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AJR 2000; 175:898-900
© American Roentgen Ray Society


Sonography Case of the Day

Case 2

Placental Site Trophoblastic Tumor

Kenneth M. Vitellas, William F. Bennett and James G. Bova

Gestational trophoblastic disease is a spectrum of trophoblastic tumors including hydatidiform mole (partial and complete), invasive mole, gestational choriocarcinoma, and placental site trophoblastic tumor [1,2,3]. It is characterized by abnormal proliferation of pregnancy-associated trophoblastic tissue with malignant potential, which can occur after a normal pregnancy, abortion, ectopic pregnancy, or molar pregnancy. The presence and course of the disease can be monitored with quantitative levels of human chorionic gonadotropin (HCG).

Placental site trophoblastic tumor (Fig. 2A,2B,2C,2D,2E,2F,2G,2H,2I,2J,2K,2L,2M) is the least common form of gestational trophoblastic disease and is potentially malignant [1,2,3]. Patients usually present with vaginal bleeding 1 week to 14 years after pregnancy. The tumor is composed of intermediate trophoblastic cells that normally play a critical role in implantation. In addition, the tumor contains little syncytiotrophoblastic tissue; thus, the HCG levels are usually normal to mildly elevated. The minimally elevated ß-HCG level that does not increase with serial determinations can help differentiate placental trophoblastic tumor from other types of gestational trophoblastic disease. Placental-site trophoblastic tumor should be suspected when the ß-HCG level is minimally elevated and there is either a decrease or no change of endometrial or myometrial mass or ß-HCG level on follow-up studies. The diagnosis is made on the basis of findings at biopsy. Ten to fifteen percent metastasize, usually to the lungs, liver, abdominal cavity, and brain.



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Fig. 2A. —38-year-old woman (gravida 1, para 0) with history of blighted ovum who presented with intermittent pelvic pain and vaginal bleeding of 3 months' duration after dilatation and curettage. Sonograms of pelvis 1 month (A and B) and 2 months (C and D) after dilatation and curettage procedure was performed for blighted ovum show stable vascular mass in lower uterine segment (arrows). Low-resistance spectral tracings were documented.

 


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Fig. 2B. —38-year-old woman (gravida 1, para 0) with history of blighted ovum who presented with intermittent pelvic pain and vaginal bleeding of 3 months' duration after dilatation and curettage. Sonograms of pelvis 1 month (A and B) and 2 months (C and D) after dilatation and curettage procedure was performed for blighted ovum show stable vascular mass in lower uterine segment (arrows). Low-resistance spectral tracings were documented.

 


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Fig. 2C. —38-year-old woman (gravida 1, para 0) with history of blighted ovum who presented with intermittent pelvic pain and vaginal bleeding of 3 months' duration after dilatation and curettage. Sonograms of pelvis 1 month (A and B) and 2 months (C and D) after dilatation and curettage procedure was performed for blighted ovum show stable vascular mass in lower uterine segment (arrows). Low-resistance spectral tracings were documented.

 


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Fig. 2D. —38-year-old woman (gravida 1, para 0) with history of blighted ovum who presented with intermittent pelvic pain and vaginal bleeding of 3 months' duration after dilatation and curettage. Sonograms of pelvis 1 month (A and B) and 2 months (C and D) after dilatation and curettage procedure was performed for blighted ovum show stable vascular mass in lower uterine segment (arrows). Low-resistance spectral tracings were documented.

 


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Fig. 2E. —38-year-old woman (gravida 1, para 0) with history of blighted ovum who presented with intermittent pelvic pain and vaginal bleeding of 3 months' duration after dilatation and curettage. Axial fast spin-echo MR images show mass of heterogeneous signal in endometrial cavity with disruption of normal low-signal junctional zone (arrows).

 


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Fig. 2F. —38-year-old woman (gravida 1, para 0) with history of blighted ovum who presented with intermittent pelvic pain and vaginal bleeding of 3 months' duration after dilatation and curettage. Axial fast spin-echo MR images show mass of heterogeneous signal in endometrial cavity with disruption of normal low-signal junctional zone (arrows).

 


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Fig. 2G. —38-year-old woman (gravida 1, para 0) with history of blighted ovum who presented with intermittent pelvic pain and vaginal bleeding of 3 months' duration after dilatation and curettage. Unenhanced (G and H) and gadolinium-enhanced (I and J) gradient echo images show hypervascular endometrial mass with extension into myometrium (arrows).

 


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Fig. 2H. —38-year-old woman (gravida 1, para 0) with history of blighted ovum who presented with intermittent pelvic pain and vaginal bleeding of 3 months' duration after dilatation and curettage. Unenhanced (G and H) and gadolinium-enhanced (I and J) gradient echo images show hypervascular endometrial mass with extension into myometrium (arrows).

 


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Fig. 2I. —38-year-old woman (gravida 1, para 0) with history of blighted ovum who presented with intermittent pelvic pain and vaginal bleeding of 3 months' duration after dilatation and curettage. Unenhanced (G and H) and gadolinium-enhanced (I and J) gradient echo images show hypervascular endometrial mass with extension into myometrium (arrows).

 


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Fig. 2J. —38-year-old woman (gravida 1, para 0) with history of blighted ovum who presented with intermittent pelvic pain and vaginal bleeding of 3 months' duration after dilatation and curettage. Unenhanced (G and H) and gadolinium-enhanced (I and J) gradient echo images show hypervascular endometrial mass with extension into myometrium (arrows).

 


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Fig. 2K. —38-year-old woman (gravida 1, para 0) with history of blighted ovum who presented with intermittent pelvic pain and vaginal bleeding of 3 months' duration after dilatation and curettage. Spin-echo gadolinium-enhanced MR images show myometrial invasion (arrows).

 


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Fig. 2L. —38-year-old woman (gravida 1, para 0) with history of blighted ovum who presented with intermittent pelvic pain and vaginal bleeding of 3 months' duration after dilatation and curettage. Spin-echo gadolinium-enhanced MR images show myometrial invasion (arrows).

 


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Fig. 2M. —38-year-old woman (gravida 1, para 0) with history of blighted ovum who presented with intermittent pelvic pain and vaginal bleeding of 3 months' duration after dilatation and curettage. Sonogram after dilatation and curettage of mass shows normal endometrium (arrows). At this time, ß-human chorionic gonadotropin level was normal.

 

Radiographically, a polypoid mass is formed that can involve the endometrium and the myometrium [2, 3]. MR imaging shows a myometrial mass isointense to normal myometrium on T1-weighted MR imaging and isointense to slightly hyperintense on T2-weighted MR imaging [1, 4]. Endometrial masses are heterogeneous. Uterine zonal anatomy is distorted with obliteration of boundaries between the endometrium and myometrium (junctional zone). Associated cystic spaces or prominent blood vessels have been described in most cases. The role of intermediate trophoblastic cells in parasitizing uterine vessels to establish uteroplacental circulation may explain the prominent vascularity described in some cases. Accurate localization with MR imaging can distinguish patients who can be successfully treated with hysterotomy rather than hysterectomy, preserving the uterus for future child-bearing [1, 4].

The other diagnoses are incorrect for various reasons. Uterine arteriovenous malformations are often caused by trauma, with the history often being spontaneous abortion followed by dilatation and curettage, therapeutic abortion, hysterectomy, cesarean section, endometrial carcinoma, or gestational trophoblastic disease [5]. The gray-scale, color Doppler, and spectral Doppler sonography features of gestational trophoblastic disease and abnormal placentation with retained products can be identical to those of uterine arteriovenous malformations. The only distinguishing feature is an elevated ß-HCG level in gestational trophoblastic disease.

Choriocarcinoma does not contain chorionic villi and is characterized by necrosis and hemorrhage with early vascular invasion resulting in distant metastasis. It consists of mixtures of trophoblastic cells with syncytial trophoblasts lacking normal organization. Follow-up imaging shows a rapidly growing mass invading both the uterine muscle and blood vessels, causing hemorrhage and necrosis. The ß-HCG level is significantly elevated. Sonographic findings are similar to those of the invasive mole.

Clinically, patients with hydatidiform mole present with vaginal bleeding and large uterus for gestational age. The hydatidiform mole is separated into two types: complete mole and partial mole. Sonographic findings vary with gestational age. In the first trimester, sonography shows an enlarged uterus containing a predominantly echogenic endometrial mass. Tiny vesicles, which can be smaller than 2 mm in diameter on pathologic examination, are too small to be seen. In the second trimester, sonography shows an enlarged uterus containing numerous tiny cystic structures (vesicular tissue) that expand the endometrial cavity. Vesicles can be as large as 2-3 cm in diameter.

Patients with invasive mole (chorioadenoma destruens) present with vaginal bleeding and uterine enlargement. The ß-HCG titer fails to decrease to normal levels after 12 weeks from evacuation, or there is an increase in ß-HCG levels after an initial decrease. Invasive mole is characterized by myometrial invasion without involvement of the endometrium. Sonography usually shows a well-defined echogenic spherical mass in the uterine myometrium.

References

  1. Brandt KR, Coakley KJ. MR appearance of placental site trophoblastic tumor: a report of three cases. AJR 1998;170:485 -487[Abstract/Free Full Text]
  2. Baz P, DeBaz, Lewis TJ. Imaging gestational trophoblastic disease. Semin Oncol 1995;22:130 -141[Medline]
  3. Green CL, Angtuaco TL, Shah HR, Parmley TH. Gestational trophoblastic disease: a spectrum of radiologic diagnosis. RadioGraphics 1996;16:1371 -1384[Abstract]
  4. Preidler KW, Luschin G, Tamussino K, Szolar D, Stiskal M, Ebner F. Magnetic resonance imaging in patients with gestational trophoblastic disease. Invest Radiol 1996;31:492 -496[Medline]
  5. Huang MW, Muradall D, Thurston WA, Burns PN, Wilson SR. Uterine arteriovenous malformations: gray-scale and Doppler US features with MR imaging correlation. Radiology 1998;206:115 -123[Abstract/Free Full Text]

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