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In the management of a chorionic disease, human chorionic gonadotropin (hCG) is the most reliable tumor marker. However, hCG has a low titer, so that it cannot be strictly distinguished from the human luteinizing hormone (hLH) by the traditional method that uses a hemagglutinin reaction (HAR) or by a radioimmunoassay (RIA). Recently, however, the detection of the beta-COOH-terminal peptide of hCG (hCG-CTP) by an enzyme immunoassay has made it possible to clearly distinguish hCG from hLH, and from April, 1987 to December, 1989, 13 trophoblastic diseases have been managed using this new technique. Results have shown that human chorionic gonadotropin-CTP, when compared to other methods of measurement, is the most sensitive tumor marker and as it is the most accurate, it should be used in careful follow-up observations of a chorionic disease.

A rare case of placentae site trophoblastic tumor (PSTT) studied by immunohistochemistry and nuclear DNA analysis is reported. The patient, a 24-year-old Japanese female, complained of amenorrhea. Dilatation and curettage revealed a small specimen that contained trophoblastic cells and caused intractable bleeding. Pelvic sonography revealed a 5-cm mass in the posterior uterine wall with multiple cystic lesions of several sizes. The cystic lesions were shown to be dilated vessels by magnetic resonance imaging (MRI) and digital subtraction angiography (DSA). Serum beta-hCG (beta subunit of human chorionic gonadotropin) was 3.7 ng/ml. Total abdominal hysterectomy revealed a well-circumscribed, yellow, soft mass in the posterior uterine wall. Microscopic findings were consistent with PSTT and the mitotic count was extremely low. Immunohistochemically, most of the tumor cells were intensely stained with human placental lactogen, whereas few were stained with human chorionic gonadotropin. The nuclear DNA content of the trophoblastic cells showed a sharp peak at the triploid range coexistent with a few cells of higher ploidy. This is the first report of sonographic findings and nuclear DNA analysis by spot cytometry in a case of PSTT.

The effectiveness of the prophylactic chemotherapy was evaluated in 420 patients with molar pregnancy. All patients were followed for 5 to 15 years after the evacuation. Twenty-two (7.5%) of 293 patients with prophylactic chemotherapy and 23 (18.1%) of 127 patients without prophylactic chemotherapy (control) developed secondary trophoblastic disease. The prophylactic chemotherapy could reduce the occurrence of secondary trophoblastic disease. In these secondary trophoblastic diseases, 5 (22.7%) of 22 patients in the prophylactic chemotherapy group and 5 (21.7%) of 23 in the control had metastatic trophoblastic disease. Choriocarcinoma after the molar pregnancy developed in two patients (0.7%) of the prophylactic chemotherapy group and two (1.6%) of the control. Prophylactic chemotherapy did not eliminate the occurrence of choriocarcinoma. The complication of the prophylactic chemotherapy was seen in 27.3% of the patients. Neither severe complication nor death were related to the toxicity.

The nuclear DNA contents of labeled and unlabeled nuclei of trophoblastic cells of 8 normal pregnancies, 2 missed abortions, and 14 cases of trophoblastic diseases were measured by Feulgen-DNA cytofluorometry combined with autoradiography. Syncytiotroblasts were rarely labeled and were considered to be inactive with regard to cell proliferation. Most of the labeled cells were cytotrophoblasts. The predominantly labeled cells ranged between 2 and 4C in cases of normal pregnancy and missed abortion, and a shift to a higher ploidy was seen in the more grave trophoblastic disease. From the point of cellular proliferation kinetics of trophoblastic cells, it is presumed that the cells in cases of normal pregnancy and type I hydatidiform mole are in the 2C cell cycle and in type II hydatidiform mole and in invasive mole there are heterogeneous cell populations, most of which are in the 2C cell cycle while the remaining are undergoing polyploidization or aneuploidization. In choriocarcinoma, the cells are not in the 2C cell cycle and also are probably undergoing polyploidization or aneuploidization in the hyper-4C area.

The nuclear DNA content of trophoblasts was measured in 25 cases of normal pregnancy, 46 cases with hydatidiform mole, ten cases with destructive mole and six cases of chorionepithelioma (choriocarcinoma). In normal pregnancy, DNA distribution in syncytiotrophoblasts and cytotrophoblasts showed a sharp peak at the diploid region, although a few cytotrophoblasts with increased DNA content were observed in the first trimester. In chorionepithelioma the DNA content of the trophoblastic cells showed extremely wide distribution without any special peak. In destructive mole, although a wide distribution was observed, the sharp peak was usually noted at the diploid range. Cases with hydatidiform mole were divided into two categories according to the DNA distribution patterns. Type I showed the patterns similar to the first trimester of normal pregnancy and type II resembled the patterns of destructive mole. In hydatidiform mole of type II, subsequent progress towards destructive mole was frequently encountered.

Twenty cases of gestational trophoblastic disease in women aged 50 or more are reported. The lesions were 7 hydatidiform mole (35%), 8 invasive mole (40%), and 5 choriocarcinoma (25%). The most common presenting symptom was abnormal vaginal bleeding. Three choriocarcinoma patients were postmenopausal and all of them had choriocarcinoma. None of the patients with hydatidiform mole or invasive mole died of the disease, but 4 of 5 choriocarcinoma patients died of the disease. Because of the high rate (56.3%) of malignant sequelae after molar evacuation, a primary hysterectomy for the treatment of hydatidiform mole in this age group is recommended. It is important to maintain a high level of suspicion for the diagnosis of gestational trophoblastic disease in the elderly women.