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Urinary E/C ratio, maternal urinary meconial index (UMI), human placental lactogen (hPL) and pregnancy specific beta-1 glycoprotein (SP1) were determined by biochemical and immunologic method. The accuracy of composite scoring method was compared with that of individual index. The results show that composite scoring method was better than the single index in predicting and diagnosis of fetal distress.

The concentration of ovine placental lactogen (oPL) in maternal plasma varies with litter size and nutritional status, making it difficult to compare these concentrations across studies. In this study, 27 Dorset and Finn-Dorset crossbred ewes with litters of known size and gestational age were used to relate concentrations of oPL in maternal plasma to placental and fetal weights. Fetal oPL concentrations also were correlated to these variables in 12 chronically catheterized singleton fetuses. The concentration of oPL in maternal plasma increased with increasing placental weight across litter sizes ranging from 1 to 3 (r = .716). When expressed per gram of placenta, oPL was greater (P less than .05) in those ewes carrying multiple fetuses. There was no correlation between maternal and fetal oPL in time-matched samples or in average values between individuals for ewes carrying singleton pregnancies. Within the singleton group, placental weight and fetal weight were well correlated (r = .761), as were the concentration of fetal plasma oPL and fetal weight (r = .699). Placental weight plus fetal oPL could explain 81% of the variation seen in fetal weight. These results imply that maternal and fetal oPL release are controlled independently and that fetal oPL affects fetal growth by a mechanism not directly related to placental size.

Early diagnosis of EP allows conservative medical and surgical therapy but also commits a proportion of patients whose EP would spontaneously resolve to therapeutic intervention. This prospective study examined the feasibility of not treating those EPs whose hCS level was low. However, three of eight subjects with EP required therapy. Thus, a single hCS alone cannot be used to identify which EPs required no therapy.

IGF-I, IGF-II, and their binding proteins (BP) were studied in sera obtained by direct puncture of umbilical cords in utero between 20 and 37 wk of gestation in 103 normal fetuses and in 16 fetuses with intrauterine growth retardation, as well as in the cord blood of 37 normal newborns of 38- to 42-wk pregnancies. In normal fetuses, IGF-I levels were approximately 50 ng/mL and IGF-II levels approximately 350 ng/mL up to the 33rd wk of pregnancy. Thereafter, both increased to reach values two to three times higher at term. Correlations were found between fetal placental lactogen levels and those of IGF-I and IGF-II, which is consistent with the hypothesis that placental lactogen is involved in the regulation of IGF synthesis in the fetus. With weight (either measured at birth or deduced from echographical data) as index of fetal size, IGF-I levels were significantly (p less than 0.001) higher in fetuses with weights above the mean for gestational age than in fetuses with weights below the mean, whereas IGF-II levels were similar in the two groups. Similarly, IGF-I (but not IGF-II) levels in fetuses with intrauterine growth retardation were significantly lower than those in normal fetuses of the same age (p less than 0.01). These findings suggest that, during the latter months of intrauterine life, IGF-I (but not IGF-II) is involved in the control of fetal size. Total fetal BP concentrations were approximately 1/3 those of adults. The fetal electrophoretic profile obtained by Western-ligand blotting bore a strong resemblance to that of subjects with growth hormone deficiency.(ABSTRACT TRUNCATED AT 250 WORDS)

Maternal plasma IGF-I and hPL concentrations were examined in 10 singleton pregnancies and in 11 twin gestations near term. hPL concentrations were higher in the twin pregnancies (14.4 +/- 2.4 micrograms/l vs 6.9 +/- 0.9 micrograms/l, P less than 0.02). In contrast, plasma IGF-I concentrations were similar in the singleton and twin pregnancies (533 +/- 45 micrograms/l vs 572 +/- 60 micrograms/l, respectively). IGF-I concentrations failed to correlate with hPL concentrations in either group separately or when all subjects were considered together. These data do not support the hypothesis that maternal IGF-I secretion is an hPL-dependent process.

Growth hormone (GH), placental lactogen (PL), prolactin (PRL), insulin-like growth factor I (IGF-I) and IGF binding protein-1 (IGFBP-1) were determined in serum by radioimmunoassays (RIAs) in 12 women during pregnancy. GH and PL were analyzed by two monoclonal antibodies (Mab 3 and Mab 1) raised against pituitary GH. Serum IGFBP-1 had reached maximum levels at midpregnancy while PRL, PL and IGF-I increased continuously during pregnancy. Mab 1, which cross-reacts with PL, measured consistently higher levels of PL in serum than a commercial PL RIA (p less than 0.01) due to interference of cross-reacting serum proteins in the Mab 1 RIA. The GH-specific Mab 3 showed decreasing GH levels in unfractionated serum throughout gestation, but detected GH-immunoreactive proteins of approximately 40-200 kD after molecular sieve chromatography of pooled serum from late pregnancy. It is suggested that the formation of GH complexes of large molecular mass account for the successive disappearance of monomeric GH during pregnancy.

Parallel to the great use of ultrasound in diagnostical purposes the interest for biological effects of ultrasound is growing every day. The present studies of the biological action of ultrasound concerned the cytogenetic investigations as well as those of animals and men. Taking into account that the extrapolation of results from animals to men is uncertain all data obtained in human population are of utmost importance. We tried to define the possible biological action of routine diagnostical ultrasound on foetoplacental unit. Women with physiological pregnancy were exposed to ultrasound during regular antenatal control-examinations in the 20th, 30th and 38th week of gestation. The follow-up concerned HPL levels in the serum 1 hour before and 1 hour after exposure to ultrasound. There was no significant difference in concentrations of the examined hormone in both blood samples.

To further deepen the understanding of growth and development of a fetal liver, we measured sizes of 108 fetal livers using ultrasound and compared them with levels of urinary estriol excretion and human placental lactogen in the sera of their mothers. The present data suggested that growth and development of a fetal liver correlated with the levels of these hormones. Measurements of the fetal liver sizes also possibly indicate the perinatal outcome.

With the object of obtaining information about the technology use employed in Danish maternity departments, a questionnaire was sent to the 58 maternity departments which existed in Denmark in May 1989. These maternity departments covered 99% of the 55,660 births in Denmark (in 1987). Deliveries at home (a total of 511) and delivers in departments with less than four deliveries annually (a total nine) were responsible for the remaining 1%. 100% of the departments returned a completed questionnaire. The following percentages are based on the deliveries included in this investigation. The review revealed that 93.5% of Danish women are delivered in departments with access to carditocographic equipment (CTG), 34% in departments where this is offered routinely to all parturient women. Sixteen departments which did not possess CTG equipment all had fewer than 400 deliveries per annum and 12 of these stated that they wished they had had CTG. Only four of the 58 maternity departments (managing 3.4% of the deliveries in 1987) never employ human placental lactogen (HPL) or oestriol (O3) analyses. The most commonly employed hormone parameter is HPL which is undertaken on appropriate indications in 51 of 54 departments and routinely in the remaining three. Scalp-pH is carried out in 13 of the Danish maternity departments. Thus 41.7% of all the parturient women have access to this analysis. However, only 20% are delivered in maternity departments where this test is employed frequently. Cord-blood-pH is employed routinely in 31.7% of the neonates. Measurement of intrauterine pressure is employed in six out of the 58 maternity departments which are responsible for 25% of Danish deliveries. It is concluded that the slightly increased employment of technology use during delivery in 1989 as compared with practice in 1984 may primarily be due to the closing of several small maternity units during the past five years. In general, the use of technologies are less intensive than in England, Germany, France and the USA.

The evaluation of hormonal adaptation of the fetoplacental unit (FPU) in pregnant women with somatic and obstetric complications has demonstrated 4 patterns of adaptation: normal, stressful, maladaptive and unstable. The distribution of FPU adaptive responses across diagnostic groups correlated with types of diseases and their duration in pregnant women. Controlled heart diseases, chronic pyelonephritis without exacerbations, mild toxemia were mostly associated with a normal FPU adaptation. Decompensated heart disease, acute episodes of chronic pyelonephritis, deteriorating toxemia, decompensated diabetes mellitus produced functional activation of FPU hormones. Pregnant women with stable hypertension in the presence of moderately severe toxemia and essential hypertension showed hormonal FPU maladaptation. Differential evaluation of FPU adaptation in pregnant women with somatic and obstetric diseases provides a guide to a range and sequence of interventions for fetal disorders.

Mature, pregnant Hereford cows (n = 17) were used to determine the effect of nutrition and body energy reserves on fetal development, concentrations of nutrients and estrogens in placental fluids, and on progesterone, estrogens and placental lactogen in maternal plasma. On d 145 of gestation, cows were assigned by breeding date to two groups and fed to achieve either a thin (TH; n = 8) or a moderate (M; n = 9) body condition score (BCS) by d 195 of gestation. Body weights, BCS, estrogens, placental lactogen and progesterone in plasma were determined weekly between d 200 and 256 of gestation. Cows were slaughtered on d 259 +/- 1 of gestation, and amnionic and allantoic fluids were sampled and analyzed for concentrations of protein, fructose and estrogens. Body weights and BCS were less (P less than .01) for TH (419 kg; 3.7) than for M (511 kg; 5.7) cows at slaughter. Uterine weights were less (P less than .07), but chorioallantoic weights were greater (P less than .07) in TH than in M cows. Cotyledonary weights were greater (P less than .05) for TH than for M cows, and total fructose in amnionic fluid was reduced (P less than .01) in TH compared with M cows. Concentrations of estradiol, estrone and placental lactogen were greater between d 240 and 256 of gestation for TH than for M cows. We conclude that nutrient intake and(or) BCS of beef cows during late gestation influence placental weight, fructose in amnionic fluid, and placental lactogen, estrone and estradiol in plasma.

Twenty pregnant women with fetal growth retardation and 20 pregnant women with appropriate for gestational age fetuses (controls) were recruited after the 28th week of gestation. Samples were collected for estimation of serum insulin and human placental lactogen (HPL) levels in the fasting state and a glucose tolerance test was carried out on all the subjects. The results showed the glucose and HPL levels to be significantly lower in the fetal growth retardation group compared to controls. There were no differences in the fasting serum insulin levels in the 2 groups. Fetal growth retardation appears to be linked with the absence of development of the physiological 'diabetogenic' state in the second half of pregnancy. This maternal hypoglycaemic state is associated with low HPL levels and not with raised maternal insulin levels as measured in the fasting state.

Purebred Ayrshire females were assigned to two groups based on the breed of fetus carried during gestation. In group 1, Limousin embryos were transferred nonsurgically into Ayrshire recipients (10 heifers and 1 cow), and in group 2, 11 Ayrshire heifers and 1 cow were inseminated artificially to Ayrshire bulls. Blood samples were collected daily from d 265 of gestation until d 15 postpartum from 5 heifers of each group. Milk yield was recorded on alternate weeks during the first 20 wk postpartum. Calf birth weight was higher (44.2 vs. 35.4 kg) and gestation was longer (297.4 vs. 280.2) in Ayrshire dams bearing Limousin fetuses than in those bearing Ayrshire fetuses. Daily milk production for the first 20 wk was lower (18.1 vs. 20.8 kg) in Ayrshire dams bearing Limousin fetuses than in those bearing Ayrshire fetuses. Prepartum decrease in progesterone concentrations and increase in estrone concentrations were faster in Ayrshire heifers bearing Limousin fetuses than in those bearing Ayrshire fetuses. Profiles of peripartum concentrations of bovine placental lactogen differed between Ayrshire carrying different families of Limousin fetuses but were similar in those carrying families of Ayrshire fetuses. The concentrations of 15-keto-13,14-dihydroprostaglandin F2 alpha were lower during the postpartum period in heifers than gave birth to Limousin calves than in those that had Ayrshire calves. In conclusion, the breed of fetus influences physiological and endocrine responses of the dam, which might have some effect on milk production of the dam.

This paper reported the serum hPL levels in 318 normal and abnormal pregnancies as determined by hPL-single radial immunodiffusion (SRID). The results indicated that serum hPL levels in the normal pregnancies increased with the advance of gestational weeks, while sustained low levels of hPL were observed in most abnormal pregnancies. Serum hPL levels varied with the severity of the pregnancy induced hypertension, fetal weight and the duration of post-term pregnancy. When the serum hPL level of the gestational woman was less than or equal to 4 mg/L, the incidence of low Apgar score was 42% (P less than 0.01). It is thought that measuring serum hPL levels is a useful index for detecting placental insufficiency and predicting fetal prognosis.

Placental lactogen (PL) was isolated from goat cotyledonary tissue by a combination of mild alkaline extraction, anion and cation exchange chromatography, chromatofocussing and molecular filtration. The product, enriched 15,000-fold from the initial extract, was homogeneous when examined by SDS-gel electrophoresis (Mr 22,500) and isoelectricfocussing indicated a pI of 8.35 with a trace contaminant of pI 8.0. When assessed by relative binding activity in radioreceptor assays (RRA), goat PL exhibited somatotropic activity equivalent to 2.2 units/mg dry weight and lactogenic activity equivalent to 28.5 units/mg. A radioimmunoassay (RIA) for goat PL is described that is highly sensitive (190 pg/tube) and has acceptable repeatability within and between assays (6 and 13%, respectively). The assay is not affected by goat pituitary extracts or partly purified goat growth hormone and prolactin. Despite the marked increase in sensitivity of the RIA over that previously available when goat PL was measured by RRA, the hormone was not detected in jugular plasma of goats before Day 44 of pregnancy; concentrations increased thereafter and highest levels were measured during the last third of pregnancy in animals bearing triplets. Measurements by RIA are in general agreement with those obtained earlier in several studies in which RRAs were used. The hormone was detected in amniotic fluid. Maternal concentrations of goat PL declined before parturition and were undetectable by 18 h post partum.

Total estrogens (TE), estradiol (E2), estriol (E3), and human placental lactogen (hPL) were determined by radioimmunoassay in the blood of 126 pregnant women during their 26th and 31st weeks of pregnancy and the results were studied in relation to maternal age and parity. Total estrogens and E2 were lowest among the youngest women (less than 20 years) and highest among women aged 20-24 years, whereas older women (25+ years) had, on the average, intermediate values. For E3 the pattern was qualitatively similar to that of TE and E2 but less striking, and no maternal age pattern was evident with respect to hPL. Within maternal age groups, TE and E2 were higher among women in the first, than among those in their second, full-term pregnancy; the difference was about seven percent for TE (P = 0.14) and about 14 percent for E2 (P = 0.05). No parity patterns were evident with respect to E3 and hPL. There were fairly strong correlations between the determinations of the same hormone in the same woman during the 26th and 31st weeks of pregnancy; Pearson correlation coefficients were 0.60 for TE, 0.78 for E2, 0.60 for E3, and 0.72 for hPL. Since the risk of breast cancer increases apparently monotonically with maternal age at birth, the present data are equivocal with respect to the hypothesis linking levels of pregnancy estrogens to risk of breast cancer in the offspring. However, the data are compatible with hypotheses linking excessive pregnancy-estrogen exposure to conditions more common among first-born individuals, including testicular cancer and cryptorchidism.

In a randomised double-blind study 568 women were given orally either 15 mmol magnesium-aspartate hydrochloride per day or aspartic acid as placebo. The outcome of pregnancy was significantly improved in the magnesium group (fewer maternal hospitalisations, reduction in preterm delivery and less frequent referral of newborn to the neonatal intensive care unit). In the 437 patients with regular intake of tablets, haematocrit, haemoglobin and calcium show a decrease up to 20 weeks of gestation (wks) and an increase during the last 8 wks, whereas magnesium stays at a low level. Oestriol and HPL are rising steadily during gestation. In all parameters, no differences were found between the magnesium and placebo group, except for a higher level of oestriol at 33 to 36 wks and a lower level above 36 wks in the magnesium group. Because of the numerous benefits throughout the pregnancy magnesium supplementation is recommended for all pregnancies.

The role of a high CRH level in normal pregnancy remains unknown. Therefore we evaluated the concentrations of CRH and the related hormones in patients with pregnancy-induced hypertension. Fourteen women with pregnancy-induced hypertension, aged 20-39, at 30-39 gestational week, were investigated. The control group consisted of 20 healthy pregnant women matched according to gestational age. Plasma CRH beta-endorphin-like immunoreactivity, cortisol, and human placental lactogen were measured by radioimmunoassay, ACTH by an immunoradiometric method. It was found that in hypertensive patients the mean CRH concentration was significantly higher (4257 +/- 840 (SEM) ng/l) than that in healthy pregnant women (1083 +/- 227 ng/l, p less than 0.001). The concentration of ACTH, however, was only slightly higher 65.0 +/- 6.0 vs 50.7 +/- 2.5 ng/l p less than 0.025, whereas the differences in beta-endorphin, cortisol and human placental lactogen were not significant. In both groups there was no correlation between the CRH level and those of the related hormones. In healthy pregnant women the CRH level closely correlated with gestational age (r = 0.76, p less than 0.001), whereas in patients with hypertension no such correlation was present (r = 0.29). We assume that the marked enhancement of plasma CRH in pregnancy-induced hypertension is probably caused by its decreased breakdown in ischemic placental tissue, but its increased synthesis in the placenta and its indirect counterregulatory hypotensive role must also be considered.

Ninety-three healthy women were investigated during normal pregnancy, and 177 blood samples were obtained at various gestational stages. In 8 of the women, serial measurements were obtained over a period of 16-34 wk from 8 to 40 wk of gestation. In 13 women, daily blood samples were obtained from day 0 to day 6 after delivery. Insulin-like growth factor I (IGF-I) and human placental lactogen (hPL) were measured by radioimmunoassays. Growth hormone (GH) was estimated by two monoclonal antibody-based radioimmunoassays insensitive to physiological concentrations of hPL: the K24 assay, which recognizes only pituitary hGH, and the 5B4 assay, which reacts with all the known pituitary as well as placental GH variants. Placental GH was distinguished from the main pituitary variant through its specific immunoreactivity pattern. Mean plasma levels of IGF-I were relatively stable until 29-30 wk gestation, then increased progressively to reach a maximum at 35-36 wk. Regardless of gestational age, individual IGF-I values exhibited a highly significant positive correlation with placental GH, reflected by 5B4 immunoreactivity, whereas the correlation between IGF-I and hPL was not statistically significant. Considering each 2-wk gestational period separately, we found a positive correlation between IGF-I and 5B4 hGH at 31-32 wk. Conversely, no evidence of correlation was found between IGF-I and hPL at any period. After delivery, IGF-I evolution exhibited a biphasic pattern, with an initial decrease to low values followed by a progressive return toward levels found in nonpregnant healthy women. These results strengthen our previous hypothesis that placental growth hormone is involved in the control mechanism of serum IGF-I levels in normal pregnant women.

It has been suggested that tobacco smoking during pregnancy reduces birth weight by lowering production rates or levels of total pregnancy estrogens. To evaluate this hypothesis, we examined total estrogen levels by radioimmunoassay in the blood of 141 pregnant women attending the maternity clinic of a major university hospital in Athens during their 26th week of pregnancy. Forty-nine of these women were regular smokers before and during their pregnancy, whereas the remaining 92 had never been regular smokers and did not smoke at all during their pregnancy. Birth weight of offspring was lower among smokers than among nonsmokers by 190.8 g, with a 90% confidence interval of 41.1 to 340.5 g, and higher among women with higher serum estrogen levels (slope b = 1.2 g per 1000 pg/ml with a 90% CI of 0.2 to 2.2 g). There was, however, only a small negative relation between tobacco smoking and serum estrogen levels; in smokers, total estrogen levels were reduced to 91% of the corresponding levels among nonsmokers.

The authors described the development of a radioimmunoassay for the determination of human placental lactogen (PL) in the blood serum of pregnant women. Methods of obtaining RIA components were developed: highly refined and stable agents of the labeled and unlabeled hormones, specific antisera and a highly effective separating agent. The test system and commercial kits were used for comparative determination of the blood PL concentration at various terms of pregnancy. Similar results were obtained. The above test system was laid in the basis of a commercial kit RIO-PL-125I (USSR).

In 311 high-risk pregnancies between 28 and 42 weeks of gestation a fetal weight estimation by ultrasound, a Doppler sonography of the umbilical artery, an analysis of estriol and HPL-levels in maternal serum and a CTG nonstress-test were performed approximately at the same time. The aim of the study was to compare the value of these methods in the diagnosis of fetal growth retardation. By variation of cut-off levels between normal and pathological range, ROC curves were created which allowed an objective comparison of methods at any cut-off level from ranges of high sensitivity to ranges of high specificity. The course of these ROC curves determine the following rank of test validity: 1. ultrasound measurement, 2. Doppler sonography, 3. HPL assay, 4. CTG nonstress-test, 5. estriol assay.

To study the potential role of GH-releasing hormone (GHRH) in maintaining circulating levels of GH during pregnancy, 302 maternal plasma samples were collected from non-fasted subjects at various stages of pregnancy and assayed for GHRH using a 'two-site' immunoradiometric assay. The GH and placental lactogen levels were also determined. In addition, maternal plasma samples taken during labour, amniotic fluid and cord blood were also assayed for these hormones. Maternal plasma GHRH levels were similar to non-pregnant levels throughout gestation despite fluctuations in GH values which were always higher than non-pregnant levels. There was no significant difference between GHRH levels in maternal plasma and cord blood although high GH levels were observed in the latter. These findings suggest that peripheral GHRH levels do not play an important role in maintaining circulating GH levels during pregnancy.

A study of the clinical course of severe pre-eclamptic toxemias shows that, in case of antihypertensive therapy, it is usually necessary to terminate the pregnancy in cases of foetal maldevelopment, in cases with foetal indication (if no intrauterine death of the foetus takes place), whereas if there is no maldevelopment it is usually a maternal indication that enforces before-term termination of pregnancy. In case of foetal maldevelopment, a drop in HPL and oestriol values was seen. This suggests that the foetal condition deteriorates under antihypertensive treatment. For the foetus, which is deficiently supplied by the placenta, pre-eclamptic toxaemia is a regulatory mechanism of circulation that enhances blood supply of the placenta, since the peripheral resistance in the placental circulation, which is free from vascular nerves, is lower than in the nerve-supplied circulation of the body, on which a hypertensive substance can act. The assumption that such a compensatory mechanism exists is supported by a number of clinical observations. This regulation, which is necessary for the development and perhaps also for the survival of the foetus, is disturbed by the antihypertensive therapy, which explains the deterioration in the condition of the foetus.

A total of 222 pregnant women had repeated hormone assays of prolactin, estriol, human chorionic gonadotrophin and placental lactogen between week 20 and delivery. The aim of this study was to investigate whether maternal serum levels of the above-mentioned hormones differed between normal and abnormal pregnancies, that is preterm, preterm small-for-date (SFD), SFD at-term and normal at-term deliveries, with special regard to fetal sex. The results of the present study indicated differences related to preterm deliveries and intrauterine growth retardation. This finding was reflected in the estriol levels when mothers of both boys and girls were included, suggesting a primary involvement of fetoplacental factors in these pathological pregnancies. However, when only mothers of girls were investigated, the development of growth retardation was mainly seen in maternal serum hPL differences, thus suggesting a placental involvement.

The concentration of human placental lactogen (HPL), in serum was measured in venous and capillary blood from 31 pregnant women. 14 women had uncomplicated pregnancies. The others had complications including preeclampsia, intrauterine growth retardation, and severe edema. The correlation between values of HPL in venous and capillary blood was high. In all cases the clinical information obtained on placental function was the same, whether HPL was measured in venous or capillary blood. The day-to-day variability was of the same order for capillary as for venous samples. It is concluded that capillary blood may well be used for measurement of HPL in pregnant women. Capillary blood could replace venous blood for measurement of HPL in the supervision of pregnancies complicated by preeclampsia or intrauterine growth retardation.

A total of 132 twin pregnancies first seen at less than 36 weeks gestation were studied prospectively to determine the epidemiological and anthropomorphic factors associated with single or dual fetal growth retardation; the clinical, biochemical and ultrasound serial measurements that are predictive of single or dual fetal growth retardation, and to design scoring systems for the prediction of fetal growth retardation. A number of factors were associated with an increased risk of fetal growth retardation, but the highest risk was present when there was an abnormality in both plasma oestriol and placental lactogen, and the biparietal diameter growth rates were divergent. Scoring systems were derived using multi-variant discriminant analysis for three clinical situations: the patient seen for the first or second time; where only clinical facilities exist and the patient was seen on three or more occasions; and where facilities exist for the biochemical tests of placental function and ultrasonic measurement of the biparietal diameters. The scoring system for the last situation had the highest predictive rate and the lowest false positive rate.

Five different products secreted by the fetoplacental unit into the maternal circulation were measured in 272 patients when they were 34 weeks pregnant. The most useful indicator of present pathology or future complications of pregnancy was a placental protein, pregnancy associated plasma protein. A which was raised in pre-eclamptic toxaemia, antepartum haemorrhage and premature labour. The highest values were recorded in pre-eclampsia before any signs of the disease were evident. Schwangerschafts protein 1 was also raised in pre-eclampsia and antepartum haemorrhage but only after the disease had presented. Placental lactogen was also raised in pre-eclampsia and its measurement may have some predictive value. Total oestriol was lowered in fetal growth retardation and the unconjugated steroid raised in pre-eclampsia and lowered in retarded fetal growth.

Authors have studied plasma human placental lactogen (HPL) an oestriol levels in 37 pregnant women affected by severe hypertensive disorders, diabetes mellitus, bad obstetric history, intrauterine growth retardation. They point out validity of associated and seriated dosages of these hormones because they are expression of foetus wellbeing and of placental function to survey high risk pregnancies.

Low implantation of the placenta may protect against the development of pregnancy-induced hypertension (PIH) and is associated with improved values in tests of placental function. PIH occurred in six of 201 (3%) consecutive patients with placenta praevia managed at the City Hospital, Nottingham, from 1 April 1973 to 30 June 1981. None of the six patients developed associated proteinuria. Of the total number of 24,549 patients delivered in the same hospital for the years 1974-1978, 3744 (15%) developed PIH. Of the patients with placenta praevia, 52% had serum levels of human placental lactogen above the 95th centile and 25% had 24-h urinary oestriol levels above the 95th centile. The birthweight distribution was not different from that of the total live births at the City Hospital, Nottingham (based on 1975-1976 deliveries).

In a study of 101 patients at term, the maternal and umbilical cord artery and vein levels of human placental lactogen (hPL) were correlated against the sex and birthweight of the fetus. No difference in hPL levels was found between cord artery and vein. The maternal hPL level correlated well with the delivered weight of the child, but no relationship could be demonstrated in the case of umbilical cord blood. Pregnancies with a female child had a higher level of hPL, which was significant only in cord samples.

Using a glucose infusion test insulin responses and insulin sensitivities were studied in 15 gestational diabetic women at 36-40 weeks gestation. In all women intravenous glucose tolerance had returned to normal at six weeks postpartum. Twelve women had a repeat glucose infusion test done 7-24 weeks (mean 17 weeks) postpartum. The results were compared with previously evaluated normal non-pregnant and normal pregnant standards and insulin responses below the normal 15th percentile were defined as "low". Twelve women had "low insulin responses in late pregnancy, and six had "low" insulin responses postpartum. The mean insulin sensitivity index of 1.34 +/- 1.21 (mean +/- SD) was significantly higher in the gestational diabetic group during pregnancy compared with a control pregnant group at 0.53 +/- 0.21 (p less than 0.01). The findings in this study support the hypothesis that gestational diabetes may arise in women who are unable to achieve adequate insulinogenic compensation to pregnancy. Increased insulin sensitivity in gestational diabetes may be a compensatory mechanism.

It has been suggested that perinatal asphyxia is not generally followed by neurological impairment unless there is preexisting chronic fetal distress. In cases of brain damage one can observe elevated levels of CK-BB. The purpose of our study was to evaluate CK isoenzymes in umbilical cord blood sera of newborns affected by chronic fetal distress. Fetal distress reflected by placental dysfunction was characterized by a diminished HPL level and decreased activity of CAP. We estimated CK isoenzymes with the use of DEAE-sepharose CL-6B column chromatography. Total CK activity was measured using kits supplied by Boehringer-Mannheim (Monotest CK-NAC aktiviert). The clinical state of examined newborns was estimated. Investigations were carried out in the group of 57 infants delivered after 37 weeks of gestation. Total CK activity in cord sera ranged from 40 to 400 U/l. Our results showed a significant rise of CK-BB activity in cord sera of newborns delivered from pregnancies with placental dysfunction (figure 2) as well as in cases of asphyxiated infants (figure 3). We were unable to demonstrate differences in total CK, CK-MM and CK-MB activities in all examined groups of newborns. Other authors have confirmed that severe asphyxia results in increase in CK-BB activity in cord blood. Infants with ominous fetal heart rate patterns have higher CK-BB activity. There are several possible sources for CK-BB activity in umbilical cord blood sera, i.e. fetal brain, lung, gastrointestinal tract, placenta and uterus. It appears that the brain is most likely the source of elevated CK-BB activity found in cord blood in cases of placental dysfunction.

The diagnostic utility of serum and urinary human chorionic gonadotropin (hCG) measurements and serum measurements of pregnancy-specific beta 1-glycoprotein (PSBG), placental lactogen, and cystine aminopeptidase (CAP) was prospectively studied in 51 consecutive patients with suspected ectopic pregnancy who underwent laparoscopy or laparotomy. CAP was not detected in the sera of any patient with ectopic pregnancy. False-positive results in each assay were found in patients with intrauterine pregnancy or missed abortion. The overall efficiency of the tests were: urine hCG slide test, 47%; urine hCG tube test, 80%; serum hCG, 86%; serum PSBG, 82%; and human placental lactogen, 60%. Although measurement of serum hCG by radioimmunoassay is the most accurate biochemical test in predicting the correct diagnosis in patients with suspected ectopic pregnancy, the relatively high efficiency of the urinary hCG tube test, coupled with its ease of performance, low cost, and rapid turnaround time, makes it the most practical screening test.

Six women in the 3rd trimester of normal pregnancy had measurements of circulating placental lactogen (hPL) levels using a continuous blood sampling technique for 10-15 h. In addition, in 3 pregnant women hPL was assayed at 10-min intervals for 60-90 min. Both these procedures showed that hPL serum levels fluctuate irregularly during normal pregnancy. The magnitude and frequency of these fluctuations make the significance of a single hPL determination less reliable as a test of placental function.

The relation between serial HPL assays in serum and placental weight-for-dates was studied in 70 randomly chosen pregnant women. Out of five different aspects of the HPL curve only a fall below the 2-3d centile without subsequent recovery was related to low placental weight. When a small-for-dates (SFD) placenta was associated with normal HPL levels, maternal body weight tended to be lower than if both placental weight and HPL levels were abnormal. This suggests that physiologically small placentae are discernible from pathologically small placentae by a normal HPL curve.

Prenatal treatment consisting of daytime bedrest, high protein diet and oral administration of allylestrenol was assessed in a prospective study of 30 patients with IUGR infants whose ultrasonically estimated body weight was less than the 10th percentile. In these pregnancies, the gestational age was confirmed in the first trimester, and the fetal weight was estimated from the BPD and AC measurements in the third trimester (Fig. 1). Following treatment, ultrasonic and biochemical determinations were performed. As results: The estimated fetal weight of 1,362 g at 32.9 g gestational weeks increased to 2,678 g at 39.2 weeks on average. The average weekly weight gain was significantly higher than the standard, and 16 cases (53.3%) were more than 10th percentile at birth (Tab. I, Fig. 2). A significant correlation (r = 0.94) between the estimated fetal weight and the birth weight was found. Following prenatal treatments, maternal plasma and urinary estriol, plasma HPL and progesterone increased significantly (Tab. II).

The influence of plasma free fatty acid (FFA) concentration on the secretion of human placental lactogen (hPL) was investigated in 16 normal young women during the last month of gestation, in order to determine whether hPL secretion is influenced in the same way as human growth hormone (hGH) during plasma FFA elevation. Maternal blood glucose (BG), plasma triglycerides (TG), FFA, immunoreactive insulin (IRI) and hPL levels were measured during and after a lipid emulsion infusion for 75 min (10 cases). The intravenous injection of 5,000 U of heparin at the 15th min of the lipid infusion was followed by a decrease in plasma triglyceride levels and by an accompanying rise in plasma FFA (rom 468 plus or minus 52 to 2,478 plus or minus 310 mueq/liter). In control experiments lipid infusion alone (3 cases) resulted in a moderate increase in FFA (718 plus or minus 157 to 1,046 plus or minus 255 mueq/liter), and separate iv heparin administration (3 cases) elevated the FFA levels from 728 plus or minus 50 to 1,649 plus or minus 153 mueq/liter). No significant change in either IRI or hPL levels was discernible in any of the tests performed. A tendency of blood glucose to increase was observed after heparin administration. It was concluded that a marked and sustained plasma FFA elevation, achieved through intravenous lipid and heparin infusion cannot alter hPL circulating levels in term human pregnancy.

The possible involvement of growth hormone (GH) and human placental lactogen (HPL) in the development of diabetic tissue damage during pregnancy was studied in 16 insulin-dependent diabetic patients (IDDM), 8 gestational diabetic patients (GD) and 14 normal pregnant women. GH and HPL were elevated in pregnancies complicated by diabetes but, in contrast to the rise of HPL, GH declined throughout pregnancy in all the groups studied. The concentrations of neither correlated with plasma glucose, insulin requirement or duration of diabetes. HPL was positively correlated with urinary albumin excretion (UAE) in all 3 groups, but with blood pressure only in the IDDM group. There was also a significant and positive correlation in all patients between HPL at the end of pregnancy and placental weight. No evidence of serious tissue damage was found in either diabetic group. The vibration sensory threshold was unaffected by pregnancy and was similar to that of normal women. However, in the IDDM group UAE increased significantly postpartum when compared with second trimester values; they also had higher UAE than the other 2 groups post-delivery. A small but significant rise in diastolic blood pressure (DBP) was found in the 3 groups studied between the second and third trimester and pre-delivery. The same trend in systolic blood pressure (SBP) was seen in the diabetic groups. The IDDM had higher systolic and diastolic blood pressures than the normal women at all stages of gestation.

Plasma levels of progesterone, 17 alpha-OH progesterone, hPL and beta-subunit hCG were measured in a group of women for 24 h after therapeutic abortion. Progesterone, hCG and hPL levels fell more rapidly than 17 alpha-OH progesterone levels. This might suggest that the main site of synthesis of 17 alpha-OH progesterone is probably in the corpus luteum of pregnancy or that the prolonged half-life of hCG maintains the corpus luteum to secrete longer. Human placental lactogen fell dramatically within 4 h but the hCG level was maintained. This difference probably reflects only the differences in half-lives of these hormones.

Because of increasing evidence for the heterogeneity of polypeptide hormones, studies of the molecular species of human placental lactogen (hPL) were initiated. When extracts of freshly delivered human placentas were passed over Sephadex G-100 in 0.05M ammonium carbonate, three immunoreactive peaks were detected. In addition to a peak corresponding to native hPL (Kav = 0.39) and one in the void volume, a consistent peak which eluted before hPL (Kav = 0.20) was present. The latter represented 2-25% of total hormonal activity and could be rerun without significant conversion to hPL. In 8M urea, the peak continued to behave as a large molecular weight form on both Sephadex chromatography and on polyacrylamide disc gel electrophoresis. Extraction procedures at both neutral and alkaline pH produced similar quantities of the larger material. [125I]iodo-hPL was not converted to the larger form by the conditions of extraction or analysis. These properties are consistent with a larger molecular weight, non-aggregated form of hPL. In comparison with the native hormone, the idsplacement curves for the larger form were parallel in radioimmunoassay studies. Sera obtained from pregnant women during various stages of gestation also showed consistent evidence for a large molecular weight form of the hormone. These observations provide direct evidence, both in placental tissue and in serum for "big" hPL.

Nine pregnant women with Rh isoimmunization who delivered newborns with hydrops fetalis were studied. The placental proteins, pregnancy specific beta 1-glycoprotein (SP1), human placental lactogen, and placental protein 5 (PP5) were measured in maternal serum by radioimmunoassays. The results indicate that both the serum human placental lactogen and PP5 levels were significantly higher than those observed in normal pregnancy. The strikingly higher circulating PP5 levels found in all nine patients with Rh isoimmunization studied suggests that serum PP5 may be specifically elevated in pregnant patients with Rh isoimmunization and hydrops fetalis.

Serial estimations were made in plasma of 17beta-oestradiol (E2), progesterone and human placental lactogen (HPL) in 43 patients and of human chorionic gonadotrophin (HCG) in 34 patients during mid-trimester abortions induced with intra-amniotic prostaglandin F2alpha (PGF2alpha. Mean plasma concentrations of all the hormones showed a progressive fall after PGF2alpha. There was no relationship between the fall in levels of progesterone, HPL and HCG and the induction-abortion interval, signs of fetal distress or of intrauterine fetal death. Both the control level and the rate of fall of E2 were related to the induction-abortion interval and a rapid decline preceded intrauterine fetal death. The relationships of the progesterone/E2 ratio and the amniotic fluid volume/progesterone ratio to the induction-abortion interval were examined. The variation in the time at which significant falls in the concentration of individual hormones occurred was probably related to their respective half-lives in plasma.