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Bowel abnormalities in the fetus--correlation of prenatal ultrasonographic findings with outcome.

OBJECTIVE: Our purpose was to correlate ultrasonographic findings with postnatal outcome in cases of fetal bowel pathologic disorders detected by either prenatal evaluation or diagnosed in the neonatal period. STUDY DESIGN: A total of 16,471 consecutive fetuses were scanned in the midtrimester or later. Fetuses were included in the study group if the prenatal ultrasonographic evaluation suggested gastrointestinal pathologic features or if gastrointestinal pathologic features were identified by postnatal evaluation. Prenatal ultrasonographic findings and postnatal outcome were collected by chart review. Prenatal ultrasonographic findings were compared with outcome. Results were compared by Fisher's exact test. Sensitivity and positive predictive values were determined. RESULTS: Of the 16,471 fetuses scanned, 15,090 (91.6%) had complete postnatal follow-up. Eighty-nine fetuses had a bowel lesion suspected by prenatal ultrasonography. Twenty-two had dilated bowel distal to the duodenum, 33 had isolated hyperechoic bowel, 20 had ascites, and 14 had a cystic abdominal mass. Twenty-two fetuses (22/89 or 25%) were found at neonatal evaluation to have a gastrointestinal lesion. In those fetuses with small-bowel lesions, the sensitivity of ultrasonography was 100% and the positive predictive value was 72.7%. For large-bowel lesions the sensitivity of ultrasonography was only 7.7%, and the positive predictive value was 18%. No ultrasonographic parameter could unequivocally differentiate between the normal and abnormal outcome groups, but progressive bowel dilatation in the third trimester and hyperperistalsis with a dilated bowel loop were frequently found in the cases of small bowel obstruction. Four of the cases of dilated bowel (18.2%) were related to cystic fibrosis. CONCLUSION: Bowel abnormalities in the fetus are manifest in diverse ultrasonographic findings, making accurate prediction of lesions difficult. The sensitivity of prenatal ultrasonography to detect large-bowel lesions was poor, although it was 100% sensitive in the detection of small-bowel lesions. Cystic fibrosis should be considered in all fetuses with bowel abnormalities suspected on prenatal ultrasonography.

Ascites↗

Sonographic identification of second-trimester fetuses with Down's syndrome.

Fetuses with Down's syndrome are more likely than normal fetuses to have a thickened nuchal skin fold and relatively short femurs on ultrasound examination in the second trimester. We evaluated these measures in more than 5500 fetuses, including 28 who were later found to have Down's syndrome by means of amniocentesis with cytogenetic analysis. Normal femur length was established as a function of biparietal diameter in 192 of the normal fetuses. We found that with use of a nuchal skin-fold thickness of 6 mm or more and a ratio of actual to expected femur length of 0.91 or less, fetuses with Down's syndrome could be identified with a sensitivity of 75 percent and a specificity of 98 percent. When other anomalies, such as an atrioventricular canal and meconium peritonitis, were added to these two criteria, the sensitivity of sonographic detection of Down's syndrome in the second-trimester fetus rose to 82 percent. The potential predictive value of these sonographic signs far exceeds that of advanced maternal age and low alpha-fetoprotein levels, which currently identify only 10 to 30 percent of affected fetuses. We recommend that fetuses with a thickened nuchal skin fold or shortened femurs on ultrasound examination be evaluated for Down's syndrome by amniocentesis and cytogenetic analysis.

Amniocentesis↗

Impairment of growth in fetuses destined to deliver preterm.

OBJECTIVE: The objective of this study was to test the hypothesis that fetuses destined to deliver preterm do not reach their individual growth potential. STUDY DESIGN: In a case control design, data on 44 preterm deliveries at < or =34 weeks were compared with data on a control group of next consecutive term deliveries. Criteria for inclusion were dating by ultrasonography at <20 weeks and no medical or obstetric complications. For each fetus, GROW v.2 software was used to generate an individual optimal growth curve and to calculate the percentile of achieved growth potential for birth weight based on 6 independent factors (maternal weight, height, parity, ethnicity, fetal sex, and gestational age) identified as determining fetal weight from multivariate logistic regression analysis of 40,000 uncomplicated term pregnancies. Birth weight percentiles based on standard norms were also calculated for each fetus. RESULTS: The number of fetuses with birth weight below the 5th, 10th, and 25th percentile of their growth potential was significantly higher in the preterm group (10, 13, and 18) compared with that in the control group (2, 2, and 6; P <.008, P <.001, and P <.008, respectively). There were no significant differences in variables defining growth potential between the case and control groups. The number of fetuses below the 5th and 10th percentile based on standard birth weight norms was not significantly different between preterm and term pregnancies (3 vs 1 and 5 vs 2; P =.37 and P =.27). Among preterm deliveries, those preceded by preterm premature rupture of the membranes had significantly fewer fetuses >75th percentile of their growth potential (2 vs 8; P =.025). Fetuses with lower gestational ages at preterm delivery achieved lower median percentiles of their growth potential. CONCLUSION: A significant proportion of fetuses destined to deliver preterm do not reach their individual growth potential compared with those delivered at term. This finding challenges our concept of preterm delivery and management strategy aimed at tocolysis.

Birth Weight↗

Instability and frequency-domain variability of heart rates in fetuses with or without growth restriction affected by severe preeclampsia.

This study investigated how the instability and frequency-domain variability in heart rates differ between fetuses affected only by severe preeclampsia and fetuses affected by both severe preeclampsia and growth restriction. From their antepartum fetal heart rates and those of control fetuses, the very short-term intermittency (C1alpha) and the spectral powers were calculated to evaluate the instability and frequency-domain variability, respectively. The fetuses affected only by severe preeclampsia showed abnormally high C1alpha and low- and high-frequency power. The fetuses affected by severe preeclampsia and growth restriction showed even higher C1alpha than that of the fetuses affected by severe preeclampsia and abnormally reduced low-frequency power. Conclusively, when compared to the heart rates of fetuses affected only by severe preeclampsia, the heart rates of fetuses affected by severe preeclampsia and growth restriction showed a greater abnormal instability and an abnormally reduced variability at low-frequency range.

Adult↗

Heteroplasmy in bovine fetuses produced by intra- and inter-subspecific somatic cell nuclear transfer: neutral segregation of nuclear donor mitochondrial DNA in various tissues and evidence for recipient cow mitochondria in fetal blood.

Varying degrees of mitochondrial DNA (mtDNA) heteroplasmy have been observed in nuclear transfer embryos, fetuses, and offspring, but the mechanisms leading to this condition are unknown. We have generated a clone of 12 bovine somatic cell nuclear transfer fetuses, using nuclear donor cells, recipient oocytes, and recipient heifers with defined mtDNA genotypes, to study nuclear-mitochondrial interactions and the origins of mtDNA heteroplasmy. Embryos were reconstructed from granulosa cells with Bos taurus mtDNA type A and recipient oocytes collected from three different maternal lineages with B. taurus mtDNA type B, B. taurus mtDNA type C, or B. indicus mtDNA. Sequence differences in the control region (CR) of B. taurus mtDNAs ranged from 6 to 11 nucleotides and differences between B. taurus and B. indicus CRs from 45 to 50 nucleotides. Fetuses were recovered from recipient heifers with B. taurus mtDNA type B on Day 80 after nuclear transfer (eight B. taurus A/B, two B. taurus A/C, and two B. taurus A/B. indicus). Agarose gel analysis of the CR by polymerase chain reaction-based restriction fragment length polymorphism failed to detect nuclear donor mtDNA in 11 investigated tissues of 10 viable fetuses and in DNA samples of two fetuses in resorption (one B. taurus A/B and one B. taurus A/C). A more sensitive analysis of 1801 plasmid clones with CR inserts derived from tissues of a B. taurus A/B. indicus fetus detected no or very low levels of heteroplasmy (0.5-0.7%). However, the analyses detected considerable amounts ( approximately 2.5% and 5%) of recipient heifer mtDNA in blood samples from two fetuses. Our data do not suggest a replicative advantage of somatic nuclear donor cell mtDNA in bovine transmitochondrial clones produced with oocytes from domestic forms of the same or a different aurochs (B. primigenius) subspecies. Detection of mtDNA from the recipient animal in the circulation of two fetuses points to leakage of the placental barrier, mimicking heteroplasmy.

Animals↗

Humeral shortening in second-trimester fetuses with Down syndrome.

Individuals with Down syndrome have abnormally short long bones. Sonography has previously revealed slightly shortened femurs and thickened nuchal folds in affected second-trimester fetuses. Humeral and femoral lengths and nuchal folds were evaluated in 400 normal second-trimester controls and in 24 consecutive Down syndrome fetuses (14-20 weeks) undergoing amniocentesis for advanced maternal age or low maternal serum alpha-fetoprotein (MSAFP). Using the 400 normal control fetuses undergoing amniocentesis, the relationship between humeral length and biparietal diameter (BPD) was: Expected humeral length = -7.9404 + 0.8492 x BPD. A ratio of measured-to-expected humeral length of less than 0.90 identified 12 of 24 fetuses (50%) with Down syndrome and 25 of 400 normals (6.25%). Twelve of the 24 Down syndrome fetuses had a nuchal fold measuring 6 mm or larger. Combining nuchal fold findings with these humeral length criteria identified 18 of 24 affected fetuses (75%) without appreciable change in specificity, yielding a positive predictive value of 4.6% for women with a risk of one in 250 (age 35) of having a Down syndrome fetus. For women with risks of one in 500 and one in 1000 of having an affected fetus based on maternal age, a shortened humerus or thickened nuchal fold yielded positive predictive values of 2.3 and 1.2%, respectively.

Adult↗

Natural history of fetuses with cleft lip.

The prospect of fetal surgery for cleft lip is predicated on our ability to accurately identify fetuses with clefts and exclude those that have associated anomalies. Prenatal ultrasound is currently the most appropriate means with which to do this. We reviewed the ultrasonographic data from two large perinatal referral institutions to determine the natural history of fetuses with cleft lip who may be candidates for fetal surgery. Forty fetuses had a cleft lip diagnosed prenatally by ultrasound. In this group, severe associated anomalies were common (30 of the 40) and multiple (23 of the 40) in a majority of fetuses. Life-threatening anomalies, such as central nervous system and cardiac anomalies, were the most common defects. As a result, many fetuses were aborted therapeutically or died in the perinatal period. Out of 12 surviving fetuses, only six had isolated clefts, and two surviving fetuses, diagnosed with isolated cleft lip, had no defect identified postnatally. This information has important implications for the perinatal management of fetuses with cleft lip and the potential role of fetal intervention.

Abnormalities, Multiple↗

Prenatal testing to predict the severity of hemolytic disease of the fetus and newborn.

The severity of hemolytic disease of the fetus or newborn can be assessed with certainty only by measurement of fetal parameters. However, these invasive procedures are not without risk for the fetus. Most erythrocyte antibodies do not cause significant hemolytic disease of the fetus or newborn and various assays are available to assist obstetricians in predicting the likely effect of maternal alloantibodies on fetal erythrocytes. Initially, immunohematologic tests are performed on maternal serum to identify antibodies with a potential for causing hemolytic disease of the fetus or newborn. Antibody concentration is measured by indirect antiglobulin technique titration, or where possible (for anti-D or -c), by quantitation. When used consecutively throughout pregnancy, these tests will reveal a trend that helps to predict the likelihood of hemolytic disease of the fetus or newborn. Functional assays (antibody-dependent cell-mediated cytotoxicity and chemiluminescence) are probably superior to serologic tests for predicting hemolytic disease of the fetus or newborn. Unfortunately, the assays do not reflect accurately the in vivo conditions for a given patient. Knowledge of the immunoglobulin subclass can help to assess the hemolytic potential of maternal antibody, but quantitative measurement of subclasses is still experimental. Diagnostic testing should be approached in a structured manner, commencing with simple serology, followed, in selected cases, by more complex functional assays and indirect fetal tests to identify those fetuses at greatest risk. This approach will enable direct fetal tests to be undertaken only when there is strong suspicion of severe hemolytic disease of the fetus or newborn.

Erythroblastosis, Fetal↗

Variation in neuropathogenicity in sheep fetuses transplacentally infected with non-cytopathogenic and cytopathogenic biotypes of bovine-virus diarrhoea virus.

Pregnant Merino ewes were inoculated intravenously between days 63 and 65 of gestation with a non-cytopathogenic (ncp) bovine-virus diarrhoea-virus (BVDV) isolate (experiment A). The histomorphological findings and the distribution of viral antigen, as revealed by immunohistochemistry in brains of fetuses from experiment A, were compared with those seen in fetal brains from a previous study (experiment B), in which pregnant ewes had been intravenously infected between days 65 and 68 of gestation with the cytopathogenic (cp) BVDV strain Indiana. The two viruses showed remarkable variations concerning their pathogenicity for the developing fetal brain. The cp BVDV had a much higher neuropathogenic potential than the ncp BVDV and induced severe intracranial malformations in most fetuses. In experiment A, exclusively relatively mild leucoencephalomalacic lesions occurred. Between fetuses of the two experiments, significant differences concerning the distribution of viral antigen and the inflammatory response were found. In the majority of fetal brains from experiment B examined at days 10, 14 and 21 post inoculation (p.i.), antigen-containing differentiated brain cells (neurons, astrocytes, oligodendrocytes) and undifferentiated cells in the periventricular germinal zones were seen throughout the different zones of the developing telencephalon and cerebellum. At 21 days p.i., a marked inflammatory response consisting of brain macrophages and other mononuclear cells occurred in the meninges and in the brain parenchyma of fetuses from experiment B. In brain sections of fetuses infected with ncp BVDV, in contrast to fetuses infected with cp BVDV, viral antigen was not detectable during the early stages (days 10 and 20) p.i., and histopathological lesions were not seen at this stage. At days 41 and 47 p.i., antigen-positive astrocytes and oligodendrocytes were found in the developing white matter of the telencephalon and cerebellum. Furthermore, antigen-containing neurons were seen in the developing cerebral cortex. Cellular infiltrations in fetal brains from experiment A were limited to the leucoencephalomalacic areas in the developing cerebral and cerebellar white matter and consisted exclusively of brain macrophages. Immunohistochemical staining in brain sections of fetuses from both experiments revealed that numerous perivascular cells contained viral antigen, whilst positive endothelial cells were exclusively found in fetuses from experiment A. From the findings of this study it was concluded that the cp BVDV stain used in experiment B has a marked tropism for the fetal brain and both its already differentiated and undifferentiated cell populations, and that the resulting brain lesions primarily are the consequence of a direct cytolysis of these cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Midpregnancy plasma zinc in normal and growth retarded fetuses--a preliminary study.

OBJECTIVE: To determine plasma zinc concentrations in normally and abnormally growing fetuses. DESIGN: Prospective observational study. SETTING: Fetal Medicine Unit, Queen Charlotte's Maternity Hospital. SUBJECTS: 53 pregnant women attending for fetal blood sampling at between 18 and 40 weeks gestation. 27 fetuses were normal (central group), 11 fetuses were growth retarded and 15 were malformed. MAIN OUTCOME MEASURES: Plasma zinc concentrations in maternal and fetal blood at time of fetal blood sampling. RESULTS: In normally growing fetuses, between 18 and 40 weeks gestation, there was no fall in maternal plasma zinc concentration; the fetal level fell by 36%. In 10 fetuses with symmetrical growth retardation, plasma zinc concentration tended to be low, but was not significantly different from that in the normal control fetuses. CONCLUSION: The results suggest that (i) placental transfer of zinc is an uphill secretory process and that it is a rate-limiting step in the accumulation of zinc by the fetus and (ii) in fetuses with symmetrical intrauterine growth retardation, a low plasma zinc is probably a parallel phenomenon and not necessarily an aetiological factor.

Female↗

The nutritional regulation of plasma prostaglandin E concentrations in the fetus and pregnant ewe during late gestation.

1. The effects of nutrient availability on the plasma concentrations of prostaglandin E (PGE) were investigated in chronically catheterized ewes and their fetuses during late gestation by varying dietary intake and by experimental manipulation of the fetal plasma concentration of glucose. The aim of the study was to determine whether varying the glucose level altered the fetal and maternal concentrations of plasma PGE. 2. Basal plasma concentrations of PGE increased with increasing gestational age in both the fetus and ewe. Fetal plasma concentrations of PGE were positively correlated with the corresponding uterine venous concentrations throughout the period of study. There was also a significant venous--arterial difference in plasma PGE concentration across the uterus at all gestational ages studied. 3. Withdrawal of food but not water for 48 h increased the plasma PGE concentration in all the fetuses studied irrespective of gestational age. In the pregnant ewe, the effects of fasting depended on gestational age. Before 130 days, fasting only increased the uterine venous concentration of plasma PGE, while after 130 days there were significant increases in both maternal arterial and uterine venous concentrations of plasma PGE. There was also a significant widening of the uterine venous--arterial difference in plasma PGE concentration during fasts begun after 130 days of gestation. Refeeding the fasted animals restored the plasma PGE levels to normal values within 24 h in both the fetus and ewe. 4. The normal daily feeding regime had no apparent effect on plasma PGE concentrations before 130 days of gestation. However, in animals nearer to term, there were significant reductions in plasma PGE in the fetus and uterine vein in the 3-6 h period after feeding. 5. The changes in plasma PGE levels during fasting and in response to the normal daily feeding regime were correlated to the changes in plasma glucose level observed in the fetus. The slope of the line relating the changes in the fetal concentrations of plasma PGE and glucose was significantly steeper in animals older than 130 days than earlier in gestation. 6. Fetal hypoglycaemia induced by fetal infusion of insulin increased fetal concentrations of plasma PGE without any apparent change in maternal plasma PGE values. In contrast, fetal hyperglycaemia produced by infusion of glucose into the fetus had little effect on plasma PGE levels in utero. 7. The results demonstrate that nutrient availability can influence uterine output and plasma concentrations of PGE in the fetus and pregnant ewe.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Neutron scattered dose equivalent to a fetus from proton radiotherapy of the mother.

Scattered neutron dose equivalent to a representative point for a fetus is evaluated in an anthropomorphic phantom of the mother undergoing proton radiotherapy. The effect on scattered neutron dose equivalent to the fetus of changing the incident proton beam energy, aperture size, beam location, and air gap between the beam delivery snout and skin was studied for both a small field snout and a large field snout. Measurements of the fetus scattered neutron dose equivalent were made by placing a neutron bubble detector 10 cm below the umbilicus of an anthropomorphic Rando phantom enhanced by a wax bolus to simulate a second trimester pregnancy. The neutron dose equivalent in milliSieverts (mSv) per proton treatment Gray increased with incident proton energy and decreased with aperture size, distance of the fetus representative point from the field edge, and increasing air gap. Neutron dose equivalent to the fetus varied from 0.025 to 0.450 mSv per proton Gray for the small field snout and from 0.097 to 0.871 mSv per proton Gray for the large field snout. There is likely to be no excess risk to the fetus of severe mental retardation for a typical proton treatment of 80 Gray to the mother since the scattered neutron dose to the fetus of 69.7 mSv is well below the lower confidence limit for the threshold of 300 mGy observed for the occurrence of severe mental retardation in prenatally exposed Japanese atomic bomb survivors. However, based on the linear no threshold hypothesis, and this same typical treatment for the mother, the excess risk to the fetus of radiation induced cancer death in the first 10 years of life is 17.4 per 10,000 children.

Female↗

Thickened nuchal fold in fetuses not at risk for aneuploidy.

Many studies have shown that a thickened nuchal fold in a second-trimester fetus is a sonographic sign suggestive of a high risk for Down syndrome. These series have included fetuses already at risk for aneuploidy because of advanced maternal age or abnormal maternal serum alpha-fetoprotein (AFP) levels. The authors describe the sonographic and karyotypic findings in 42 women younger than age 35 years whose fetuses were noted to have a thickened nuchal fold. Forty fetuses were not at risk for Down syndrome. Fourteen of the 42 fetuses (33%) had abnormal karyotypes; 11 had Down syndrome and one each had XXX, XO, and XYY. If the five cases with low maternal serum AFP levels are excluded, nine of the 37 fetuses (24%) with thickened nuchal folds had abnormal karyotypes. Amniocentesis would have been performed in one of those nine fetuses because of hydrocephalus. Thus, eight of 36 fetuses (22%) with thickened nuchal folds and no other indications for amniocentesis had abnormal karyotypes. When a thickened nuchal fold is present, the yield of abnormal karyotype is high (22%), making it possible to identify patients who would benefit from cytogenetic evaluation but who would not otherwise be candidates.

Adult↗

Insulinlike growth factor 1 in controls and growth-retarded fetuses.

OBJECTIVES: To establish a reference range of insulinlike growth factor 1 (IGF-1) values in normal fetuses and to assess whether intrauterine growth retardation is associated with increased or decreased IGF-1 levels. METHODS: Retrospective analysis of blood samples collected from 64 fetuses who underwent blood sampling at 18-38 weeks' gestation was performed: 40 fetuses, who were considered controls, were appropriately grown for gestational age and were found unaffected by the condition for which they were tested; the remainder (n = 24) underwent fetal blood sampling to assess fetal karyotype and acid-base balance following ultrasonic diagnosis of intrauterine growth retardation. (In this group, 8 survived, and 16 died during the perinatal period). IGF-1 was measured using a radioimmunoassay after acid-ethanol extraction in order to avoid interference by the binding proteins. All samples from controls and growth-retarded fetuses were measured using the same batch, and the intra-assay coefficient of variation of the test ranged from 4.1 to 6.1%. RESULTS: In control fetuses, IGF-1 serum levels increased linearly with gestational age. In growth-retarded fetuses, IGF-1 levels were not significantly different from the reference range (median Z-score -0.3; range -4.4 to 291) and did not correlate with fetal size, hematocrit, and acid-base balance values. There was a significant difference in IGF-1 and pH values when the fetuses were divided into two groups based on the perinatal outcome: those who survived had values of IGF-1 mostly within the normal range, whereas the fetuses who died in utero or postnatally had significantly decreased pH and elevated IGF-1 values (median Z-score 2.1; 95% confidence interval 0.4-13.9; p = 0.04). CONCLUSIONS: This study confirms previous observations that IGF-1 levels parallel the increase in fetal size which occurs with advancing gestation. Increased levels of IGF-1 may indicate a terminal process in the fetal adaptation to placental failure.

Case-Control Studies↗

Development of semitendinosus muscle in pig fetuses with spinal cord lesions.

The effect of upper motor neuron regulation on the development of the semitendinosus muscle was studied in the fetus. A region of the fetal spinal cord at the level of the upper cervical vertebrae was destroyed by cauterization at 45 days of gestation. Fetuses with intact spinal cords served as controls. One cauterized fetus and one control fetus were obtained from each of six crossbred sows at 110 days of gestation. From each fetus one semitendinosus muscle was removed for histochemistry and the contralateral muscle was removed, weighed and utilized for biochemical analyses. Body weights and muscle weights were not significantly different (p greater than 0.05) between the two groups. Transverse sections (cryostat) of muscle were stained for lipid and the following enzymes: acid ATPase, NADH-TR, and esterase. Lipid and enzyme cytochemistry showed that sections from cauterized and control fetuses had identical fiber type patterns. Motor endplates, as studied with esterase reactions, were not affected by spinal cord cauterization. Mean values for percentage of muscle dry weight, DNA, RNA, protein, glycogen content and minimum fiber diameters were similar for cauterized and control fetuses (p greater than 0.05). These data illustrate that in the porcine fetus the central nervous system proximal to the alpha-motoneuron exerts little control over muscle cell development.

Adenosine Triphosphatases↗

The clinical value of umbilical artery Doppler velocimetry in the management of intrauterine growth-retarded fetuses before 32 weeks' gestation.

The objective of this study was to investigate the clinical utility of umbilical artery Doppler velocimetry in the management of very premature growth-retarded fetuses. The study comprised 34 fetuses between 26 and 34 weeks' gestation, diagnosed ultrasonically as suffering from intrauterine growth retardation. Based on the umbilical artery Doppler findings, patients were divided into 3 groups: group 1 (10 fetuses) with normal Doppler systolic/diastolic (S/D) ratios (within 2 SD of the mean for gestational age); group 2 (9 fetuses) with significant abnormal umbilical artery S/D ratios (above 2 SD of the mean for gestational age), and group 3 (15 fetuses) with absent or reverse end-diastolic flow. Fetal outcome was assessed in terms of neonatal mortality and morbidity, i.e. low umbilical artery pH (pH < 7.20) and Apgar scores. In group 1, all fetuses had a stable, normal S/D ratio; in group 2, 2 fetuses (22%) showed deterioration in the Doppler findings and were transferred to group 3, while in group 3, 3 of 15 fetuses (20%) showed improvement in the absence of end-diastolic flow and were thus transferred to group 2. Emergency cesarean section due to antenatal deterioration of the biophysical profile occurred in only 1 patient (10%) in group 1, compared to 33 and 87% in groups 2 and 3, respectively (p < 0.05). The other 9 patients in group 1 had normal vaginal deliveries at 36-37 weeks' gestation, with no perinatal complications. The mean expectant interval from admission to delivery in group 3 was 8.2 days, while in groups 1 and 2 it was 23.8 and 22.2, respectively (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Clearance of calcium across in situ perfused placentas of intrauterine growth-retarded rat fetuses.

Maternofetal clearance of 45Ca and 51Cr-EDTA (diffusional marker) were simultaneously measured across in situ perfused placentas of intrauterine growth-retarded (IUGR) and control rat fetuses on d 20 of gestation. IUGR was induced by uterine artery and vein ligation on d 17 of gestation. Control fetuses and their placentas were taken from sham-operated dams. We hypothesized that calcium transfer would be impaired across placentas of IUGR fetuses. The mean body wt of IUGR fetuses was 42% lower, and the mean nose-anus length was 16% lower than those of control fetuses. The mean total calcium content of IUGR fetuses was significantly lower than that of control fetuses, but not when it was normalized to body wt. The mean maternal whole blood ionized calcium concentration was not significantly different in the two groups. The materno-fetal clearance of 45Ca across IUGR placentas was significantly lower than that across control placentas (IUGR = 35.2 +/- 1.9 micro L/min/g placenta, mean +/- SEM; control = 93.1 +/- 12 microliters/min/g placenta, p less than 0.002). In contrast, the maternofetal clearance of 51Cr-EDTA, the reference diffusional marker, was not significantly different across IUGR and control placentas. We conclude that maternofetal transfer of calcium is reduced across placentas of IUGR rat fetuses.

Animals↗

Serum insulin-like growth factors and insulin-like growth factor binding proteins in the human fetus. Relationships with growth in normal subjects and in subjects with intrauterine growth retardation.

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)

Body Constitution↗