Amniotic fluid is crucial for the well-being of the fetus. Recent studies suggest that dehydration in a pregnant woman leads to oligohydramnios. We assessed the variation in the amniotic fluid index (AFI) during the summer and non-summer seasons and evaluated neonatal outcomes. We retrospectively reviewed electrical medical records of pregnant women who visited the Konkuk University Medical Center for antenatal care, between July 2005 and July 2019. A total of 19,724 cases from 6438 singleton pregnant women were included after excluding unsuitable cases. All AFI values were classified as 2nd and 3rd trimester values. Additionally, borderline oligohydramnios (AFI, 5–8) and normal AFI (AFI, 8–24) were assessed according to the seasons. The average AFI between the summer and non-summer season was statistically different only in the 3rd trimester; but the results were not clinically significant. In the 3rd trimester, the summer season influenced the increased incidence of borderline oligohydramnios. The borderline oligohydramnios group showed an increased small-for-gestational-age (SGA) rate and NICU admission rate. In the summer season, the incidence of borderline oligohydramnios was seen to increase. This result would be significant for both physicians and pregnant women.

Maternal circulating angiogenic factors are established biomarkers in preeclampsia, but their early profiles in fetal growth impairment without preeclampsia remain unclear. We quantitatively synthesized data from observational studies measuring maternal serum placental growth factor (PlGF), soluble fms-like tyrosine kinase-1 (sFlt-1), or their ratio before 29 weeks and before clinical recognition of growth impairment in singleton pregnancies without preeclampsia, subsequently classified as fetal growth restriction (FGR), small for gestational age (SGA), or unaffected. PubMed, Embase, and the Cochrane Library were searched through April 2026; 22 studies were included. In random-effects meta-analysis, PlGF was lower in affected pregnancies (standardized mean difference [SMD] −0.38; 95% CI −0.63 to −0.13; I² = 92.0%; 19 studies), whereas sFlt-1 did not differ (SMD 0.03; 95% CI −0.27 to 0.34; I² = 79.5%; 12 studies) and the ratio was higher in the primary analysis (SMD 0.39; 95% CI 0.08 to 0.70; I² = 80.0%; seven studies). This pattern suggests that the ratio signal was influenced largely by lower PlGF. Bivariate analysis of five PlGF accuracy studies yielded a summary sensitivity of 0.29 and specificity of 0.86. Despite substantial heterogeneity, reduced PlGF was the most consistent early angiogenic feature in pregnancies subsequently classified as FGR/SGA without preeclampsia. Its low sensitivity does not support its use as a stand-alone screening test, but these findings warrant further evaluation of PlGF within multimarker prediction models.

Preeclampsia (PE) has traditionally been regarded as a pregnancy-limited hypertensive disorder; however, accumulating evidence increasingly positions it as a pivotal early-life vascular stress test that manifests underlying vulnerabilities and accelerates biological aging. Women with a history of PE exhibit a heightened susceptibility to premature-onset multi-systemic diseases, specifically cardiovascular, ovarian, renal, and metabolic decline. This suggests that PE acts as a catalyst for accelerated aging, driven by shared pathophysiological pathways that represent common mechanisms of systemic senescence. This review provides a comprehensive analysis of the epidemiological links and pathogenic drivers underpinning accelerated systemic aging following PE, with a specific focus on the cardiovascular-ovarian axis. Epidemiological data consistently demonstrate that women with prior PE exhibit significantly reduced anti-Müllerian hormone (AMH) levels, translating to an estimated 1.5-year acceleration in reproductive aging. In parallel, PE is associated with a twofold increase in lifetime cardiovascular disease (CVD) risk and the onset of chronic hypertension occurring an average of 7.7 years earlier. However, reconciling the phenotypic heterogeneity of PE and transcending the constraints of non-experimental designs are essential for firmly establishing this accelerated aging paradigm. At the molecular level, PE and ovarian aging converge on shared pathways—including mitochondrial dysfunction, oxidative stress, inflammation, and epigenetic dysregulation—collectively defining a distinct pathogenic ovarian–vascular aging axis. Proposed geroscience-based strategies advocate for refined risk stratification by incorporating molecular aging biomarkers—such as epigenetic clocks and inflammatory profiles—alongside conventional clinical indicators. This integrative framework facilitates the early identification of high-risk aging phenotypes, enabling targeted monitoring and timely interventions to preemptively modulate accelerated aging pathways. Pharmacological approaches within this framework emphasize the judicious repurposing of established agents, such as metformin, statins, and SGLT2 inhibitors, while emerging gerotherapeutics, including senolytics and senomorphics, provide a conceptual foundation for targeting the fundamental biological drivers of senescence. Although these geroprotective strategies, including the repurposing of established agents and the use of senolytics, offer innovative conceptual frameworks for targeting the fundamental drivers of senescence, they remain largely exploratory and require further clinical validation. Such strategies offer novel opportunities to shift the clinical focus from treating isolated comorbidities to modulating the shared molecular substrates of aging, ultimately promoting healthy aging and functional longevity in the elderly female population.

Maternal angiogenic imbalance is a hallmark of preeclampsia (PE), but whether it differs between PE-associated and isolated fetal growth restriction (FGR)/small-for-gestational-age (SGA) pregnancies is unclear, particularly before clinical recognition. We searched PubMed, Embase, and CENTRAL for observational studies comparing maternal soluble fms-like tyrosine kinase-1 (sFlt-1), placental growth factor (PlGF), or their ratio between these phenotypes. Analyses were stratified by sampling context and pooled as Hedges’ g using random-effects models. Twenty-three studies (630 PE-associated, 1476 isolated FGR/SGA pregnancies) were included. After clinical recognition, PE-associated FGR/SGA showed a higher sFlt-1/PlGF ratio (g = 1.04, 95% CI 0.51 to 1.57), higher sFlt-1 (1.05, 0.73 to 1.38), and lower PlGF (−0.60, −0.82 to −0.38) than isolated FGR/SGA; differences in the same directions were present before clinical recognition (ratio 0.86, 0.38 to 1.33; sFlt-1 0.38, 0.12 to 0.64; PlGF −0.46, −0.77 to −0.16). The sFlt-1 difference was larger after clinical recognition in the test for subgroup differences (p = 0.002) but not in meta-regression (p = 0.064), and this between-context contrast is therefore reported as exploratory; the PlGF difference was similar in both contexts. These group-level differences do not establish individual-level prediction, discrimination or threshold performance. PE-associated and isolated FGR/SGA should therefore be distinguished in biomarker research, and angiogenic thresholds derived in suspected PE require validation before application to normotensive FGR/SGA.

Background/Objectives: Congenital uterine anomalies (CUAs) are associated with adverse pregnancy outcomes, but large-scale data, particularly in Asian populations, remain limited. We evaluated obstetric and neonatal outcomes in women with CUAs using a large national Korean cohort. Methods: This population-based retrospective cohort study used the Korean National Health Insurance Service database and included 878,000 singleton deliveries between 2018 and 2023. CUAs were identified using International Classification of Disease, 10th Revision (ICD-10) codes and categorized as double, septate, bicornuate, or unicornuate uterus. Outcomes were compared with women without CUA using multivariable logistic regression adjusted for maternal age, parity, chronic hypertension, and pregestational diabetes mellitus. Results: CUAs were identified in 6038 women (0.68%), most commonly double uterus. Risks were higher for Cesarean delivery (adjusted odds ratio [aOR] 2.57, 95% confident interval [CI] 2.38–2.77), breech presentation (6.42, 5.91–6.99), placenta previa (1.79, 1.45–2.22), and placental abruption (3.01, 2.26–4.01). Neonates were more likely to be preterm (2.43, 2.10–2.80), small for gestational age (1.90, 1.70–2.10), and to experience respiratory distress syndrome (2.04, 1.63–2.55) and intraventricular hemorrhage (3.04, 2.00–4.62). Conclusions: CUAs are associated with increased risks of adverse obstetric and neonatal outcomes, with subtype-specific variations, warranting tailored prenatal counseling and management.

Background/Objectives: S100A14 has been implicated in cellular signaling and tissue remodeling, but its relationship with histologic chorioamnionitis (HCA) remains unknown. We evaluated its placental expression and discriminatory performance for HCA in preterm birth. Methods: This retrospective cohort included 233 women with singleton spontaneous preterm births. Placental tissues were evaluated by immunohistochemistry for S100A14, MMP-2, ERK, and p38. Expression was compared by HCA status, and correlations were evaluated using Spearman coefficients. Multivariable logistic regression was adjusted for gestational age at delivery and preterm prelabor rupture of membranes (PPROM) status. Discriminatory performance was assessed using receiver operating characteristic analysis. Results: S100A14 scores were higher in placentas with HCA than without HCA (5.61 vs. 2.97, p < 0.001) and remained independently associated with HCA after adjustment (adjusted odds ratio per 1-point increase, 1.50; 95% confidence interval, 1.31–1.71; p < 0.001). MMP-2 expression was also elevated in HCA, whereas ERK and p38 expression did not differ by HCA status. S100A14 correlated most strongly with MMP-2 (ρ = 0.531, p < 0.001). Among 173 participants with complete data, the areas under the curve were 0.780 for placental S100A14, 0.717 for placental MMP-2, and 0.660 for maternal serum CRP at admission; the difference between S100A14 and CRP was statistically significant (p = 0.023), whereas the difference between S100A14 and MMP-2 was not (p = 0.126). At an optimal cutoff of 5.0, sensitivity was 55.2% and specificity was 80.2%. Conclusions: Placental S100A14 expression was independently associated with HCA and showed moderate tissue-level discriminatory ability for HCA. Its modest sensitivity limits its utility as a stand-alone diagnostic marker. Further studies are required to determine whether S100A14 or related molecular signals can be detected and validated in specimens obtainable before delivery.