J. Haapalahti

Maternal adrenocorticotrophic hormone and cortisol during labour and vaginal delivery.

Plasma concentrations of ACTH (by radioimmunoassay) and cortisol (by competitive protein binding) were measured in eight healthy parturients during labour and vaginal delivery. The concentration of both ACTH and cortisol increased during labour; the maximum values were recorded immediately prior to delivery. The changes correlated well with the degree of cervical dilatation. Both the mean (±SEM) ACTH (275.3±39.5 pg./ml.) and cortisol (2.33±0.49 μmol./l.) recorded before delivery were significantly elevated compared with the initial values (ACTH: 89.3±39.5 pg./ml.; cortisol: 0.86±0.20 μmol./l.).

Effects of ritodrine and isoxsuprine with and without dexamethasone during late pregnancy.

beta-Adrenergic agents are used to inhibit preterm labor and glucocorticoids to accelerate fetal pulmonary maturation. A study was designed to investigate the metabolic effects of intravenous infusion of ritodrine (150 to 100 microgram/min) or isoxsuprine (200 to 150 microgram/min) in a series of 28 patients with gestations of 28 to 40 weeks, with and without concomitant dexamethasone therapy. Ritodrine was more potent than isoxsuprine in increasing the circulating levels of cyclic AMP, glucose, insulin, and triglycerides. The diabetogenic effect of both ritodrine and isoxsuprine was so slight that it did not have any clinical significance in women with normal glucose tolerance. The results were similar when these beta-adrenergic tocolytics were given to women concomitantly with intramuscular dexamethasone therapy, although dexamethasone appeared to minimally impair carbohydrate metabolism. Both ritodrine and isoxsuprine caused a significant fall in serum iron and potassium, and this effect was unaltered by dexamethasone. Serial serum potassium levels should be obtained during long-term infusion of beta-mimetics.

ACTH levels in amniotic fluid during pregnancy.

The fetal pituitary‐adrenal axis plays an important role in the regulation of fetal development. In order to obtain information about fetal ACTH secretion at different gestational ages, a total of 109 amniotic fluid ACTH determinations was performed by ra.dioimmunoassay. There was a significantly higher level of ACTH during 26 to 30 weeks of pregnancy (429 ±180–4 pg/ml) than in early (208–7±90–6 pg/ml) and in late (172–7±97–4 pg/ml) pregnancy; fetal sex, uterine contractions and maternal complications in pregnancy did not affect levels. The ACTH level in the first urine of six newborn infants (160‐Oib40‐6 pg/ml) approximated to that in the amniotic fluid in late pregnancy. Our results support the assumption of a fetal origin for ACTH in amniotic fluid. The high secretion of ACTH at the beginning of the last trimester of pregnancy may stimulate the development of the adrenal cortex and result in the increased cortisol secretion necessary for fetal lung maturation.

THE FUNCTION OF THE ANTERIOR PITUITARY‐ADRENAL CORTEX AXIS IN HYPEREMESIS GRAVIDARUM

In order to study the function of the pituitary‐adrenal axis, serum ACTH and cortisol levels were estimated before and after insulin induced hypoglycaemia in nine women with hyperemesis gravidarum, seven women in normal early pregnancy and in eight non‐pregnant controls. Before hypoglycaemia, the basal ACTH level in the hyperemesis group (102.4±62.9 pg/ml) was higher than in normal early pregnancy (67.5±19.2 pg/ml; p<0.05) or in non‐pregnant controls (54.8±25.2 pg/ml; p<0.01). Correspondingly, the mean cortisol value in hyperemesis (0.47±0.16 μmol/1) was higher than in normal early pregnancy (0.39±0.10 μmol/1; p>0.05) or in non‐pregnant controls (0.32±0.13 μmol/1; p<0.01). After insulin the elevation of ACTH (p>0.05) and cortisol (p<0.01) was observed in every group. The level of ACTH and cortisol was highest in hyperemesis group. Our results do not support the idea that hypofunction of the pituitary‐adrenal axis contributes to the aetiology or pathogenesis of hyperemesis gravidarum. The high ACTH level might be evidence of the psychic instability of hyperemesis gravidarum patients.

Follicle stimulating hormone, thyrotrophin, human growth hormone and prolactin in hyperemesis gravidarum.

To investigate the functional capacity of the anterior pituitary gland in hyperemesis gravidarum, the serum levels of follicle stimulating hormone (FSH), thyrotrophin (TSH), human growth hormone (HGH) and prolactin were measured before and after the combined administration of gonadotrophin and thyrotrophin releasing hormones (GnRH, TRH), and insulin in seven normal pregnancies, nine with hyperemesis and eight nonpregnant subjects. There was no difference between normal pregnancy and hyperemesis for FSH and TSH, but the basal level of HGH was lower and that of prolactin higher in hyperemesis although their responses following stimulation were similar. Thus there seems to be no hypofunction of the anterior pituitary gland in hyperemesis gravidarum.

THE PLACENTAL AND FETAL RESPONSE TO THE INTRA‐AMNIOTIC INJECTION OF PROSTAGLANDIN F2α IN MIDTRIMESTER ABORTIONS

The placental and fetal response to the intra‐amniotic injection of prostaglandin F2α (PGF2α) for midtrimester abortions was evaluated. Maternal blood samples for radioimmunological determinations of serum progesterone, human placental lactogen (HPL) and alpha‐fetoprotein (AFP) were taken before and serially until 24 hours after the injection of 40 mg (nine patients) or 75 mg (seven patients) of PGF2α. Fetal heart action was monitored ultrasonically during the same period. The average induction‐abortion interval was 22.6 hours and was independent of the dose of PGF2α used. The mean progesterone and HPL levels showed a significant fall half an hour after PGF2α. The constant decreases began only at 5 hours and later. The mean AFP levels increased rapidly after 5 hours following injection of PGF2α. The fetal heart stopped at a mean of 10.4 hours (range 0.5 to 25 hours) after the injection of PGF2α. No relationship between the time of fetal death or rises in AFP and the induction‐abortion interval could be detected. The primary hormonal response of the placenta and the efficacy of exogenous PGF2α were not related, indicating the possibility that the abortifacient property of PGF2α is not related to its primary effect on placental hormone synthesis or release.

The effect of labour on ACTH and cortisol levels in amniotic fluid and maternal blood.

Levels of adrenocorticotrophic hormone (ACTH) and cortisol were measured in amniotic fluid during labour and in maternal blood during and after labour. There was a significant rise of maternal ACTH and cortisol levels during labour and a significant decrease after delivery in all 14 patients studied. There were no significant changes in amniotic fluid ACTH and cortisol levels during labour. The initial level of ACTH in amniotic fluid (162·7 pg/ml) was higher than that in maternal circulation (120·2 pg/ml). The correlation between maternal and amniotic fluid ACTH was not significant while the corresponding correlation for cortisol values was.

The effect of oral thyrotropin-releasing hormone on thyroid function and the composition of breast milk in puerperal women.

To determine the effect of oral administration of thyrotropin‐releasing hormone (TRH) on the thyroid function and on the composition of breast milk in the early puerperium, six lactating women were treated with a single dose of 40 mg of synthetic TRH and six women were treated with placebo. Serial serum samples taken before and between one and 25 hours after TRH administration were assayed with specific radioimmunoassays for thyrotropin (TSH), triiodothyronine (T3) and total thyroxine (T4). Milk samples were collected three times a day and their major fatty acids were determined by gas‐liquid chromatography and were compared with those obtained from normal lactating women. A statistically significant TSH elevation was observed between one and six hours after TRH administration, with a peak value of 23.7 ± 10.6 mU/liter at three hours. The T3 concentration rose between three and nine hours after TRH administration, with a peak of 6.3 ± 1.2 nmole/liter at six hours. The T4 elevation was statistically significant between six and 12 hours after TRH administration. The fatty acid content of milk samples from women treated with TRH did not differ from the normal series. A single daily dose of oral TRH thus caused a temporary thyroid stimulation. It is doubtful whether this could lead to hyperthyroidism since the levels of thyroid hormones became normal within ten hours after TRH administration.