfunction and systemic inflammation. Oxidative stress, mitochondrial abnormalities, and immune dysregulation further exacerbate the condition. Genetic and epigenetic modifications, including polymorphisms in the Fms-like tyrosine kinase 1 (FLT1) gene and altered microRNA (miRNA) expression, play critical roles. Emerging therapeutic strategies targeting oxidative stress, inflammation, angiogenesis, and specific molecular pathways like the heme oxygenase-1/carbon monoxide (HO-1/CO) and cystathionine gamma-lyase/hydrogen sulfide (CSE/H2S) pathways show promise in mitigating preeclampsia’s effects. PE is a complex disorder with multifactorial origins involving abnormal placentation, endothelial dysfunction, systemic inflammation, and oxidative stress. Despite advances in understanding its pathophysiology, effective prevention and treatment strategies remain limited. Continued research is essential to develop targeted therapies that can improve outcomes for both mothers and their babies.

Gestational diabetes (GD) is a metabolic disorder characterized by glucose intolerance during pregnancy, significantly impacting maternal and fetal health. Its global prevalence is approximately 14%, with risk factors including obesity, family history of diabetes, advanced maternal age, and ethnicity, which are linked to cellular and molecular disruptions in glucose regulation and insulin resistance. GD is associated with short- and long-term complications for both the mother and the newborn. For mothers, GD increases the risk of developing type 2 diabetes, cardiovascular diseases, and metabolic syndrome. In the offspring, exposure to GD in utero predisposes them to obesity, glucose intolerance, and metabolic disorders later in life. This review aims to elucidate the complex cellular and molecular mechanisms underlying GD to inform the development of effective therapeutic strategies. A systematic review was conducted using medical subject headings (MeSH) terms related to GD’s cellular and molecular pathophysiology. Inclusion criteria encompassed original studies, systematic reviews, and meta-analyses focusing on GD’s impact on maternal and fetal health, adhering to PRISMA guidelines. Data extraction captured study characteristics, maternal and fetal outcomes, key findings, and conclusions. GD disrupts insulin signaling pathways, leading to impaired glucose uptake and insulin resistance. Mitochondrial dysfunction reduces ATP production and increases reactive oxygen species, exacerbating oxidative stress. Hormonal influences, chronic inflammation, and dysregulation of the mammalian target of rapamycin (mTOR) pathway further impair insulin signaling. Gut microbiota alterations, gene expression, and epigenetic modifications play significant roles in GD. Ferroptosis and placental dysfunction primarily contribute to intrauterine growth restriction. Conversely, fetal macrosomia arises from maternal hyperglycemia and subsequent fetal hyperinsulinemia, resulting in excessive fetal growth. The chronic inflammatory state and oxidative stress associated with GD exacerbate these complications, creating a hostile intrauterine environment. GD’s complex pathophysiology involves multiple disruptions in insulin signaling, mitochondrial function, inflammation, and oxidative stress. Effective management requires early detection, preventive strategies, and international collaboration to standardize care and improve outcomes for mothers and babies.

Preeclampsia remains a major cause of maternal and perinatal morbidity and mortality worldwide, yet progress in biomarker discovery and predictive modeling has translated only modestly into clinically meaningful risk stratification. Over the past two decades, numerous biomarkers and predictors reflecting placental–angiogenic dysfunction, maternal cardiovascular maladaptation, and inflammatory–metabolic stress have been proposed, alongside increasingly sophisticated statistical and machine learning approaches. However, many predictive strategies continue to treat preeclampsia as a single disease entity and rely on static thresholds applied at isolated gestational time points. Accumulating biological and clinical evidence instead suggests that preeclampsia represents a heterogeneous syndrome composed of partially overlapping mechanistic phenotypes whose relative contributions vary across pregnancy and across individuals. In this narrative review, we argue that further progress in prediction is likely to depend less on the identification of additional biomarkers and more on how biological heterogeneity and temporal dynamics are integrated into predictive frameworks. We synthesize current evidence supporting multimarker approaches, phenotype-informed frameworks, and longitudinal risk trajectories that conceptualize prediction as a dynamic process rather than a binary classification task. We also examine the complementary roles of classical statistical models and machine learning, emphasizing that calibration, external validation, interpretability, transportability, and clinical usability are essential, alongside discrimination, for successful clinical implementation. Finally, we outline key research priorities for the next generation of predictive studies, including mechanistically grounded phenotyping, dynamic risk updating across gestation, rigorous evaluation across diverse populations, and explicit linkage of risk stratification to preventive interventions and clinical decision-making. Together, these directions support a shift toward an integrative, longitudinal, and clinically anchored approach to preeclampsia prediction.

Background Perinatal mortality, encompassing late stillbirths and neonatal mortalities, is a key indicator of maternal and neonatal health. Despite advances in health care, there have been alarming increased in perinatal mortality rates in Mexico. This study investigated the influence of social determinants on perinatal death in a Latin American middle-income country, aiming to inform equitable and effective health policies. Methods A prospective cohort study was conducted with pregnant women from Mexico City. Data on the following clinical and social factors were collected: pregestational body mass index (pBMI), lupus, antiphospholipid syndrome (APS), preeclampsia, foetal growth restriction (FGR), social vulnerability, poverty, household overcrowding, and gender-based violence. Nested logistic regression models were developed to identify significant predictors of perinatal mortality, with the results reported as odds ratios (ORs) and 95% confidence intervals (CIs). Results Among the 3,890 participants, there were 76 cases of perinatal mortality. Significant clinical predictors of perinatal mortality included higher pBMI (OR = 1.088, 95% CI 1.026–1.153), APS (OR = 10.049, 95% CI 1.843–54.803), and FGR (OR = 2.929, 95% CI 1.399–6.135), whereas high social vulnerability (OR = 5.332, 95% CI 2.485–11.443) and medium social vulnerability (OR = 3.084, 95% CI 1.528–6.222) emerged as significant social predictors of perinatal mortality. A comprehensive model incorporating both clinical and social determinants achieved an AUC of 0.921, with a detection rate of 67.1% and a false-positive rate of 10%, this indicating a significant improvement in perinatal mortality prediction. The inclusion of social determinants progressively enhanced predictive performance, underscoring their critical role in risk assessment. Conclusions Clinical and social determinants significantly influence perinatal mortality. Addressing social inequalities and integrating social determinants into perinatal care could improve maternal and neonatal health outcomes. However, limitations such as reliance on self-reported data, ecological-level indicators for social vulnerability, and potential constraints on generalizability should be considered. These findings emphasize the need for targeted health policies to reduce social vulnerabilities and enhance health care access in middle-income countries.

Background Laparoscopic cholecystectomy is known for its minimally invasive nature, but postoperative pain management remains challenging. Despite the enhanced recovery after surgery (ERAS) protocol, regional analgesic techniques like modified perichondral approach to thoracoabdominal nerve block (M-TAPA) show promise. Our retrospective study evaluates M-TAPA’s efficacy in postoperative pain control for laparoscopic cholecystectomy in a middle-income country. Methods This was a retrospective case-control study of laparoscopic cholecystectomy patients at Hospital General de Mexico in which patients were allocated to the M-TAPA or control group. The data included demographic information, intraoperative variables, and postoperative pain scores. M-TAPA blocks were administered presurgery. Outcomes: opioid consumption, pain intensity, adverse effects, and time to rescue analgesia. Analysis of variance (ANOVA) compared total opioid consumption between groups, while Student’s t test compared pain intensity and time until the first request for rescue analgesia. Results Among the 56 patients, those in the M-TAPA group had longer surgical and anesthetic times ( p  < 0.001), higher ASA 3 scores (25% vs. 3.12%, p  = 0.010), and reduced opioid consumption ( p  < 0.001). The M-TAPA group exhibited lower postoperative pain scores ( p  < 0.001), a lower need for rescue analgesia ( p  = 0.010), and a lower incidence of nausea/vomiting ( p  = 0.010). Conclusion Bilateral M-TAPA offers effective postoperative pain control after laparoscopic cholecystectomy, especially in middle-income countries, by reducing opioid use and enhancing recovery.

Background: In healthy pregnancies, components of the Renin-Angiotensin system (RAS) are present in the placental villi and contribute to invasion, migration, and angiogenesis. At the same time, soluble fms-like tyrosine kinase 1 (sFlt-1) production is induced after binding of ANG-II to its receptor (AT-1R) in response to hypoxia. As RAS plays an essential role in the pathogenesis of COVID-19, we hypothesized that angiogenic marker (sFlt-1) and RAS components (ANG-II and ACE-2) may be related to adverse outcomes in pregnant women with COVID-19; Methods: Prospective cohort study. Primary outcome was severe pneumonia. Secondary outcomes were ICU admission, intubation, sepsis, and death. Spearman’s Rho test was used to analyze the correlation between sFlt-1 and ANG-II levels. The sFlt-1/ANG-II ratio was determined and the association with each adverse outcome was explored by logistic regression analysis and the prediction was assessed using receiver-operating-curve (ROC); Results: Among 80 pregnant women with COVID-19, the sFlt-1/ANG-II ratio was associated with an increased probability of severe pneumonia (odds ratio [OR]: 1.31; p = 0.003), ICU admission (OR: 1.05; p = 0.007); intubation (OR: 1.09; p = 0.008); sepsis (OR: 1.04; p = 0.008); and death (OR: 1.04; p = 0.018); Conclusion: sFlt-1/ANG-II ratio is a good predictor of adverse events such as pneumonia, ICU admission, intubation, sepsis, and death in pregnant women with COVID-19.

Evidence from studies in the general population suggests an association between vitamin D insufficiency/deficiency and COVID-19 susceptibility and disease severity. The present study was performed on 165 third-trimester pregnant women at the time of delivery. Seventy-nine women tested negative for SARS-CoV-2. From 86 women testing positive, 32 were asymptomatic, 44 presented a mild form of the disease, and 10 experienced severe symptoms. Serum 25-OH vitamin D levels were measured on blood samples collected on admission. Low vitamin D levels were detected in symptomatic but not asymptomatic COVID-19 patients compared to healthy women (p = 0.0227). In addition, 20 (45.4%) pregnant women in the mild COVID-19 group and 6 (60%) in the severe group were vitamin D deficient (p = 0.030). On the other hand, lasso regression analysis showed that 25-OH vitamin D deficiency is an independent predictor of severe COVID-19 with an odds ratio (OR) of 5.81 (95% CI: 1.108–30.541; p = 0.037). These results show the relationship between vitamin D deficiency in pregnant women and the severity of COVID-19 infection and support the recommendation to supplement with vitamin D to avoid worse COVID-19 outcomes during pregnancy.

Background: HIV infection continues to be a global public health challenge, affecting approximately 1.7 million reproductive-aged women. Protease inhibitor-based highly active antiretroviral therapy (PI-HAART) has significantly reduced the risk of vertical transmission of HIV from mother to child. Nevertheless, concerns linger regarding the long-term effects, particularly on body composition, notably subcutaneous fat tissue (SFT). Although HIV-associated lipodystrophy syndrome (LS) has been well documented in adults and older children, its impact on fetuses exposed to PI-HAART remains underexplored. This study aims to evaluate SFT in the fetuses of HIV-pregnant women exposed to PI-HAART, assessing the potential clinical implications. Methods: We conducted a comparative study between HIV-pregnant women receiving PI-HAART and an HIV-negative control group. Fetometry measurements were obtained via 3D ultrasound. SFT in the fetal arm and thigh segments was assessed. Data were analyzed using lineal multivariate regression and receiver-operating characteristics (ROC)-curve analysis. Results: Fetuses exposed to PI-HAART exhibited a significant reduction in subcutaneous fat, particularly in the proximal third-middle union of the femur (coefficient: −2.588, p = 0.042). This reduction was correlated with lower newborn serum glucose levels (65.7 vs. 56.1, p = 0.007; coefficient: −1.277, p = 0.045). Conclusions: Our study sheds light on the connection between PI-HAART, fetal subcutaneous fat, and neonatal health. These findings might reveal the long-lasting effects of PI-HAART on newborns and children’s well-being. Our results emphasize the need for a more balanced approach to managing pregnant women with HIV in developing countries and open new venues for research on the impact of intrauterine PI-HAART exposure on energy metabolism and fetal programming.

The early identification of women with an increased risk of preeclampsia (PE) is desirable, but apart from soluble fms-like tyrosine kinase-1 (sFlt-1), few biomarkers have previously been identified as relevant for predicting preeclampsia. Since kinases and phosphatases regulate critical biological processes and previous evidence suggests a potential role of these molecules in preeclampsia, we performed this systematic review and metanalysis. The objective was to determine if there are kinases and phosphatases whose serum levels are different between women with and without PE, being relevant biomarkers of PE. We followed the recommendations of Cochrane and the Preferred Reported Items for Systematic Reviews and Metanalysis (PRISMA) to perform this study. The MESH terms preeclampsia, kinases, phosphatases, angiopoietins, soluble tyrosine protein kinase receptor (sTIE2), and cellular-mesenchymal-epithelial transition factor (c-MET) were combined to find relevant articles in the PubMed, PROSPERO, and Cochrane databases. Then, a qualitative and quantitative analysis was performed in R Studio software. From 580 abstracts identified, 37 were included in the final analysis, which comprised 24,211 pregnant women (2879 with PE and 21,332 women without PE [HP]. The pooled analysis showed that serum creatine kinase (CK) (SMD: 2.43, CI 95% 0.25–4.62) was significantly higher in PE, whereas sTIE2 and anti-angiogenic factor soluble c-Met (sMet)were significantly lower in PE than in HP (SMD: −0.23, CI95% −0.37 to −0.09; and SMD:0.24, CI95% 0.01–0.47, respectively). Adenosine monophosphate-activated protein kinase (AMPK), angiopoietin-1 (ANG-1), angiopoietin-2 (ANG-2), the ratio angiopoietin-1/angiopoietin-2, acid phosphatase, and alkaline phosphatase were not different between women with PE and HP. In summary CK, sTIE2, and c-MET are relevant biomarkers of PE. It is desirable to incorporate them into current models for PE prediction to evaluate their utility as biomarkers.

Background/Objectives: Insulin resistance during pregnancy is a key factor underlying gestational diabetes mellitus (GDM) and other adverse perinatal outcomes (APOs). While traditional markers, such as HOMA-IR, are used to evaluate insulin resistance, they may be inaccessible in resource-limited settings. The triglyceride–glucose (TyG) index has emerged as a practical alternative. This study aimed to assess whether or not a TyG index > 8.6 during the first trimester of pregnancy is associated with an increased risk of APOs, including GDM, preeclampsia, and other maternal and neonatal complications. Methods: A prospective cohort study was conducted involving 333 pregnant women in Mexico City, divided into two groups: Group 1 (TyG index > 8.6, n = 153) and Group 2 (TyG index ≤ 8.6, n = 180). Primary outcomes included gestational diabetes mellitus (GDM), hypertensive disorders of pregnancy, preeclampsia, preterm birth, cesarean section, and large-for-gestational-age (LGA) and small-for-gestational-age (SGA) neonates. Logistic regression models were used to calculate the adjusted relative risk (aRR) and 95% confidence intervals (CIs), adjusting for maternal age, pregestational weight, and body mass index (BMI). Results: Women with a TyG index > 8.6 had a significantly higher pregestational weight and BMI than those with a TyG index ≤ 8.6. Group 1 demonstrated a higher risk of GDM (RR 2.05; 95% CI: 1.23–3.41) and preeclampsia (RR 2.15; 95% CI: 1.10–4.21). After adjusting for maternal age, pregestational weight, and BMI, these associations remained significant: GDM (aRR 1.87; 95% CI: 1.0–2.5) and preeclampsia (aRR 2.18; 95% CI: 1.1–5.0). No significant associations were found between an elevated TyG index and other APOs, including LGA, SGA, preterm birth, or cesarean delivery. Conclusions: A first-trimester TyG index > 8.6 is significantly associated with an increased risk of GDM and preeclampsia, highlighting its potential as a predictive marker for adverse perinatal outcomes. These findings underscore the utility of the TyG index as a practical, cost-effective tool for early risk stratification, particularly in resource-limited settings. Further multi-center research is needed to validate these results and refine population-specific thresholds.