Urogenital Imaging

Gestational trophoblastic disease

(GTD), a proliferative disease of the trophoblast. It has various clinical manifestations, ranging from the relatively benign hydatidiform mole to the more malignant invasive mole to metastatic choriocarcinoma. The beta-subunit of human chorionic gonadotrophin (beta-hCG) serves as a useful marker of disease aggressiveness and progression.

The most benign and common form of GTD is the hydatidiform mole. Risk factors include advanced maternal age and prior history of molar pregnancy, which carries a 2040 times relative risk. Remarkable geographical differences are seen in the prevalence of this disease: ranging from 1 in 1200 to 2000 pregnancies in the U.S. to 1 in 500 in France to 1 in 100 in Indonesia.

A hydatidiform mole may be either diploid (complete or classic mole) or triploid (incomplete or partial mole) in its chromosomal make-up. All genetic material of the complete mole is of paternal origin. Most commonly, the complete mole is 46,XX, resulting from fertilization of an ovum without functional genetic material by a X-chromosome sperm, which then duplicates to achieve the normal diploid number. Less commonly, a complete mole may be 46,XY, thought to be the result of fertilization by two different haploid sperms. The incomplete or partial mole is the result of fertilization of a normal ovum by two sperms. Pathologically, the following features are seen in the hydatidiform mole:

  • marked oedema and enlargement of the chorionic villi;

  • lack of villous blood vessels;

  • proliferation of the lining trophoblast of the chorionic villi; and

  • absence of fetal tissue.

    Sonography remains the primary modality in the evaluation of the hydatidiform mole. A second-trimester mole appears as a large, moderately echogenic soft tissue mass in the uterine cavity, containing numerous small cystic spaces, which represent the markedly hydropic chorionic villi. The myometrium may be seen as less echogenic soft tissue surrounding the more echogenic mass. First-trimester moles are more difficult to diagnose sonographically and have a variety of appearances, ranging from a small echogenic mass without the characteristic vesicular architecture to an appearance simulating a blighted ovum or threatened abortion. Doppler interrogation of the trophoblastic tissue reveals a low-impedance, high-flow state, in distinction to the low-flow, higher-impedance states seen in patients with nonviable gestations or degenerating fibroids.

    CT imaging is the study of choice in staging extrapelvic metastases. Extrauterine disease occurs via haematogenous spread, most commonly to the lungs (80%), followed by vagina (30%), pelvis (20%), liver and brain (10%). MRI is useful for assessing the primary uterine lesion and residual abnormalities in patients with persistently elevated hCG levels or an enlarged uterus.

    On MRI (Fig.1) the primary uterine lesion is a medium signal intensity mass on T1-weighted images, and a heterogeneous high and low signal intensity lesion on T2-weighted images. Because these tumours are highly vascular, multiple vessels can be identifed, along with intralesional haemorrhage. The zonal anatomy of the uterus is obscured, and the boundary between the tumour and the myometrium is ill-defined and irregular. Tumour penetration through the uterine wall can also be seen. With therapy, the return of normal uterine zonal anatomy precedes the reduction in tumour volume and regression of pelvic hypervascularity.

    Complications of GTD include theca lutein cysts and haemorrhage, within both the mole and adjacent tissues. High levels of hCG stimulate the formation of theca lutein cysts. Sonographically, multilocular cysts are seen, corresponding to the multiseptated cysts containing amber-coloured or serosanguinous fluid seen pathologically. These cysts can persist for 2-4 months after molar evacuation.

    Hydropic degeneration of the placenta, occurring in 1-3% of pregnancies, can mimic GTD. Engorgement of the chorionic villi can be present following a missed abortion. However, absence of proliferation of the lining trophoblast distinguishes this entity from GTD. As the two entities present with similar sonographic appearances, distinction is made by evaluating the hCG level and by pathologic examination. Degenerating leiomyomas may also mimic the cystic appearance of a hydatidiform mole, though myomas tend to be sound-attenuating.

  • GTD is treated by suction evacuation of the uterus, followed by endometrial curettage to determine the presence and extent of myometrial invasion. Radiographic examination of the chest, including CT, is performed to assess for metastatic disease. Serum beta-hCG is followed until the level is normal; hCG level usually falls towards zero in 10–12 weeks after evacuation.

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    Fig.1

    Oblique coronal T1-weighted gradient echo MRI section after intravenous gadolinium, demonstrating fluid with an enhancing mass in the endometrial cavity, due to gestational trophoblastic disease. The uterus is bicornuate.
    Gestational trophoblastic disease, Fig.1