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Clinically, patients with complete hydatidiform mole typically present with hyperemesis gravidarum or uterine size larger than expected for the estimated gestational age (2). The serum beta-hCG level is usually considerably higher than expected for the estimated gestational age. This is variable, however, and the level may be within the expected range for a first trimester pregnancy. Ultrasonography (US) is used primarily to rule out a normal intrauterine pregnancy. However, the imaging appearance may also allow one to suggest the diagnosis of complete hydatidiform mole.
US helps confirm uterine enlargement in more than 60% of cases. A moderately echogenic, central uterine mass is seen on sonograms. Although earlier reports (12) described a "snowstorm" or "granular" appearance of multiple echogenic foci, more modern equipment usually allows identification of numerous, discrete, anechoic (cystic) spaces within a central area of heterogeneous echotexture (Figure 3, Figure 4). Contrary to earlier assertions, the small cystic areas correspond to the hydropic villi characteristically seen at gross pathologic examination, rather than to areas of hemorrhage. Hemorrhage is not a typical pathologic feature of complete hydatidiform mole, although it is occasionally seen with choriocarcinoma.
The appearance of complete hydatidiform mole is extremely variable in the first trimester. One may see a large, central fluid collection that mimics an anembryonic gestation (12) (Figure 5) or abortion (missed or incomplete) (9). Occasionally, there is merely a central mass of variable echogenicity, presumably because the villi are too small to see with sonography at this time (13) (Figure 6).
The coexistence of a fetus with a complete hydatidiform mole is uncommon (in contrast to the partial hydatidiform mole), occurring in 1%-2% of cases (Figure 7). This condition is usually the result of dizygotic twinning; thus, the fetus (in contrast to the mole) is chromosomally normal. However, fetal survival until term is unlikely because of the maternal complications of the mole itself. In the occasional case in which there are not overwhelming clinical grounds to treat the complete hydatidiform mole and the fetus is sonographically normal, one may elect to perform amniocentesis. If a normal (diploid) karyotype is obtained, the diagnosis of complete hydatidiform mole is made (and that of partial hydatidiform mole is excluded), and the patient might be given the option of attempting to carry the gestation to term (14).
Another clue to the diagnosis of GTD is ovarian enlargement with cyst formation (seen in up to 40% of cases). These theca lutein cysts are a form of ovarian hyperstimulation and result from high circulating levels of beta-hCG typically associated with GTD (Figure 4, Figure 8). Theca lutein cysts are multiloculated, are often bilateral, and resolve after treatment of the intrauterine process. Other causes of theca lutein cysts include twin gestations, fetal hydrops, pharmacologic stimulation (especially with human maternal gonadotropin) (15), and, occasionally, a normal pregnancy. Some authors believe that the presence of theca lutein cysts should alert one to an increased probability of one of the more aggressive forms of GTD, that is, invasive mole or choriocarcinoma (2). Although occasionally complicated by hemorrhage or rupture, these cysts usually resolve within a few months of removal of the causative factor (13).
Nonneoplastic complications of complete hydatidiform mole may be seen. Hyperthyroidism may occur because of the thyroid-stimulating properties of beta-hCG. Although such an effect is weak, it may be offset by the very high serum concentrations of the hormone. Anemia may occur as a result of plasma volume expansion; although this phenomenon is seen in patients with normal gestations, it may be exaggerated in patients with GTD and may be further complicated by concomitant vaginal bleeding. Despite the occurrence of these and other complications (including toxemia and coagulopathy), treatment is curative in approximately 85% of patients (9,16).
Typically, therapy for complete hydatidiform mole consists of dilatation and suction curettage (at which time the diagnosis is confirmed). Occasionally, recurrence of complete hydatidiform mole may occur. More important, 15% of women with complete hydatidiform mole will develop recurrent disease in the form of invasive mole or choriocarcinoma. These women cannot be identified at the time of initial diagnosis. Herein lies the difficulty: Because of the unpredictable outcome in a given patient with a presumptive diagnosis of complete hydatidiform mole based on laboratory, radiologic, and microscopic features, all patients are followed up with successive serum beta-hCG measurements to allow early detection of persistent gestational trophoblastic neoplasia (ie, invasive mole and choriocarcinoma) (2,6). The clinical diagnosis of complete hydatidiform mole is reached only when serial testing shows progressive decrease in the serum beta-hCG level (confirming the absence of persistent gestational trophoblastic neoplasia). In view of the importance of serial monitoring of beta-hCG levels during the 1st year after treatment of complete hydatidiform mole, pregnancy, which would adversely affect the specificity of an abnormally elevated beta-hCG level, should be avoided during this time (6).
Complete Hydatidiform Mole