This study aimed to evaluate the prevalence of sexual dysfunction among women diagnosed with gestational trophoblastic disease (GTD) who were undergoing outpatient follow-up at a university hospital. A cross-sectional study was conducted involving 73 women aged ≥ 18 yr. Data were collected using a structured questionnaire addressing sociodemographic and clinical characteristics, in addition to the Sexual Quotient - Female Version (SQ-F) to assess sexual function. Most participants were aged 18-30 yr (58.9%), married (74.0%), and reported using oral contraceptives (52.1%). Based on the total SQ-F score, 63.0% (n = 46) of participantsdemonstrated adequate sexual satisfaction. However, 15.0% reported experiencing dyspareunia, and 45.2% reported difficulty maintaining concentration during sexual activity. Sexual dysfunction was significantly associated with smoking (Prevalence ratios (PR) = 2.88; p = 0.015) and residence in rural areas (PR = 3.47; p = 0.003). Although the overall prevalence of sexual dysfunction was not higher than national estimates, the findings identify specific vulnerabilities that may adversely affect sexual health. These factors should be considered in the comprehensive clinical management of women with GTD.

Background: Gestational choriocarcinoma is a highly aggressive trophoblastic neoplasm. Historically, the presence of chorionic villi was considered discordant with the diagnosis of choriocarcinoma. We report a case of early gestational choriocarcinoma arising in a post-molar setting with residual chorionic villi, creating a diagnostic pitfall. Case report: a 51-year-old woman with a prior complete hydatidiform mole showed plateauing β-human chorionic gonadotropin (β-hCG) levels. She underwent total laparoscopic hysterectomy. Histologic examination of the uterine mass revealed a malignant biphasic-to-triphasic trophoblastic proliferation with marked atypia, brisk mitotic activity, extensive hemorrhage, and necrosis, situated immediately adjacent to a single residual molar villus. Immunohistochemistry showed strong β-human chorionic gonadotropin expression in syncytiotrophoblasts, a elevated Ki-67 index (∼80%), focal human placental lactogen (hpL) expression, and absence of p63 staining, confirming choriocarcinoma and excluding other trophoblastic tumors. Conclusion: this case demonstrates that the presence of chorionic villi does not exclude a diagnosis of choriocarcinoma and underscores the necessity of rigorous clinicopathologic correlation.

Introduction Gestational trophoblastic disease (GTD) is characterized by abnormal trophoblastic proliferation, with hydatidiform mole being its most common form. Markedly elevated serum human chorionic gonadotropin (hCG) concentrations in molar pregnancy can stimulate thyroid-stimulating hormone receptors, resulting in thyroid dysfunction. This study aimed to evaluate thyroid hormone levels and their correlation with serum β-human chorionic gonadotropin (β-hCG) concentrations in patients with molar pregnancy and to compare thyroid function between complete and partial hydatidiform mole. Materials and methods This prospective observational study was conducted in the Department of Obstetrics and Gynaecology, Srirama Chandra Bhanja (SCB) Medical College and Hospital, Cuttack, Odisha, India, from January 2022 to December 2023. Eighty-eight women with histopathologically confirmed hydatidiform mole were included after excluding 26 patients who had received initial treatment elsewhere and were referred exclusively for oncological management. Serum β-hCG, thyroid-stimulating hormone (TSH), free triiodothyronine (free T3), free thyroxine (free T4), total triiodothyronine (total T3), and total thyroxine (total T4) were measured before uterine evacuation. Thyroid hormone profiles were compared between complete and partial mole, and correlations between serum β-hCG and thyroid hormone parameters were analyzed using Pearson's correlation coefficient. Results Among 15,844 deliveries, 88 women with histopathologically confirmed hydatidiform mole were analyzed, yielding a hospital-based frequency of 5.5 per 1,000 deliveries. Complete mole constituted 57 (64.8%) cases and partial mole 31 (35.2%). Patients with complete mole had significantly lower TSH (0.82±0.71 vs. 1.96±0.82 µIU/mL; p<0.001) and significantly higher free T3, free T4, total T3, total T4, and β-hCG levels than those with partial mole (all p<0.001). Serum β-hCG demonstrated a significant negative correlation with TSH (r=-0.61; p<0.001) and positive correlations with free T3 (r=0.73), free T4 (r=0.69), total T3 (r=0.65), and total T4 (r=0.67) (all p<0.001). Conclusion Complete hydatidiform mole was associated with significantly higher serum β-hCG concentrations and more pronounced thyroid dysfunction than partial hydatidiform mole. Serum β-hCG concentrations demonstrated a significant negative correlation with TSH and positive correlations with free and total T3 and T4 levels, supporting a close association between trophoblastic activity and thyroid function. These findings suggest that thyroid dysfunction may be particularly relevant in women with complete hydatidiform mole or markedly elevated serum β-hCG concentrations; however, larger multicentric studies with adjustment for potential confounding factors and longitudinal follow-up are warranted to clarify the clinical significance of these associations.

A complete hydatidiform mole coexisting with a normal fetus in a twin gestation (CHMCF) is an extremely rare form of abnormal multifetal gestation characterized by the coexistence of a normal fetus and its placenta alongside a complete hydatidiform mole, with a markedly increased risk of persistent gestational trophoblastic disease (PTD) in the mother. Embryo transfer, as a key procedure in assisted reproductive technology, achieves conception by transferring in vitro-fertilized embryos into the uterine cavity. Although it addresses infertility, it may also present distinct clinical scenarios involving rare gestational complications. This report describes a case of a complete hydatidiform mole coexisting with a fetus in a twin gestation after embryo transfer. By integrating serial changes in serum β-human chorionic gonadotropin (β-hCG) levels, ultrasonographic features, chromosomal analysis, and histopathological findings, we summarize the diagnostic and management course and review the relevant literature.

BackgroundGestational trophoblastic disease refers to a group of tumors defined by abnormal trophoblastic proliferation. This disease produces a distinct tumor marker, beta-human chorionic gonadotropin, which can be useful for diagnosis and follow-up. The objective of this study was to investigate the variations in serum beta-human chorionic gonadotropin levels after uterine evacuation as well and the progression of gestational trophoblastic neoplasia.Materials and methodsThis retrospective cohort study was conducted at Tu Du Hospital, Vietnam, between January 2019 and December 2020. All patients diagnosed with molar pregnancy were analyzed retrospectively based on serial serum beta-human chorionic gonadotropin levels following uterine evacuation. Post-evacuation outcomes, including relapsed molar pregnancy and gestational trophoblastic neoplasia, were also monitored.ResultsWe enrolled 560 patients with molar pregnancy, including 298 with complete hydatidiform mole and 262 with partial hydatidiform mole. Severe symptoms were more common in those with complete hydatidiform mole. Over the follow-up period, 97 cases of gestational trophoblastic neoplasia were noted. The data show that the median time to gestational trophoblastic neoplasia diagnosis was 8.75 ± 4.41 (4-26) weeks. In terms of variations in the serum beta-human chorionic gonadotropin levels, the generalized estimating equation model showed a faster decline in the complete hydatidiform mole group than in the partial hydatidiform mole group. Similarly, regression in serum beta-human chorionic gonadotropin levels was significantly more rapid in patients who progressed to gestational trophoblastic neoplasia than in those with relapsed molar pregnancy (-11,593 vs. -20,651.22 and -12,946.26 vs. -46,329.23 mUI/mL, p < 0.001).ConclusionsSurveillance of serum beta-human chorionic gonadotropin levels remains essential for gestational trophoblastic neoplasia monitoring in patients with molar pregnancy following surgical evacuation. The post-evacuation serum beta-human chorionic gonadotropin level regression curve helps distinguish gestational trophoblastic neoplasia from hydatidiform moles. Further evidence is required to strengthen these findings.

Background/Objectives: Biallelic mutations of NLRP7, a maternal-effect gene encoding a key component of the subcortical maternal complex, are the major monogenic cause of recurrent hydatidiform mole (RHM) and confer a substantial lifetime risk of gestational trophoblastic neoplasia (GTN), including choriocarcinoma. Although oocyte donation is currently the standard reproductive option, anecdotal live births from autologous oocytes in carriers of specific missense variants raise mechanistic and clinical questions that have not been integrated. We aimed to synthesize the current understanding of NLRP7 biology, oncogenic mechanisms in GTN, and genotype-stratified reproductive outcomes, and to propose a genetic permissiveness framework that links cancer surveillance with reproductive decision-making. We also place this monogenic disease in an epidemiological context, given the marked geographical variation in molar pregnancy incidence. Methods: PubMed, Embase and Web of Science were searched from January 2006 to December 2025 using terms related to NLRP7, hydatidiform mole, GTN, choriocarcinoma, maternal-effect genes, genomic imprinting, and assisted reproduction. Original studies, case series, expert consensus statements, and reviews were included. Results: NLRP7 loss disrupts subcortical maternal complex assembly, maternal-DMR methylation, trophoblast differentiation, and HLA-C-dependent immune privilege; in choriocarcinoma, NLRP7 is conversely reported to be up-regulated, where it has been implicated in tumor proliferation and immune evasion through inflammasome-independent pathways. Genetic permissiveness for autologous-oocyte pregnancy is mutation-type dependent: complete loss-of-function variants confer near-zero permissiveness, whereas missense variants with retained partial function may permit rare normal pregnancies. Conclusions: A genetic-permissiveness framework integrating variant-level functional data, GTN risk, and reproductive priorities can support shared decision-making in this rare but high-stakes clinical scenario, and it identifies clear directions for future translational research. We emphasize, however, that this framework has not been prospectively validated and should be regarded as hypothesis-generating rather than as a clinically established decision-making model. Recognizing the biallelic NLRP7 mutation as a heritable cancer-predisposition state further supports genotype-informed, risk-stratified oncological surveillance.

Partial hydatidiform mole (PHM) is a rare pathological subtype of gestational trophoblastic disease (GTD). Tubal pregnancy complicated with PHM is an extremely rare clinical condition with atypical preoperative manifestations, which easily leads to clinical misdiagnosis. Definitive diagnosis primarily relies on intraoperative exploration combined with postoperative histopathological and immunohistochemical verification. This study reports a case of tubal PHM in a 31-year-old nulliparous female presenting with 54 days of amenorrhea and persistent lower abdominal distending pain. Preoperative examinations revealed markedly elevated serum β-human chorionic gonadotropin (β-hCG) levels and a unilateral adnexal mixed mass. The patient underwent emergency laparoscopic left salpingectomy, and the final diagnosis of tubal PHM was confirmed by postoperative pathological examination. The patient achieved uneventful postoperative recovery, with serum β-hCG declining steadily in a logarithmic pattern and no metastatic lesions identified during follow-up. This article systematically elaborates the clinical manifestations, pathological features, diagnostic challenges, individualized treatment strategies, and standardized follow-up principles of tubal PHM, aiming to improve clinicians' awareness of differential diagnosis and standardized management of this rare disease, and provide a credible clinical reference for the diagnosis and treatment of rare ectopic gestational trophoblastic lesions.

Complete hydatidiform mole with a coexisting live fetus in a twin pregnancy is exceptionally rare and carries major maternal and fetal risks. We describe two such pregnancies to illustrate management options. The first followed frozen-thawed single blastocyst transfer and presented at 13 weeks with a live fetus, a separate molar mass, an intramural fibroid, markedly elevated serum beta-human chorionic gonadotropin, and biochemical hyperthyroidism. Multidisciplinary assessment led to hysterotomy with removal of the fetus, molar tissue, and fibroids, followed by rapid recovery and no gestational trophoblastic neoplasia. The second was a spontaneously conceived twin pregnancy with a live 9-week fetus and multicystic molar tissue that was evacuated by suction curettage. An initial decline in beta-human chorionic gonadotropin was followed by a low-level plateau that resolved after a single low-dose methotrexate cycle. These cases highlight the need for individualized, multidisciplinary care and close biochemical follow-up.