This chapter should be cited as follows:
Verri D, Glob Libr Women's Med
ISSN: 1756-2228; DOI 10.3843/GLOWM.419743

The Continuous Textbook of Women’s Medicine Series – Gynecology Module

Volume 10

Ultrasound in gynecology

Volume Editors: Professor Antonia Testa, Agostino Gemelli University Hospital, Rome, Italy
Professor Simona Maria Fragomeni, Agostino Gemelli University Hospital, Rome, Italy

Chapter

Ultrasound Diagnosis and Management of Trophoblastic Disease

First published: January 2026

AUTHOR(S)

Debora Verri, MD

Gynecology and Breast Care Center, Mater Olbia Hospital, Italy

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INTRODUCTION

Gestational trophoblastic disease (GTD) is a group of rare disorders arising from abnormal trophoblastic proliferation and includes both premalignant and malignant conditions. The premalignant forms are partial hydatidiform mole (PHM) and complete hydatidiform mole (CHM), collectively referred to as molar pregnancies. The malignant forms of GTD, known as gestational trophoblastic neoplasia (GTN), include invasive hydatidiform mole (IHM), choriocarcinoma, placental site trophoblastic tumor (PSTT) and epithelioid trophoblastic tumor (ETT).

The currently used classification system is the World Health Organization (WHO) Classification (2020),¹ encompassing also placental site nodules (PSN) as well as exaggerated placental site reactions (EPS), which are considered tumor-like, benign trophoblastic lesions, without predisposition to malignant transformation.

Trophoblastic cells produce the pregnancy hormone, human chorionic gonadotropin (hCG). All forms of gestational trophoblastic disease, apart from PSTT and ETT (which arise from the intermediate trophoblast) normally produce high levels of hCG making it a useful biomarker for diagnosis, disease progression, treatment response and surveillance.²

While a molar pregnancy can progress to any of the malignant forms of GTN, choriocarcinoma, PSTT and ETT may arise following any type of antecedent pregnancy.

This chapter provides an overview of the diagnosis, management and surveillance of the different types of GTD. By integrating the latest WHO and FIGO classifications, it details the pathogenetic and sonographic distinctions between PHM and CHM. It also explores the risk stratification of GTN, evaluating therapeutic strategies ranging from single-agent chemotherapy to advanced immunotherapy.

MOLAR PREGNANCY

Molar pregnancies are characterized by ‘grape-like’ clusters formed by swollen hydropic villi and are categorized into two types: complete and partial hydatidiform moles.

CHM and PHM are the commonest form of GTD affecting around 1–2 per 1000 pregnancies in most western countries.³

CHM occurs from the fertilization of an empty ovum by one sperm, with subsequent duplication, or from fertilization of an empty ovum by two sperm; both scenarios result in androgenetic diploid tissue (46XX, 46XY). In contrast, PHM typically arises from an ovum fertilized by two sperm, resulting in triploid biparental genome (69XXY, 69 XXX or 69XYY).⁴

They typically present with bleeding in the first trimester of pregnancy (sometimes associated with severe anemia), high serum levels of hCG (> 2 MoM) and abnormal ultrasound findings. Other clinical features reported are: uterine enlargement, hyperemesis and hyperthyroidism (due to the high levels of hCG, hCG sharing an alpha subunit with thyroid-stimulating hormone), early pre-eclampsia and respiratory distress (explained by pulmonary embolization of the trophoblastic tissue or by lung metastasis). However, nowadays, use of ultrasound allows earlier diagnosis of molar pregnancy, enabling prompt intervention and thereby reducing the likelihood of severe clinical manifestations. Despite this diagnostic advance, there is no reduction in the incidence of malignant postmolar forms.

Ultrasound is more reliable in the diagnosis of CHM when compared to PHM. In the first trimester, the detection rate of CHM is 95% whilst, for PHM, it is only 20%. The positive predictive value of ultrasound in the diagnosis of molar pregnancy ranges from 48–88%.⁵

A characteristic ultrasound finding of CHM is a uterine cavity filled with a heterogeneous mass, with avascular anechoic cystic areas, with absence of fetal development (Figure 1). This finding is commonly referred to as a ‘snowstorm' appearance. It is also possible to find theca lutein ovarian cysts, due to the high levels of β-hCG (Figure 2).⁶^,⁷^,⁸

Complete mole in the first trimester.

Ovarian theca lutein cyst.

In PHM, a fetus may be visualized on ultrasound, sometimes with initial cardiac activity. However, the fetus is typically triploid and, therefore, may present with congenital malformations, symmetric growth restriction and poor pregnancy outcomes, including miscarriage or intrauterine fetal demise. The placenta is enlarged and contains cystic spaces, producing the characteristic 'Swiss cheese' appearance.⁶^,⁸

The sonographic detection of PHM remains a diagnostic challenge. In the differential diagnosis, it is necessary to consider: (1) placental chorioangioma, (2) subchorionic hematoma, (3) mesenchymal dysplasia and (4) complete hydatidiform mole coexisting with a viable fetus (CHMFM). CHMFM is a rare condition (about 1/22,000–1/100,000 pregnancies) that is associated with obstetric complications (antepartum hemorrhage, early severe pre-eclampsia or eclampsia, placenta previa, pPROM and premature birth), fetal complications (spontaneous loss, intrauterine death and growth restriction) and/or maternal complications (thyrotoxicosis and persistent trophoblastic disease). It is estimated from the literature that less than 50% of these pregnancies will result in the birth of live babies and up to 63% of women affected by this condition will develop a GTN after delivery.

The diagnosis of molar pregnancy must be confirmed by histological examination. When distinguishing between a non-molar hydropic abortus, partial mole and complete mole, overlapping features may lead to misclassification, particularly in early gestation. Thus, the following ancillary diagnostic techniques can be helpful in the differential diagnosis:

immunohistochemistry shows negative staining for p57 in complete mole, since the protein kinase inhibitor is expressed by a maternal gene; p57 is instead expressed in partial mole and hydropic abortion
in CHM, cytogenetics shows a monoparental diploid karyotype of paternal origin (with the exception of familial recurrent hydatidiform mole), while in PHM it shows a biparental triploid genome
gene amplification of the short tandem repeats (STRs) of microsatellites also allows a precise diagnosis of partial and complete mole.⁴^,⁹^,¹⁰^,¹¹

Histological examination is essential to achieve a correct diagnosis.

For women who want to preserve their fertility, uterine evacuation by dilatation curettage, ideally performed under ultrasound guidance, is the preferred method for those with suspected hydatidiform mole.¹²

Following surgical treatment, all women with a histological diagnosis of molar pregnancy require careful hCG monitoring, to detect malignant change (postmolar GTN). The progression of a previous molar pregnancy to GTN occurs in 15–20% of cases of CHM and 0.5–5% of PHM.

PHM does not require prolonged follow-up, a confirmatory negative value of hCG levels 1 month after normalization is sufficient. However, in the case of CHM, follow-up of up to 6 months after hCG normalization is desirable, given the greater risk of recurrence.¹³

Risk of recurrence is low (< 2%) following a single molar pregnancy, but increases significantly for patients who experience one or more recurrences. While, in several studies, fertility and reproductive outcomes after a previous molar pregnancy have been demonstrated to be similar to those of the general population, the risk of a new hydatidiform mole has been reported to increase with successive molar pregnancies and is higher for CHM than for PHM.¹⁴

GESTATIONAL TROPHOBLASTIC NEOPLASIA

Postmolar GTN (invasive mole and choriocarcinoma)

The diagnosis of postmolar GTN is usually made during the post-treatment surveillance of serum β-hCG levels. In 2000, the International Federation of Gynaecology and Obstetrics (FIGO) defined the diagnostic criteria for postmolar gestational trophoblastic neoplasia (Table 1).¹⁵

International Federation of Gynaecology and Obstetrics (FIGO 2000) criteria for diagnosis of postmolar gestational trophoblastic neoplasia.¹⁵

Histological evidence of invasive mole or choriocarcinoma

Plateau or increasing^*hCG after evacuation of partial or complete mole

The hCG level remains elevated for 6 months or more after evacuation of partial or complete mole

*A plateau or increase is defined as four or more equivalent values of hCG over at least 3 weeks (days 1, 7, 14 and 21) and two consecutive increases in hCG of 10% or greater over at least 2 weeks (days 1, 7 and 14).

About 50% of GTNs arise after molar pregnancy, the remaining malignant forms may develop after miscarriage, ectopic pregnancy or full-term pregnancy. In addition to abnormal vaginal bleeding, other initial symptoms may be related to bleeding in metastatic organs (liver, spleen, intestine, lung or brain), respiratory symptoms from pulmonary metastases or neurological symptoms from brain or bone marrow metastases. β hCG is a specific marker for this group of pathologies. Once the diagnosis of postmolar GTN has been made, the patient should be rapidly re-evaluated in a referral center for GTD for subsequent staging of the disease (Table 2).¹⁵

International Federation of Gynaecology and Obstetrics (FIGO 2000) staging of gestational trophoblastic neoplasia (GTN).¹⁵

Stage I	Disease confined to the uterus
Stage II	GTN spread beyond the uterus but limited to genital system
Stage III	GTN spread to lungs, with or without involvement of the genitourinary system
Stage IV	All other metastatic sites

Pelvic ultrasound allows evaluation of the extent of the disease in the pelvis. It is difficult to distinguish invasive mole and choriocarcinoma from other malignant forms of GTD sonographically. They are generally heterogeneous myometrial nodules, isoechoic or hypoechoic, hypervascularized on color Doppler and with poorly defined margins compared to the surrounding myometrium (Figure 3). Cystic cavities are often recognized within these nodules and arteriovenous (AV) shunts due to neoangiogenesis are common (Figure 4).⁷^,¹⁶

Postmolar gestational trophoblastic neoplasia, showing lesion in both endometrial cavity and myometrium (a), mainly myometrial lesion (b) and global uterine lesion (c).

Postmolar gestational trophoblastic neoplasm showing a myometrial lesion with an arteriovenous fistula with high velocity turbulent flow on color Doppler.

Pelvic MRI may be considered for staging before starting treatment. In accordance with the guidelines of the European Organisation for Treatment of Trophoblastic Diseases (EOTTD) published in 2020,¹⁷ chest X-ray is indicated to evaluate lung metastases in patients with postmolar GTN, which represent the most frequent secondary lesions. In the presence of lung metastases, also confirmed by chest CT, brain MRI and abdominal CT or MRI should be performed to look for other metastases.

Treatment of postmolar GTN (invasive mole and choriocarcinoma) is generally by chemotherapy.¹⁸^,¹⁹ These diseases are highly chemosensitive with an excellent prognosis and a cure rate of almost 100%, allowing the preservation of fertility.

The therapeutic regimens used are based on the 2000 FIGO prognostic scoring system (Table 3)¹⁵ in which the total score is obtained by adding the individual scores for each prognostic factor. According to the scoring system, patients are considered at low risk (risk score of 6 and below) or at high risk (risk score above 6) of developing resistance to single-drug chemotherapy.

International Federation of Gynaecology and Obstetrics (FIGO 2000) prognostic scoring system for postmolar gestational trophoblastic neoplasia.

Prognostic factor	Score
Prognostic factor	0	1	2	4
Age (years)	< 40	≥ 40	–	–
Antecedent pregnancy	Mole	Miscarriage	Term	–
Interval from end of antecedent pregnancy to start of chemotherapy (months)	< 4	4–6	7–12	> 12
Pretreatment hCG (IU/l)	< 10³	> 10³–10⁴	> 10⁴–10⁵	> 10⁵
Number of metastases	0	1–4	5–8	> 8
Site of metastases	No metastases or only lung	Spleen, kidney	Gastrointestinal tract	Liver, brain
Largest tumor diameter (cm)	–	3–4	> 5	–
Prior chemotherapy	–	–	Single drug	≥ 2 drugs

Low-risk patients are typically treated with single-agent chemotherapy, most commonly methotrexate or actinomycin D, with an overall complete remission rate approaching 100%. However, within this group, increasing FIGO score is associated with a higher risk of chemoresistance, and it is widely reported that only approximately one third of patients with a score of 5–6 achieve remission with single-agent therapy alone. Accordingly, in low-risk GTN, a FIGO score of 5–6 and a diagnosis of choriocarcinoma appear to be associated with an increased risk of resistance to single-agent chemotherapy.

In the literature, low-risk patients have been the subject of numerous clinical studies aimed at identifying predictive factors for resistance to single-agent chemotherapy, in order to select patients who may benefit from upfront multi-agent therapy. Some studies suggest that, in low-risk women, the uterine artery pulsatility index (UA-PI) on Doppler velocimetry is a predictive factor of resistance to first-line treatment with methotrexate.²⁰^,²¹^,²² It has been proposed that the degree of tumor vascularization, as assessed by Doppler ultrasonography, may provide additional prognostic information beyond the FIGO scoring system for the early identification of low-risk women who may require second-line therapy. However, this approach has not yet been validated or incorporated into the FIGO scoring system.

Multi-agent chemotherapy regimens are used to treat high-risk GTN. The most commonly used is EMA-CO (etoposide, methotrexate, actinomycin D, cyclophosphamide, vincristine) or alternatively EP-EMA (etoposide, cisplatin, etoposide, methotrexate, actinomycin D).

Approximately 20% of high-risk patients will relapse following primary chemotherapy, though the majority (about 80%) can be salvaged with further treatment. There are different options for patients who relapse after initial treatment. Moreover, the advances in immunotherapy in recent years, alongside the fact that invasive mole and choriocarcinoma strongly express PD-L1, has led to checkpoint inhibitor use in GTN.²³^,²⁴

Patients with a diagnosis of GTN, before starting treatment, should be referred to a specialist GTD centers to optimize management.

Overall survival of women with high-risk GTN is around 95%, and 86.4% of recurrences occur within the first year after normalization of β-hCG. Thus, patients should be counseled to avoid conceiving during the first year following the end of treatment.

Follow-up after chemotherapy for postmolar GTN should include close monitoring of β-hCG for at least 12 months, in order to identify possible recurrences, which are more frequent in this period (72.7% for low-risk GTN and 86.4% for high-risk GTN). The overall duration of follow-up, for postmolar GTN, is recommended to be a minimum of at least 5 years from the end of chemotherapy; current evidence suggests that relapses beyond 7 years are exceptional.

Placental site trophoblastic tumor and epithelioid trophoblastic tumor

PSTT and ETT are associated with lower β-hCG levels than invasive mole and choriocarcinoma, as they arise from the intermediate trophoblast. They may develop several years after any type of antecedent pregnancy.

On ultrasound, PSTT and ETT show heterogeneous myometrial nodules with cystic cavities or solid masses that occupy the endometrial cavity and invade the myometrial wall. On Doppler, they generally show minimal or moderate vascularization (Figure 5). The differential diagnosis is therefore with other forms of GTN, retained placental material and arteriovenous malformations.⁷

Placental site trophoblastic tumor.

Histological diagnosis by resection or biopsy of the primary tumor or metastases is essential. These tumors are less sensitive to chemotherapy with a greater capacity for lymphatic spread than invasive mole and choriocarcinoma.

PSTT and ETT should not be scored and instead requires staging according to FIGO (Table 2), to define the extent of the disease and the most appropriate management. Surgery, when possible, should represent the mainstay of treatment. Hysterectomy should be performed in Stage-I disease. Adjuvant treatment (multi-agent chemotherapy) should be considered in the presence of poor prognostic factors (interval from the prior pregnancy > 4 years, high hCG levels, high mitotic index). However, if fertility preservation is desired, especially in localized lesions, conservative management such as uterine evacuation, hysteroscopic resection and/or chemotherapy may be considered.

For intermediate trophoblast tumors, there are no data on the best follow-up schedule. The 2020 EOTTD guidelines suggest intensive monitoring for the first year post-treatment and continued follow-up for at least 10 years. Follow-up and imaging should be defined by the local GTD referral center.¹⁷

CONCLUSION

GTD encompasses a heterogeneous group of pregnancy-related disorders with distinctive clinical behavior and generally favorable outcomes when appropriately managed. Accurate diagnosis relies on the integration of clinical features, serial β-hCG monitoring, histopathology and imaging, particularly ultrasound, which is essential for initial assessment, staging and treatment surveillance. Risk-adapted therapy and long-term follow-up, ideally coordinated through specialized referral centers, allow high cure rates while preserving fertility. Continued advances in imaging techniques and systemic therapies are expected to further refine individualized management strategies.

PRACTICE RECOMMENDATIONS

Gestational trophoblastic disease comprises a group of rare benign and malignant tumors arising from placental trophoblastic tissue.
Hydatidiform mole or molar pregnancy is categorized into two types: complete (CHM) and partial (PHM) mole.
CHM arises when an empty egg is fertilized by one or two sperm, resulting in a genome with only paternal DNA; PHM occurs when a viable egg is fertilized by two sperm, leading to a triploid biparental genome.
Symptoms of a CHM include vaginal bleeding in the first trimester, severe nausea with high β-hCG level and abnormal ultrasound findings.
Ultrasound typically reveals a uterine cavity filled with anechoic cystic clusters in the case of CHM ('snowstorm appearance') and fetal tissue in the case of PHM.
Histopathological examination confirms the diagnosis after tissue removal by suction dilatation and curettage (D&C), preferably performed under ultrasound guidance in patients who wish to preserve fertility.
Regular β-hCG monitoring post-treatment is essential to detect any progression to gestational trophoblastic neoplasia (GTN), as hydatidiform moles are considered premalignant
The progression of a molar pregnancy into a GTN occurs in 15–20% of CHM and 0.5–5% of PHM.
Reproductive outcomes after a previous molar pregnancy are similar to those of the general population; the risk of a new hydatidiform mole has been reported to increase with successive molar pregnancies and is higher for CHM than for PHM.
Malignant GTD, also known as GTN, encompasses invasive mole, choriocarcinoma, placental site and epithelioid trophoblastic tumors.
GTN should be suspected in any woman with a history of any type of pregnancy who presents with persistent or irregular vaginal bleeding, or with unexplained metastatic disease or acute symptoms compatible with metastases to the lungs, brain, gastrointestinal tract or urinary tract.
The diagnosis of postmolar GTN (invasive mole and choriocarcinoma) is usually made during post-treatment surveillance of serum β-hCG levels according to the 2000 FIGO criteria.
Pelvic ultrasound allows evaluation of the extent of postmolar GTN within the pelvis. Lesions typically appear as heterogeneous myometrial nodules that are isoechoic or hypoechoic, hypervascular on color Doppler imaging, and have poorly defined margins compared with the surrounding myometrium. Cystic cavities are frequently identified within these nodules, as well as arteriovenous shunts.
Postmolar GTN shows high chemosensitivity, with a cure rate approaching 100% and treatments allow fertility preservation.
Therapeutic regimens are based on the FIGO prognostic scoring system: low-risk patients (score 0–6) are treated with single-agent chemotherapy (methotrexate or actinomycin D), whereas high-risk patients (score ≥7) require multi-agent chemotherapy (e.g. EMA/CO).
Low-risk patients show an overall complete remission rate close to 100% while approximately 20% of high-risk patients will relapse following primary chemotherapy with an overall survival around 95%.
In high-risk patients about 85% of recurrences occur within the first year after normalization of β-hCG. Thus, patients should be advised to avoid conceiving during the first year following the end of treatment.
Follow-up after the end of chemotherapy for postmolar GTN should include close monitoring of β-hCG for at least 12 months. The overall duration of follow-up is recommended to be at least 5 years from the end of chemotherapy. Future fertility is not affected by the treatment.
Placental site trophoblastic tumor (PSTT) and epithelioid trophoblastic tumor (ETT) arise from intermediate trophoblast and are associated with lower β-hCG levels than invasive mole and choriocarcinoma; moreover, they may develop years after any type of pregnancy.
On ultrasound, PSTT and ETT show heterogeneous myometrial nodules with cystic cavities or solid masses that occupy the endometrial cavity and invade the myometrial wall with minimal or moderate vascularization observed on color Doppler.
PSTT and ETT should not be scored and instead require staging according to FIGO, to define the extent of the disease and the most appropriate management.
Surgery, when possible, should represent the mainstay of treatment because of the lower chemosensitivity compared with postmolar GTN; adjuvant treatment can be considered if there are poor prognostic factors.
For intermediate trophoblastic tumors, intensive monitoring for the first year post-treatment and continued follow-up for at least 10 years are required.
Patients with a diagnosis of GTN should be referred to specialized gestational trophoblastic disease (GTD) centers before starting treatment to optimize management.

CONFLICTS OF INTEREST

The author(s) of this chapter declare that they have no interests that conflict with the contents of the chapter.

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