Gestational trophoblastic disease (GTD) arises from abnormal placenta and is composed of a spectrum of premalignant to malignant disorders. Changes in epidemiology of GTD have been noted in various countries. In addition to histology, molecular genetic studies can help in the diagnostic pathway. Earlier detection of molar pregnancy by ultrasound has resulted in changes in clinical presentation and decreased morbidity from uterine evacuation. Follow-up with human chorionic gonadotropin (hCG) is essential for early diagnosis of gestational trophoblastic neoplasia (GTN). The duration of hCG monitoring varies depending on histological type and regression rate. Low-risk GTN (FIGO Stages I-III: score <7) is treated with single-agent chemotherapy but may require additional agents; although scores 5-6 are associated with more drug resistance, overall survival approaches 100%. High-risk GTN (FIGO Stages II-III: score ≥7 and Stage IV) is treated with multiagent chemotherapy, with or without adjuvant surgery for excision of resistant foci of disease or radiotherapy for brain metastases, achieving a survival rate of approximately 90%. Gentle induction chemotherapy helps reduce early deaths in patients with extensive tumor burden, but late mortality still occurs from recurrent treatment-resistant tumors.
Background: Amniotic mesenchymal stem cells (AMSCs) have been demonstrated as effective in tissue repair and regeneration. Trophoblast dysfunction is associated with several types of pregnancy complications. The aim of this study is to investigate the effects of AMSCs on the biological activities of human trophoblasts, as well as their molecular mechanisms.
Placental trophoblasts constitute the interface between the fetal and maternal environments and physically prevent maternal-fetal viral transmission. However, congenital human cytomegalovirus (HCMV) infection in the early stages of pregnancy results in severe symptoms in the fetus. HCMV is the most common causative agent of intrauterine infection.
Twin pregnancies consisting of one normal fetus and one complete mole are very rare. The main concerning risks associated with the continuation of such pregnancy are hyperthyroidism, theca lutein cysts, preeclampsia, and the development of GTD (gestational trophoblastic disease) spectrum (neoplasia) in the mother, which is due to high human chorionic gonadotropin (HCG) values, and intrauterine death and prematurity in the coexistent normal fetus. We report the successful outcome of conservative management in a healthy mother and baby.
Reproductive success hinges on the presence of a robust and functional placenta. Examining the placenta provides insight about the progression of pregnancy and valuable information about the normal developmental trajectory of the fetus. The current limitations of using bulk RNA-sequencing (RNA-seq) analysis stem from the diverse composition of the placenta, hindering a comprehensive description of how distinct trophoblast cell expression patterns contribute to the establishment and sustenance of a successful pregnancy.
Offspring of women with gestational diabetes mellitus (GDM) face an increased risk of long-term neurodevelopmental abnormalities. This study explores the altered expression of key placental fatty acid transport proteins-FATP2, FATP4, FATP6, FABP4, and FAT/CD36-in GDM patients, and the potential of docosahexaenoic acid (DHA) to mitigate neurodevelopmental risks in offspring by enhancing their expression through activation of peroxisome proliferator-activated receptor γ (PPAR-γ). Our findings demonstrate that placental FATP4 expression is reduced in GDM patients.
