Gestational Trophoblastic Disease

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Chapter 208 Gestational Trophoblastic Disease

INTRODUCTION

Description: Gestational trophoblastic diseases include choriocarcinoma, molar pregnancy (hydatidiform mole and invasive mole), and placental-site trophoblastic tumor. They are abnormalities of pregnancy that arise entirely from abnormal placental proliferation. They are classified as being either complete, in which no fetus is present, or incomplete (partial), in which both fetus (generally abnormal) and molar tissues are present.
Prevalence: Molar pregnancy—1 of 1000 to 1500 pregnancies in the United States, as high as 10 per 1000 pregnancies in Asia; choriocarcinoma—1 of 40,000 pregnancies.
Predominant Age: Greatest during the early and late reproductive years.
Genetics: Complete—mostly 46,XX (paternal in origin, although mitochondrial DNA remains maternal in origin). Incomplete—triploid (69,XXY or 69,XXX; all of paternal origin).

ETIOLOGY AND PATHOGENESIS

Causes: Unknown.
Risk Factors: Maternal age (older than 40: 5.2 times risk), Asians living in Southeast Asia, folate deficiency, prior molar pregnancy (2% recurrence rate).

CLINICAL CHARACTERISTICS

Signs and Symptoms

• Present as a pregnancy but associated with more profound hormonal changes, leading to exaggerated symptoms of pregnancy in many patients
• Uterine size that is inappropriate for dates (larger or smaller, 30%)
• Painless vaginal bleeding (95%, generally between 6 and 16 weeks of gestation)
• Hypertension, pre-eclampsia, proteinuria, nausea and vomiting (hyperemesis, 8%), visual changes, tachycardia, and shortness of breath all possible (pregnancy-induced hypertension in the first trimester of pregnancy is virtually diagnostic)
• Incomplete molar pregnancies—symptoms of an incomplete or missed abortion (90%), including vaginal bleeding (75%)

DIAGNOSTIC APPROACH

Differential Diagnosis

• Choriocarcinoma
• Missed abortion
• Threatened abortion

Associated Conditions: Hyperemesis, hypertension, hyperthyroidism, pre-eclampsia, proteinuria, nausea and vomiting, visual changes, tachycardia, and shortness of breath. Bilateral adnexal masses (theca lutein cysts) occur in 15% to 20% of patients.

Workup and Evaluation

Laboratory: Complete blood count, quantitative measurement of β-human chorionic gonadotropin (β-hCG; to establish risk and serial to follow success of therapy), the patient’s blood type and Rh status should be established to allow for Rh immune globulin therapy (if needed) or blood replacement. Clotting function studies and blood cross-matching are advisable before the evacuation of a large uterus. (Chorionic gonadotropin levels often exceed 100,000 ImU/mL.)
Imaging: Ultrasonography can establish the diagnosis. A baseline chest radiograph to check for metastatic disease should be obtained.
Special Tests: Absence of fetal heart sounds (in complete mole).
Diagnostic Procedures: History and physical examination. Edematous trophoblastic fragments may be passed vaginally through a partially dilated cervical os, alerting the clinician to the diagnosis.

Pathologic Findings

Edematous trophoblastic fronds. Karyotype: incomplete; triploid (80%); complete; 46,XX (95%).

MANAGEMENT AND THERAPY

Nonpharmacologic

General Measures: Evaluation and diagnosis, general supportive measures.
Specific Measures: The treatment of molar pregnancies is surgical: evacuation of the uterine contents. This is most often accomplished via suction curettage. Because of the large size of some molar pregnancies and a tendency toward uterine atony, concomitant oxytocin administration is advisable and blood for transfusion must be immediately available, should it be needed.
Diet: No specific dietary changes indicated.
Activity: No restriction.

Drug(s) of Choice

None. (Oxytocin or methylergonovine maleate [Methergine] is used to help contract the uterus during surgical evacuation.) Primary or recurrent malignant trophoblastic disease is generally treated with chemotherapy (methotrexate, actinomycin D, chlorambucil, or cyclophosphamide [Cytoxan], singly or in combination).

FOLLOW-UP

Patient Monitoring: After the uterus has been emptied, the patient must be closely followed for at least 1 year for the possibility of recurrent benign or malignant disease. Any change in the patient’s examination, an increase in β-hCG titers, or a failure of the β-hCG level to fall below 10 mIU/mL by 12 weeks after evacuation must be evaluated for the possibility of recurrent benign or malignant disease. Serum hCG levels are generally monitored every 2 weeks until three consecutive tests are negative, then monthly for 6 to 12 months. (Proteolytic enzymes and heterophilic antibodies found in 3% to 4% of individuals can cause a falsely positive hCG test [up to 800 ImU/mL have been reported] and can lead to inappropriate therapy.)
Prevention/Avoidance: None.
Possible Complications: Gestational trophoblastic neoplasia is notable for the possibility of malignant transformation, although less than 10% of patients develop malignant changes. In general, the larger or more advanced the molar pregnancy, the greater the risk of pulmonary complications, bleeding, trophoblastic emboli, or fluid overload during evacuation.
Expected Outcome: Approximately 80% of molar pregnancies follow a benign course after initial therapy. Between 15% and 25% of patients develop invasive disease, and 3% to 5% eventually have metastatic lesions. The prognosis for patients with primary or recurrent malignant trophoblastic disease is generally good (>90% cure rate). The theca lutein cysts often found in molar pregnancies may take several months to regress after evacuation of the uterine contents. Fewer than 5% of patients will require hysterectomy to achieve a cure for choriocarcinoma.

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MISCELLANEOUS

Pregnancy Considerations: Pregnancy should be delayed for at least 1 year after a molar pregnancy to avoid confusion between normal pregnancy and recurrent disease. These patients have no higher rate of abortions, stillbirths, congenital anomalies, prematurity, or other complications of pregnancy with future gestations. The placenta from any subsequent pregnancies should be sent for histologic evaluation.
ICD-9-CM Codes: 630, 236.1 (Invasive or malignant).

REFERENCES

Level I

Covens A, Filiaci VL, Burger RA, et alGynecologic Oncology Group. Phase II trial of pulse dactinomycin as salvage therapy for failed low-risk gestational trophoblastic neoplasia: a Gynecologic Oncology Group study. Cancer. 2006;107:1280.

Goldstein DP, Goldstein PR, Bottomley P, et al. Methotrexate with citrovorum factor rescue for nonmetastatic gestational trophoblastic neoplasms. Obstet Gynecol. 1976;48:321.

Homesley HD, Blessing JA, Rettenmaier M, et al. Weekly intramuscular methotrexate for nonmetastatic gestational trophoblastic disease. Obstet Gynecol. 1988;72:413.

Level II

Bracken MB. Incidence and aetiology of hydatidiform mole: an epidemiological review. Br J Obstet Gynaecol. 1987;94:1123.

Matsui H, Iitsuka Y, Suzuka K, et al. Early pregnancy outcomes after chemotherapy for gestational trophoblastic tumor. J Reprod Med. 2004;49:531.

Level III

American College of Obstetricians and Gynecologists. Diagnosis and treatment of gestational trophoblastic disease. ACOG Practice Bulletin 53. Obstet Gynecol. 2004;103:1365.

Berkowitz RS, Goldstein DP. Gestational trophoblastic disease. Cancer. 1995;76:2079.

Berkowitz RS, Goldstein DP. Chorionic tumors. N Engl J Med. 1996;335:1740.

Grimes DA. Epidemiology of gestational trophoblastic disease. Am J Obstet Gynecol. 1984;150:309.

Lewis JLJr. Diagnosis and management of gestational trophoblastic disease. Cancer. 1993;71:1639.

Smith HO. Gestational trophoblastic disease epidemiology and trends. Clin Obstet Gynecol. 2003;46:541.

Soper JT. Gestational trophoblastic disease. Obstet Gynecol. 2006;108:176.

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