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Endocrine tumors in pregnancy
Published in Nadia Barghouthi, Jessica Perini, Endocrine Diseases in Pregnancy and the Postpartum Period, 2021
A complete hydatidiform mole is a result of a paternal homologous chromosome pattern. This occurs when a single sperm (90%) or dispermy (10%) fertilizes an egg with absent nuclear DNA.1,2 The most common resulting karyotype is 46XX (85%) and less likely 46XY.6
DRCOG MCQs for Circuit B Questions
Published in Una F. Coales, DRCOG: Practice MCQs and OSCEs: How to Pass First Time three Complete MCQ Practice Exams (180 MCQs) Three Complete OSCE Practice Papers (60 Questions) Detailed Answers and Tips, 2020
Hyperemesis gravidarum:Does not recur in subsequent pregnancies.Metoclopramide may induce oculogyric crises.May be associated with multiple pregnancy.May be associated with a hydatidiform mole.May be associated with jaundice.
Miscarriage and Gestational Trophoblastic Disease
Published in Arianna D'Angelo, Nazar N. Amso, Ultrasound in Assisted Reproduction and Early Pregnancy, 2020
Treatment of hydatidiform moles involves evacuation of the uterus. In the majority of cases, this completely resolves the disease, but in a small number of cases, it recurs (persistent mole) and further treatment is necessary. Persistent moles may progress to invasion into the myometrium (invasive mole) or development into a malignancy (choriocarcinoma) that can metastasize. These complications, particularly persistent mole, occur in approximately 20% of complete moles and much less frequently with partial moles.
Management of trophoblastic tumors : review of evidence, current practice, and future directions
Published in Expert Review of Anticancer Therapy, 2023
Antoine Deleuze, Christophe Massard, Fanny Le Du, Benoit You, Claudia Lefeuvre-Plesse, Pierre-Adrien Bolze, Thibault de la Motte Rouge
Gestational trophoblastic diseases (GTD) are a group of premalignant and malignant diseases originating from abnormalities during the fertilization process leading to a global dysregulation of trophoblast proliferation and differentiation. The exact incidence of GTD varies worldwide and remains uncertain due to the heterogeneity in diagnosis and case recording processes between countries. In western Europe and the United States, the reported incidence of hydatidiform moles is 1 to 3 in 1000 pregnancies, respectively, and has been shown to be slightly higher in Asia [1]. Epidemiologic studies have not been able to determine genetic or cultural factors explaining these disparities. The extremes of maternal age and prior molar pregnancy are the most significant risk factors of GTD with a 7.5-fold higher risk for women >40 years and a 10–20-fold higher risk after a first occurrence of hydatidiform mole [2,3]. Spontaneous abortion has also reported to be associated with a 2-to-3-fold higher risk of hydatidiform mole. Few familial cases of recurrent CMH have been described and have been found to share a missense NLRP7 gene mutation on chromosome 19q [4–7].
A case report on recurrent partial moles in three consecutive pregnancies
Published in Journal of Obstetrics and Gynaecology, 2022
Prashida Guha Sarkar, Saroj Dalmia, Pinky Khatri
Hydatidiform moles are abnormal conceptions, occurring in about one in 500–1000 pregnancies (Seckl et al. 2000). Complete moles are diploid and androgenic in origin and have no evidence of foetal tissue. Most (90%) arise secondarily to fertilisation of an empty ovum with duplication of a haploid sperm. In contrast, partial moles show evidence of foetal tissue and are triploid in origin, containing one set of maternal haploid chromosomes and two sets of paternal haploid chromosomes, derived from dispermic fertilisation of an ovum (90%). On histology, a PM pregnancy shows presence of foetal tissue, focal hydropic change to the villi and some excess trophoblast proliferation. Ploidy status and immunohistochemistry staining for p57, a paternally imprinted gene, help in distinguishing partial from CM pregnancies (Tham et al. 2003).
Detection of Parental Contribution to Molar Genome Leads to Diagnosis of Recurrent Hydatidiform Mole in a Family with NLRP7 Variants
Published in Fetal and Pediatric Pathology, 2022
Rong-Yue Wang, Yu-Juan Li, Li Zhen, Fan Jiang, Cong-Min Gu, Dong-Zhi Li
Hydatidiform mole (HM) is a complication of pregnancy characterized by varying degrees of trophoblastic proliferation and vesicular swelling of placental villi, while the embryonic development is severely abnormal or absent. The diagnosis is usually made only after histopathological examination of uterine curettage specimens, which allows the classification of moles as complete HM (CHM) or partial HM (PHM) based on the degree of trophoblast proliferation and the presence or absence of fetal tissues [1]. CHM and PHM are genetically different in that CHM is androgenetic diploid, containing two sets of paternal chromosomes, while PHM is triploid with one maternal and two different paternal sets of chromosomes [2]. Occasional diploid CHMs have both maternal and paternal genomes. This type of biparental CHM (BiCHM) has clinical implication as it has been associated with recurrent HM (RHM) [3]. In this study, we report a RHM which was identified by the detection of BiCHM.