P. C. T. Chew

Elevated peritoneal fluid luteinizing hormone and prolactin concentrations in infertile women with endometriosis

In this study, we compared (Mann‐Whitney U‐test) the peritoneal fluid FSH, LH and PRL levels, measured by RIA, at the follicular and luteal phases of the menstrual cycle in women with (n = 43; age 25–44 years) and with no evidence of endometriosis (n = 35; age 25–39 years) who were considered as controls. Both follicular and luteal phase FSH concentrations of women with endometriosis were not statistically different (n = 22 vs 18; 0.32–5.8 vs 0.50–8.2 IU/l, P = 0.247; n = 13 vs 14; 0.6–6.5 vs 0.66–6.7 IU/l, P = 0.604) compared to their respective controls. In contrast to FSH, the concentrations of LH at follicular (n = 19 vs 17; 3.1–34.2 vs 2.3–12.2 IU/l, P = 0.01) and luteal (n = 17 vs 15; 2.1–95.4 vs 1.3–17.9 IU/l, P = 0.02) phases of the test group was significantly elevated at both phases of the cycle. With respect to differences in PRL concentrations at follicular phase no significant change (n = 21 vs 16; 1030–5800 vs 1305–4650 mIU/l; P = 0.255) was observed. The greatest difference in luteal PRL concentrations (P = 0.007) was obtained between the women with endometriosis and controls (n = 17 vs 17; 1895–8600 vs 1041–5000 mIU/l). The results suggest that disordered synchronization of neuroendocrine mechanisms controlling LH and PRL may be the underlying abnormality causing infertility in our group of patients with endometriosis

CONTROL OF GONADOTROPHIN SECRETION BY STEROID HORMONES IN CASTRATED MALE TRANSSEXUALS. I. EFFECTS OF OESTRADIOL INFUSION ON PLASMA LEVELS OF FOLLICLE‐STIMULATING HORMONE AND LUTEINIZING HORMONE

Twenty‐four infusions of oestradiol (E2) in graded doses ranging from 0–200 μg administered over a period of 7 hours were carried out in eleven healthy male transsexuals who had undergone sex reassignment at least 3 months previously. Plasma levels of follicle‐stimulating hormone (FSH), luteinizing hormone (LH) and E2 were analysed by radioimmunoassay, while sex hormone binding globulin (SHBG) was measured using 3H‐testosterone as the saturating ligand. Infusion of 5–200 μg of E2 raised plasma E2 to levels ranging from 38·4–367·8 pg/ml which represent 83%–800% of levels found in a control group of sixty‐three normal males. SHBG capacity remained unchanged at all doses of E2 studied. No change in plasma levels of FSH and LH was observed in control infusions and infusion of 5 μg of E2. From 10 μg‐200 μg, suppression of plasma levels of FSH was noted at the 5–7 hour period. The suppression increased up to 20 μg and thereafter the levels of FSH remained constant. On the other hand, the suppression of LH increased up to the highest E2 dose (200 μg) studied. Further, significant suppression of LH occurred earlier than the 5–7 hours as the dose of E2 increased. These observations are consistent with the conclusions that: (1) E2 plays a part in the regulation of secretion of FSH and LH in men; and (2) at doses higher than physiological, E2 exerts a differential effect on the secretion of FSH and LH.

THE EFFECT OF CLOMIPHENE ON UNCASTRATED AND CASTRATED MALE TRANSSEXUALS

Clomiphene was administered at a daily dose of 100 mg for 5 consecutive days to two groups of male subjects. There were three uncastrated male transsexuals (Group A) and nine castrated male transsexuals (Group B). In the uncastrated subjects Clomiphene enhanced the secretion of follicle‐stimulating hormone (FSH), luteinizing hormone (LH) and testosterone (T) starting from day 3 of treatment. The magnitude of the increment ranged from 150%–250% over the mean basal plasma level for LH, 113%–262% for FSH and 12%–68% for T. In contrast, Clomiphene suppressed both FSH and LH in the castrated subjects. Equal suppression of both the gonadotrophins were observed. The levels of FSH and LH in plasma on day 3 were suppressed to 66.4% and 66.2% of their respective mean basal levels. Two days after the termination of treatment, suppressions were maintained. These results suggest that Clomiphene acts as an anti‐oestrogen in uncastrated male transsexuals and in castrated male transsexuals who have subphysiological levels of oestradiol it acts as a weak oestrogen.

Plasma oestriol in normal pregnancy in an Asian population.

Serial plasma oestriol levels were measured by a radioimmunoassay in 49 normal pregnancies. Plasma oestriol rose from 43 ng/ml (149.1 nmol/1) at 22 weeks to 357 ng/ml (1237.91 nmol/1) at 40 weeks. The rise was gradual etween 22 and 32 weeks and steep between 32 and 40 weeks. No significant relationship could be found between lasma oestriol and parity, maternal age, maternal height, maternal weight or fetal sex. However, a significant but low correlation was found between birth weight and plasma oestriol prior to labour and also oestriol increments from 30 weeks to delivery. The average day to day coefficient of variation of plasma oestriol in 11 patients was found to be 16.2 per cent.

Testosterone in the molar vesicle fluid and theca-lutein cyst fluid.

Testosterone was estimated by radioimmunoassay in molar vesicle fluid in 41 patients and theca‐lutein cyst fluid in three patients with hydatidiform moles. The testosterone concentration in the molar vesicle fluid ranged from 0.4 ng/ml to 28.1 ng/ml with a mean±SEM of 6.0±1.0 ng/ml while in the theca‐lutein cyst fluid, it ranged from 4.7 ng/ml to 23.5 ng/ml. Oestradiol‐17β and human chorionic gonadotrophin (HCG) were also estimated in the molar vesicle fluid. The oestradiol‐17β concentration ranged from 0.1 ng/ml to 26.2 ng/ml with a mean±SEM of 10.7±1.1 ng/ml. HCG concentration ranged from 18 000 to 150000 mIU/ml with a mean±SEM of 49 800 ± 5 000 mIU/ml. A positive correlation was found between testosterone and oestradiol‐17β (r =+0.37; P<0.01) but not between testosterone and HCG (r = 0.32; 0.1>P>0.05). Our findings suggest that molar trophoblast is the major source of testosterone.

Testosterone production with hydatidiform moles--in vitro and in vivo studies.

Fresh molar tissues obtained from seven patients were incubated in vitro with dehydroepiandrosterone and androstenedione. The testosterone concentration in molar tissue ranged from 5.4 ng/g wet weight to 43.8 ng/g wet weight. Both precursors were readily converted to testosterone indicating that 17‐hydroxysteroid dehydrogenase and 3β‐hydroxysteroid dehydrogenase are present in molar trophoblast. A 50 mg dose of dehydroepiandrosterone was infused into patients with hydatidiform mole before and after uterine evacuation. There was a testosterone peak preceding an oestrogen rise which disappeared after uterine evacuation. It is suggested that the elevated testosterone level in molar pregnancy is mainly due to the conversion of dehydroepiandrosterone in the molar trophoblast.

PLASMA LEVELS OF OESTRIOL-17β OESTRIOL AND HUMAN PLACENTAL LACTOGEN DURING BED REST

Plasma unconjugated oestradiol‐17/2, total oestriol and human placental lactogen levels were measured in twelve healthy volunteers admitted for bed rest in the last trimester of pregnancy. No significant alteration in levels was observed.

Pregnancies in Patients with Prosthetic Heart Valves: A Review and Report of 2 Further Cases

Summary: Improvement of cardiac status following prosthetic valve replacement has made this procedure an accepted method in the treatment of damaged valves. With its wider use, an increasing number of women of reproductive years will present to the obstetrician. We report 2 successful pregnancies in patients with Starr‐Edwards valve prostheses. The risk of pregnancy in such patients is reviewed in the light of reports in the literature.

PLASMA TESTOSTERONE IN MOLAR PREGNANCY: CORRELATION WITH GESTATIONAL AGE, UTERINE SIZE, THECA-LUTEIN CYST AND SERUM HCG

Plasma testosterone and serum HCG were measured by radioimmunoassay in 46 patients with intact molar pregnancy. There was no significant difference in plasma testosterone between patients with theca‐lutein cyst and those without the cyst. This suggests that ovarian contribution to the elevated testosterone in molar pregnancy is probably a minor one. No correlation was found between plasma testosterone and uterine size. However, a positive correlation (r =+O·3567, P<0·00l) was found between plasma testosterone and HCG and a rising trend in plasma testosterone was observed with increasing gestation. These results suggest that molar trophoblast is probably the major source of elevated testosterone in the maternal circulation.

Prognostic Value of Plasma Oestradiol‐17β and Human Placental Lactogen in High‐risk Pregnancies

Summary: Serial estimations of plasma oestradiol‐17(E2) and human placental lactogen (HPL) were made in 58 high‐risk pregnancies. In pregnancies complicated by marked hypertension, intrauterine growth retardation, and intra‐uterine death, plasma E2 did not reflect fetal well‐being accurately, unlike HPL which was accurate in predicting fetal outcome. In diabetic pregnancy, plasma E2 and HPL levels were similar to those found in normal pregnancy.