The main complications causing practically 75% of all maternal deaths are severe bleeding, infections, and high blood pressure during pregnancy (preeclampsia (PE) and eclampsia). The usefulness of ncRNAs as clinical biomarkers has been explored in an extensive range of human diseases including pregnancy-related diseases such as PE. Immunological dysregulation show that the Th1/17:Th2/Treg ratio is “central and causal” to PE. However, there is evidence of the involvement of placenta-expressed miRNAs and lncRNAs in the immunological regulation of crucial processes of placenta development and function during pregnancy. Abnormal expression of these molecules is related to immune physiopathological processes that occur in PE. Therefore, this work aims to describe the importance of miRNAs and lncRNAs in immune dysregulation in PE. Interestingly, multiple ncRNAS are involved in the immune dysregulation of PE participating in type 1 immune response regulation, immune microenvironment regulation in placenta promoting inflammatory factors, trophoblast cell invasion in women with Early-Onset PE (EOPE), placental development, and angiogenesis, promotion of population of M1 and M2, proliferation, invasion, and migration of placental trophoblast cells, and promotion of invasion and autophagy through vias such as PI3K/AKT/mTOR, VEGF/VEGFR1, and TLR9/STAT3.

Background: Preeclampsia (PE) is a syndromic disorder that affects 2% to 8% of pregnancies and is diagnosed principally when hypertension appears in the second-d half of pregnancy. WHO estimates the incidence of PE to be seven times higher in developing countries than in developed countries. Severe preeclampsia/eclampsia is one of the most important causes of maternal mortality, associated with 50,000 to 100,000 annual deaths globally as well as serious fetal and neonatal morbidity and mortality, especially in developing countries. Even though evidence from family-based studies suggest PE has a heritable component, its etiology, and specific genetic contributions remain unclear. Many studies examining the genetic factors contributing to PE have been conducted, most of them are focused on single nucleotide polymorphisms (SNPs). Given that PE has a very important inflammatory component, is mandatory to examine cytokine-SNPs for elucidating all mechanisms involved in this pathology. In this review, we describe the most important cytokine-polymorphisms associated with the onset and development of PE. We aim to provide current and relevant evidence in this regard. Methods: We searched English databases such as PubMed and the National Center for Biotechnology Information. The publication time of the papers was set from the establishment of the databases to February 2022. All studies about Th1/Th2/Th17 cytokines polymorphisms were included in our study. Results: SNPs in IFN-γ, TNF-α, IL-4, IL-6, IL-10, IL-17A, and IL-22 are associated with the development, early-onset and severity of PE, being the Th1/Th2/Th17 responses affected by the presence of these SNPs. Conclusions: The changes in Th1/Th2/Th17 response modify processes such as placentation, control of inflammation, and vascular function. Nonetheless, association studies have shown different results depending on sample size, diagnostic, and population.

Placenta accreta spectrum (PAS) disorders are characterized by abnormal trophoblastic invasion into the myometrium, leading to significant maternal health risks. PAS includes placenta accreta (invasion < 50% of the myometrium), increta (invasion > 50%), and percreta (invasion through the entire myometrium). The condition is most associated with previous cesarean deliveries and increases in chance with the number of prior cesarians. The increasing global cesarean rates heighten the importance of early PAS diagnosis and management. This review explores genetic expression and key regulatory processes, such as apoptosis, cell proliferation, invasion, and inflammation, focusing on signaling pathways, genetic expression, biomarkers, and non-coding RNAs involved in trophoblastic invasion. It compiles the recent scientific literature (2014–2024) from the Scopus, PubMed, Google Scholar, and Web of Science databases. Identifying new biomarkers like AFP, sFlt-1, β-hCG, PlGF, and PAPP-A aids in early detection and management. Understanding genetic expression and non-coding RNAs is crucial for unraveling PAS complexities. In addition, aberrant signaling pathways like Notch, PI3K/Akt, STAT3, and TGF-β offer potential therapeutic targets to modulate trophoblastic invasion. This review underscores the need for interdisciplinary care, early diagnosis, and ongoing research into PAS biomarkers and molecular mechanisms to improve prognosis and quality of life for affected women.

Placenta accreta spectrum (PAS) disorders are characterized by abnormal trophoblastic invasion into the myometrium, leading to significant maternal health risks. PAS includes placenta accreta (invasion 50%), and percreta (invasion through the entire myometrium). The condition is most associated with previous cesarean deliveries, and its incidence increases with the number of cesareans. Other risk factors include advanced maternal age, multiparity, and various uterine surgeries. The increasing global cesarean rates heighten the importance of early PAS diagnosis and management. The study reviewed molecular mechanisms driving PAS, focusing on signaling pathways, genetic expression, biomarkers, and non-coding RNAs involved in trophoblastic invasion. It explored genetic expression and key regulatory processes such as apoptosis, cell proliferation, invasion, and inflammation. The manuscript was compiled from recent scientific literature (2014 – 2024) from the Scopus, PubMed, Google Scholar, and Web of Science databases. Placenta Acreta Spectrum; acreta; increta; percreta; trophoblast invasion; miRNAs, lncRNAs; genetic expression; biomarkers; signaling pathways were the employed keywords to compile relevant literature. The PAS is an important obstetric health problem that challenges maternal health risks associated with abnormal trophoblastic invasion that relies on abnormal placentation, uterine scarring, and impaired decidualization. Identifying new biomarkers like AFP, sFlt-1, β-hCG, PlGF, and PAPP-A aids early detection and management. Understanding genetic expression and non-coding RNAs is crucial for unraveling PAS complexities. Besides, aberrant signaling pathways like Notch, PI3K/Akt, STAT3, and TGF-β offer potential therapeutic targets to modulate trophoblastic invasion. This review underscores the need for interdisciplinary care, early diagnosis, and ongoing research into PAS biomarkers and molecular mechanisms to improve prognosis and quality of life for affected women.

Rationale: A pregnancy with incomplete mole is very rare case. Hydatidiform mole (HM) with live fetus is associated with a risk of a wide variety to maternal and fetal complications. The incidence of a normal live fetus and an incomplete mole such as the case we describe is extremely rare. Patient concern: We report a case of multiparous 34-year-old at Culiacan Mexico woman with incomplete mole coexisting with normal fetus, pregnant 35.3 weeks who presented anemia grade II. Diagnosis: The initial diagnosis of the mole was by ultrasound. Interventions: KERR-type cesarean section and bilateral tubal occlusion. The newborn was morphologically normal, and she did not require intervention or treatment. Outcomes: The newborn was feminine, morphologically normal, weighing 2380 g and 47 cm, APGAR score 8 to 9, delivered prematurely, and there was a large placental plate. The blood loss on surgery was estimated at 1000 mL. Histopathology report of an incomplete hydatidiform mole, negative for malignancy. Histopathology diagnostic was confirmed by immunohistochemistry staining for p57KIP2. Lessons: Although the incidence of this pregnancy is very rare, early recognition, diagnosis and divulge of the cases of medical community is very important for patient care.

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