The term “molar pregnancy” is commonly used to describe disorders of the villous anatomy which results from a lack, maldevelopment or regression of the villous vasculature that make the drainage of fluid supplied by the trophoblast impossible. When these changes are associated trophoblastic hyperplasia on histology they are described as hydatidiform moles (HM) which are classified into either complete hydatidiform moles (CHM) where the trophoblastic hyperplasia is diffuse, fetal development is absent and the morphological changes are generalised, or partial hydatidiform moles (PHM) which characteristically display trophoblastic hyperplasia with focal villous hydropic changes and evidence of fetal development. The vast majority of CHM and triploid PHM miscarry spontaneously during the first three months of pregnancy. Following uterine evacuation, around 15% and between 0.5-5.6% of patients with a CHM and PHM develop gestational trophoblastic neoplasia (GTN) requiring chemotherapy and thus it is essential that patients with HM are diagnosed early in pregnancy and provided with follow-up. The molar transformation of the placental tissue in HM is a progressive phenomenon secondary to the oedema of the villous mesenchyme and the typical cystic molar changes found on ultrasound are often not visible before 9 weeks of gestation. Most patients with HM are likely to be first seen in an early pregnancy unit.

Molar pregnancies, characterized by abnormal placental tissue growth, are rare but clinically significant conditions. Advancements in ultrasound and hCG assays have transformed the diagnosis of molar pregnancies. Maintaining a high index of suspicion is important for proper diagnosis, especially in cases of first-trimester vaginal bleeding. Certain clinical and laboratory features help distinguish between complete and partial molar pregnancies, including subtle sonographic findings and hCG levels. Histologic confirmation remains essential. The primary therapeutic approach for molar pregnancies is suction dilation and curettage, often with ultrasound guidance. Rhogam administration is important for Rhesus-negative patients, and uterotonics and blood products should be made immediately available during evacuation procedures. Hysterectomy is considered for presumed complete molar pregnancies in patients who have completed childbearing. Postoperative surveillance of serum hCG levels is critical for detecting postmolar gestational trophoblastic neoplasia. This case outlines diagnostic criteria for postmolar GTN, including hCG trends and potential complications. It also emphasizes the importance of contraception for accurate postoperative monitoring. Despite an increased risk of recurrence with a history of molar pregnancy, subsequent normal pregnancies are common following treatment. Early first-trimester ultrasounds and post-pregnancy hCG assessments are recommended for favorable outcomes in future pregnancies.

Gestational trophoblastic disease (GTD) incorporates a spectrum of placental related disorders, with both benign and malignant (Gestational trophoblastic neoplasia (GTN)) subtypes. Upon initial presentation, one should establish diagnosis (GTD versus GTN), the requirement for chemotherapy and whether monitoring has been concluded by a specialist trophoblastic centre. Women with a prior history of GTD or GTN that have completed monitoring, or early pregnant GTD patients, do not require specialist pregnancy management. Dissimilarly, early pregnant GTN patients, particularly those treated for high-risk disease, or women with a twin pregnancy involving a complete hydatidiform mole and viable co-existent foetus should receive detailed antenatal counselling and be managed under consultant-led care. Patients with a twin mole and viable co-existent foetus have a high risk of antenatal, intrapartum and post-partum complications. Fortunately, in women with a prior history of trophoblastic disease, live birth rates equal the general population, with no increased risk of disease relapse.