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Serum unconjugated estradiol-17β (E2) was measured by a rapid radioimmunoassay method using a specific antibody. Serial estimations of serum E2were performed in 10 pregnancies and 3 twin pregnancies complicated by hypertensive disorder of pregnancy, 2 cases of bad obstetric history, 8 cases of uncomplicated twin pregnancy, and 3 uncomplicated triplet pregnancies. Serum E2was also measured in 7 instances of intrauterine death. In 2 of the 10 patients with hypertensive disorder of pregnancy resulting in delivery of dysmature, growth-retarded babies, serial serum E2showed a falling trend, with two or more successive values below the standard deviation range for normal pregnancy. A similar pattern was obtained in a case of bad obstetric history resulting in neonatal death of a dysmature, growth-retarded infant. In all 3 cases, serum E2was below 10 ng/ml. In 6 cases of intrauterine death due to placental dysfunction, serum E2levels were low (between 0.375 and 6.46 ng/ml), while serum E2was normal in 1 case of intrauterine death not due to placental dysfunction. Serum E2was higher in uncomplicated twin and triplet pregnancies than in single pregnancies. The advantages and potential value of serum E2measurement as an index of placental function are discussed.

Serum unconjugated estradiol-17β (E2) was measured by a radioimmunoassay method using a specific antibody raised against 6-oxo-estradiol-17β succinyl bovine serum albumin conjugate. Serum E2estimation was performed on 294 normal single pregnancies from 6 weeks to 42 weeks' gestation, 28 samples from uncomplicated twin pregnancies, and 12 samples from uncomplicated triplet pregnancies. In late pregnancy, serum E2levels fluctuated throughout the day and were lowest at night. Unconjugated E2rose slowly from a mean ± SE of 2.10 ± 0.56 ng/ml at 6 to 7 weeks' gestation to 8.03 ± 0.97 ng/ml at 30 weeks' gestation. From the 30th week of pregnancy, unconjugated E2rose much more rapidly until term to reach a nadir at 41 weeks' gestation with a mean ± SE of 35.85 ± 2.96 ng/ml. It dropped to 24.00 ± 3.67 ng/ml at 42 weeks. There was a wide scatter of serum E2values during pregnancy. Serum E2concentrations in uncomplicated twin and triplet pregnancies were usually much higher than for single pregnancies or within the normal range for single pregnancies. The significance of these findings is discussed.

Conjoined twins in a triplet pregnancy are very rare. Failure to diagnose a thoracopagus in a case of known triplet pregnancy resulted in obstructed labor which necessitated an emergency cesarean section. The single infant survived, but the thoracopagus died apparently from asphyxia.

The source of the large amounts of circulating progesterone and the smaller quantities of 17α-hydroxyprogesterone in Hydatidiform Mole was studied by measuring progesterone, 17α-hydroxyprogesterone and 20α-hydroxyprogesterone in petroleum ether extracts of mole vesicle fluid and theca lutein cyst fluid following chromatography. The progesterone concentration in 10 samples of mole vesicle fluid ranged from 261–1493 ng/ml (mean 724 ng/ml) and was 8.6 times higher than the concentration in the serum. The chromatogram of the theca lutein cyst fluid showed a large peak of progesterone followed by two large secondary peaks of 20α-hydroxyprogesterone and 17α-hydroxyprogesterone. In 3 patients with benign Hydatidiform Mole, progesterone and human chorionic gonadotrophin rapidly decreased during the first 48 hours following evacuation of the mole. Thereafter, progesterone disappeared from the serum before HCG in one case, together with HCG in the second, and remained at low concentrations for 3 months in the third patient despite negative (below 0.6 IU/ml) HCG assays. The studies show that the mole trophoblast is the principal source of progesterone and the ovaries are a secondary source. Theca lutein cysts are the principal source of 17α-hydroxyprogesterone.

Progesterone and human chorionic gonadotrophin (HCG) were measured in the sera of 25 patients with hydatidiform mole, 10 patients with choriocarcinoma and 200 normal pregnancies by a competitive protein-binding assay and a haemagglutination-inhibition assay respectively. Elution of the petroleum ether extract of mole serum on Sephadex LH-20 showed that the main fraction (92.8%) was progesterone, followed by a small peak of 20 α-hydroxyprogesterone. In 21 intact hydatidiform moles, the mean serum progesterone of 106.0 ng/ml (range 17.8–263 ng/ml) was higher than for normal pregnancy. Serum HCG (mean 833 IU/ml) was similarly elevated. Low concentrations of progesterone (0–17.3 ng/ml) and HCG (15–160 IU/ml) were present in 4 patients who had aborted. The mean serum progesterone was not further elevated in patients with theca lutein cysts of the ovary. There was no correlation between the serum progesterone and the uterine size, serum HCG or malignant sequelae. In 10 cases of choriocarcinoma, the serum progesterone ranged from 1.3–61 ng/ml (mean 16.9 ng/ml), the serum HCG from 0–960 IU/ml (mean 158 IU/ml) but there was no correlation between the two values. The evidence suggests a hyperactive steroidogenesis in hydatidiform mole and poor steroidogenesis in choriocarcinoma. An HCG secretion occurs in both cases.