Maternal and paternal alcohol consumption and miscarriage

Summary. To explore the role of parental alcohol consumption in miscarriage we interviewed 80 women who miscarried about their own and their partners' drinking habits. A control group of 81 gestational-age-matched women whose pregnancy ended in the delivery of a healthy infant at term were similarly questioned. The use of alcohol by women and men was equally frequent in both groups. Before pregnancy, the mean alcohol consumption per week had been about 1–2 drinks for the women and 4–5 drinks for the men. During the presumed day of conception, 13% of the women who miscarried and 11% of the women in the control group had drunk on average 3–4 drinks; the other women had been abstinent at this time. Of the partners, 13% and 15%, respectively, had taken a mean of 4–5 drinks. In both groups 58% of the subjects continued to consume alcohol during pregnancy. The mean consumption was about one drink a week by the women who miscarried and half a drink a week in the control group. Of women who miscarried, 36 had a blighted ovum and in this subgroup alcohol consumption in both women and men was similar to that in the other women who miscarried and their partners, suggesting that alcohol is not causally related to the development of a blighted ovum. These results suggest that moderate maternal or paternal alcohol consumption does not increase the risk of miscarriage.     

MATERNAL SERUM PROLACTIN AND ITS RESPONSE TO TRH IN NORMAL AND COMPLICATED EARLY PREGNANCY

Maternal serum prolactin levels (PRL) were measured by radioimmunoassay in thirty-four women with either normal or complicated early pregnancy. The basal PRL level (mean +/- S.D.) of 33.4 +/- 16.4 ng/ml in normal pregnancy (n = 15) was similar to the level of 32.7 +/- 18.8 ng/ml in threatened abortion (n = 11) and 32.8 +/- 16.9 ng/ml in hyperemesis gravidarum (n = 8). Two patients, one with blighted ovum and the other with subsequent spontaneous abortion, demonstrated PRL levels lower than the range of 20-63 ng/ml in the control group. The PRL response to 200 microgram of synthetic thyrotropin releasing hormone (TRH) administered intravenously was similar throughout the patient groups. The basal level of PRL in the whole series was more closely related to the level of serum oestradiol (r = 0.778, P less than 0.001) than to that of serum progesterone (r = 0.442, P less than 0.05). However the increments of PRL following TRH administration did not correlate with either oestradiol or progesterone.     

Labetalol does not alter the placental and fetal blood flow or maternal prostanoids in pre-eclampsia

Summary. The effect of intravenously administered labetalol (1 mg/kg) on placental and fetal blood flow was studied in 13 pre-eclamptic women. Although the maternal blood pressure decreased, no changes occurred in the blood flows in the intervillous space, the umbilical vein or the fetal descending aorta, nor did the indices of peripheral vascular resistance in the fetal aorta change, but the placental vascular resistance did decrease. Labetalol had no effect on prostacyclin or thromboxane A₂ as measured by urinary 6-keto-prostaglandin F_1α and serum thromboxane B₂ respectively. These findings are clinically relevant since they suggest that labetalol reduces maternal blood pressure without interfering with the placental or fetal blood flow.     

Vaginal and abdominal delivery increases maternal urinary 6-keto-prostaglandin F1α excretion

Summary. To study the role of the antiaggregatory and vasodilatory prostacyclin (PGI₂) during human delivery, serial urine samples collected from 13 women delivered vaginally and from eight delivered abdominally were assayed for 6-keto-prostaglandin F_1α (6-keto-PGF_1α a breakdown product of PGI₂) by high-performance-liquid-chromatography and radioimmunoassay. In women delivered vaginally the mean urinary 6-keto-PGF_1α concentration was 41.9 (SE 8.3) ng/mmol creatinine, before the onset of labour and increased progressively to a maximum of 186.5 (SE 47.6) ng/mmol creatinine 2 h after delivery irrespective of the use of oxytocin and epidural analgesia. In women delivered by caesarean section under epidural anaesthesia, the urinary 6-keto-PGF_1α rose from 33.4 (SE 4.2) ng/mmol creatinine to 2153 (SE 314) ng/mmol creatinine 2 h after section. In both groups the increased levels had fallen by 24 h postpartum to levels below those found before delivery. In neonatal urine 6-keto-PGF_1α concentrations were some 12–30 times higher than those in postpartum urine. Thus, vaginal and abdominal delivery is accompanied by significant increases in maternal PGI₂ release, perhaps in the myometrium and/or intrauterine tissues. This may be of significance in the regulation of fetoplacental blood flow and in the prevention of intra- and postpartum thrombosis.     

Amniotic fluid prostaglandins do not reflect human fetal lung maturation

Summary. Experimental data suggest the involvement of classic prostaglandins (PG), prostacyclin (PGI,) and thromboxane A₂ (Tx A₂ ) in fetal pulmonary development. To explore this possibility in man, we assayed serial amniotic fluid samples from 33 women for 13, 14 -dihydro-15-keto-PGF_2α (M-PGF_2α a metabolite of PGF_2α), 6-keto-PGF_1α (a breakdown product of prostacyclin (PGI₂)), and thromboxane B₂ (a metabolite of TxA₂) as well as for the lecithin/sphingomyelin (L/S) ratio and phosphatidylglycerol. No difference in these prostanoids was seen between the samples with the immature (< 2) or mature 2) L/S ratio, or between the samples with undetectable or detectable phosphatidylglycerol. The L/S ratio matured in 16 women and phosphatidylglycerol became detectable in 19 women during serial smpling, but even in these women the changes in the amniotic fluid prostanoids were inconsistent. It is concluded that the amniotic fluid M-PGF_2α, 6-keto-PGF_1α, and TxB₂ do not reflect fetal pulmonary maturity.     

EFFECTS OF ORAL AND INTRAVENOUS TRH AND METOCLOPRAMIDE ON PRL AND TSH SECRETION IN WOMEN

Pituitary secretion of PRL and TSH is under the control of inhibitory dopaminergic and stimulatory TRH-mediated mechanisms. To evaluate the relationships between these regulatory systems, ten healthy women were treated with oral TRH (20 mg twice daily), a dopamine blocking drug, metoclopramide (MC) (10 mg t.d.s.) or placebo for 1 week (from 8th to 14th cycle day). Serum concentrations of PRL, TSH, T3 and T4 were determined before, at the end, and 3 days after the treatments. In addition, PRL and TSH responses to i.v. TRH (200 μg) or MC (10 mg) were studied at the end of the oral treatments. Oral TRH treatment was accompanied by increases in basal T3 and T4 concentrations, no change in PRL, and a decrease in TSH 3 days after the end of treatment. Oral TRH did not modify the PRL response to i.v. MC while it eliminated the TSH response to i.v. MC, possibly because of elevated concentrations of thyroid hormones. Oral MC treatment raised the concentrations of PRL, T3 and T4, and also potentiated the PRL response to i.v. TRH, whereas the TSH response remained unaltered. These results demonstrate that dopaminergic and TRH-mediated mechanisms are related in the control of PRL and TSH secretions, perhaps directly or through thyroid hormones.     

Haemostatic Parameters in Cushing's Syndrome

ABSTRACT. Ikkala E, MyllylÄ G, Pelkonen R, Rasi V, Viinikka L, Ylikorkala O. (Finnish Red Cross Blood Transfusion Service and Helsinki University Central Hospital, Helsinki, Finland.) Haemostatic parameters in Cushing's syndrome. We have studied haemostatic parameters in 12 patients with Cushing's syndrome. Three patients had prolonged bleeding times, and in all seven patients whose bleeding times were measured 3–6 months after surgical treatment the postoperative bleeding times were shorter (mean 7.5 min) than the pretreatment times (mean 12.3 min). In ADP- or adrenaline-induced aggregation the second wave was lacking in six and the degree of aggregation was borderline or subnormal in five patients. One patient had, in addition, a severe defect in collagen-induced aggregation. However, thromboxane B₂ production of the platelets from both endogenous and exogenous arachidonic acid was unaffected. Factor VIII:C, RAg and Rcof activities were all elevated, and in patients with severe disease F VIIIR:Ag and F VIII:Rcof activities were markedly more elevated than F VIII:C activity. The changes in both primary haemostasis and in factor VIII activities correlated clearly with the clinical severity of the disease.     

Causes of stillbirth: a clinicopathological study of 243 patients

Summary. The clinical and autopsy findings in all stillbirths during the years 1974—1979 at the Helsinki University Central Hospital were analysed. There were 243 stillborn infants of whom 200 died before labour. According to the autopsy findings asphyxia accounted for 38% and major malformations for 17% of the deaths, but because of fetal maceration no diagnosis could be made at autopsy in 43%. The cause of death suggested by the clinical findings was placental failure in 57%, cord complication in 12% and major malformations in 17%. The cause of death remained unsolved in 9%. The importance of routine ultrasound and a- fetoprotein screening for the detection of unrecognized risk patients is emphasized.