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PubMedDate not supplied

Assessment of risk for chromosomal abnormalities at 10-14 weeks of gestation by nuchal translucency and maternal age in 5,210 fetuses at a single centre.

OBJECTIVE: To evaluate the screening of chromosomal abnormalities by nuchal translucency (NT) measurement. METHODS: Assessment of risk for chromosomal abnormalities by NT and maternal age in 5,210 single fetuses with karyotype and outcome already known. RESULTS: Risk was > or =1 in 300 in 640 (12.2%) of all fetuses, in 575 (11.1%) of the normal fetuses, in 38 (80.8%) of the fetuses affected by trisomy 21, and in 65 (89%) of the fetuses affected by chromosomal abnormalities. Risk was > or =1 in 200 in 477 (9.1%) of all fetuses, in 418 (8.1%) of the normal fetuses, in 35 (74.4%) of the fetuses affected by trisomy 21, and in 59 (80.8%) of the fetuses affected by chromosomal abnormalities. Risk was > or =1 in 100 in 270 (5.1%) of all fetuses, in 216 (4.2%) of the normal fetuses, in 33 (70.2%) of the fetuses affected by trisomy 21, and in 54 (73.9%) of the fetuses affected by chromosomal abnormalities. CONCLUSIONS: Risk generated by NT and maternal age is effective in screening for chromosomal abnormalities.

Adult↗
PubMed1993

Elevated levels of umbilical cord plasma corticotropin-releasing hormone in growth-retarded fetuses.

CRH is synthesized in the hypothalamus and released in response to stress into the portal hypophyseal blood; an additional site of synthesis, the placenta, is present only during pregnancy. Placental CRH is released into the maternal and fetal circulation during human pregnancy, and we hypothesized that the chronic fetal stress associated with fetal growth retardation may stimulate placental CRH release. We measured plasma CRH concentrations in the umbilical cord blood of 28 growth-retarded fetuses and 28 normally grown fetuses matched for gestational age and mode of delivery. Plasma ACTH, dehydroepiandrosterone sulfate (DHEAS), and cortisol were also measured in the umbilical cord samples to determine if CRH levels were correlated with levels of pituitary and adrenal hormones. The mean umbilical cord plasma CRH level in the growth-retarded fetuses was 206 +/- 25.8 pmol/L, which was significantly higher than that in the normally grown fetuses matched for gestational age, presence or absence of labor, and mode of delivery (49.4 +/- 16.7 pmol/L; P < 0.01). The mean plasma ACTH level in the growth-retarded fetuses (5.7 +/- 1.2 pmol/L) was significantly higher than that in the normally grown fetuses (3.3 +/- 0.7 pmol/L; P < 0.05). The mean cortisol concentration in the growth-retarded fetuses was 260 +/- 32.5 nmol/L, and that in the normally grown fetuses was 220 +/- 40 nmol/L. The mean DHEAS level was significantly lower in the growth-retarded fetuses (4.8 +/- 0.6 mumol/L) than that in the normally grown fetuses (7.7 +/- 0.6 mumol/L; P < 0.001). There was a significant correlation between umbilical cord plasma CRH and both ACTH and cortisol concentrations as well as a significant negative correlation between CRH and DHEAS levels in the growth-retarded fetuses. The umbilical cord plasma CRH level is extremely elevated in growth-retarded fetuses compared to that in normal fetuses. Placental CRH, like hypothalamic CRH, may be stimulated in conditions of chronic stress and may modulate fetal pituitary-adrenal function in high risk pregnancies.

Adrenocorticotropic Hormone↗
PubMed1991

Glucose gradients of maternal vein-umbilical vein and umbilical vein-umbilical artery in normally grown and growth-retarded fetuses.

The present study was designed to investigate the roles of maternal-fetal glucose transport and fetal glucose utilization in the regulation of fetal growth. Maternal venous blood, umbilical arterial and venous blood were sampled simultaneously in 60 full-term appropriate-for gestational age (AGA) fetuses and 48 small-for-gestational-age (SGA) fetuses. The cases were divided into four groups: group 1 consisted of 35 AGA fetuses, group 2 consisted of 25 AGA fetuses, group 3 consisted of 25 SGA fetuses, and group 4 consisted of 22 SGA fetuses. The mothers of group 1 and 3 were given 2.5% glucose in 0.9% normal saline and those of groups 2 and 4 by cesarean section received normal saline or Ringer's lactate at least one hour prior to delivery of the fetus SGA fetuses were found to have hypoglycaemia of umbilical venous blood, increased (maternal vein-umbilical vein) MV-UV and decreased UV-UA (umbilical vein-umbilical artery) glucose gradients, all of which disappeared after maternal glucose supplementation. However, hypoinsulinemia and lower insulin/glucose ratio in SGA fetuses persisted either with or without maternal parenteral glucose infusion. Increased MV-UV and decreased UV-UA glucose gradients suggests placental dysfunction and poor glucose utilization in SGA fetuses. The lower fetal insulin/glucose ratio may imply pancreatic dysfunction in SGA fetuses, which did not respond to glucose challenge from the maternal side. It seems that in SGA fetuses, placental dysfunction interferes with maternal-fetal transfer with resulting fetal hypoglycemia; on the other hand, pancreatic dysfunction leads to poor glucose utilization and retarded intrauterine growth. However, the mechanism that primarily accounts for pancreatic dysfunction in these fetuses remains to be resolved.

Blood Glucose↗
PubMed1988

Effect of stage of gestation, litter size and uterine space on the incidence of mummified fetuses in pigs.

Factors associated with incidence of mummified fetuses at 7, 9, 11, 13 and 15 wk of gestation were determined in a cross-sectional design involving 209 pregnant pigs. Percentage of observed mummies increased from 2.1 to 12.2% as gestation progressed. Incidence of mummies at 7 wk of gestation was not different between litters of nine fetuses or fewer and those of 10 fetuses or more. During the period of 7 to 15 wk of gestation, the incidence of mummies remained constant at about 1% in litters of nine fetuses or fewer, whereas in litters of 10 fetuses or more the incidence increased linearly from 1 to 12% (P less than .01). In litters of nine fetuses or fewer, a mummy occupied no less space than a live fetus until 13 wk of gestation. In litters of 10 fetuses or more, a mummy occupied less space than did a live fetus after 7 wk of gestation. An increase in the incidence of mummies in larger litters was associated with uterine space per fetus below that needed for development and survival. The 12% fetal loss in late gestation was associated with less uterine space per fetus. Length of uterine horns, litter size and stage of gestation together accounted for 12% of the variation in incidence of mummies (P less than .001). A longer uterus had greater space per fetus, a larger number of live fetuses and a lower incidence of mummies.

Animals↗
PubMed2006

[Role of ST-analysis of fetal ECG in intrapartal fetus monitoring with presumed growth retardation].

OBJECTIVE: Evaluation of the role of ST analysis of fetus ECG for early detection of developing acute hypoxia in the course of delivery of fetuses with presumed growth retardation. A comparison with present way of intrapartal fetus monitoring. Impact on the number of surgical births for indications of threatening fetus hypoxia. Influence of the method on perinatal results and postnatal adaptation of the newborns. TYPE OF STUDY: A prospective study. SETTING: Gynecology-Obstetrics Clinic, Masaryk University and Teaching Hospital Brno. METHOD: Forty seven women with a growth retardation of the fetus diagnosed before delivery who gave birth in the Teaching Hospital in Brno during 2003-2005 and intrapartal ST analysis of fetus ECG was subsequently used, were enrolled into this prospective study (group A). The control group consisted of 87 deliveries taking place in the same period of time and concerning women with fetuses suffering from growth retardation and monitored by standard methods (group B). The standard methods included cardiotocography (CTG), supplemented with pulse oximetry (IFPO) if needed. The diagnosis of intrauterine fetus growth retardation was established on the basis of the results of repeated prepartal ultrasound fetus biometry with estimation of the mass, which corresponded to a group below 10 percentile for the given gestational age. The numbers of vaginal deliveries and surgically treated delivery due to threatening fetus hypoxia (Cesarean section, forceps delivery) were recorded. The authors evaluated postpartal pH from umbilical artery, independently for the group of values of pH < 7.00, the group of pH 7.00-0.10 and pH 7.10 or more. The values of Apgar score were evaluated for the first, fifth and tenth minute, respectively. The neonatologist followed the duration of stay of the newborn at the Newborn Intensive Care Unit, the Intermediate Care Unit, total duration of hospitalization, the occurrence of sepsis in the early newbotn period, the occurrence of hyperbilirubinemia, and the conclusion of neurological examination. All the results were evaluated statistically by the chi2 test, Kruskal-Wallis test or the Anova method. RESULTS: There was no statistically significantly difference in the number of delivery ended by surgery for threatening fetus hypoxia (p = 0.856) or the detection rate of intrapartal hypoxia according to pH values of umbilical blood divided into the three groups (p = 0.657, p = 0.958, p = 0.730, respectively). The values of Apgar score differed in favor of the group A significantly only in the first minute at the level of 5% opf significance (p = 0.018). The values of Apgar score in the fifth and tenth minute did not show any significant difference (P = 0301 and p = 0313, respectively). There was no statistically significant difference in neonatological results between the group A and B. CONCLUSION: The use of ST analysis of fetal ECG in the course of delivery of fetuses with presumed intrauterine growth retardation did not show any significant difference from the presently used methods (CTG supplemented with IFPO if needed). In using the method there was not any effect on the number of surgically treated deliveries for indications of threatening acute fetus hypoxia or perinatal results and postnatal adaptation of the newborns.

Cardiotocography↗
PubMed1984

Teratogenic effects of dosage levels and time of administration of carbamazepine, sodium valproate, and diphenylhydantoin on craniofacial development in the CD-1 mouse fetus.

The objective of this investigation was to study the teratogenic effects of dosage levels and time of administration of three anticonvulsant drugs (carbamazepine [CMZ], sodium valproate [NaV], and diphenylhydantoin [DPH]) on craniofacial development in the CD-1 mouse fetus. Pregnant females were intubated on each of days 8-10, 11-13, 14-16, and 8-16 of gestation with the following dose levels for each drug: 375, 563, 938 mg/kg CMZ; 225, 338, 563 mg/kg NaV; 50, 75, 125 mg/kg DPH. Appropriate control groups were maintained for each drug. On gestation day 17, pregnant females were killed and implantation sites were recorded as live, dead, or resorbed. All live fetuses were examined for craniofacial defects. Results of examination of 1,398 fetuses indicated that CMZ, NaV, and DPH were teratogenic and embryotoxic at all dose levels. This study indicated that the observed decrease in mean fetal weight was drug-, dose-, and time-dependent. There was a drug-, dose-, and time-dependent increase observed in the number of dead fetuses, whereas the number of resorbed fetuses was observed to be only time-dependent. The observed frequencies of hydrocephalies, secondary palatal clefts, and submucous palatal clefts were significant for all three factors (drug, dose, and time) whereas the observed frequencies of hematomas and exencephalies were significant only for drug and time. Cleft lips were observed only in the highest dose level of DPH. Uterine horn distribution of defects indicated that fetuses located at the proximal end of the horns were less subject to major defects than those fetuses located at the distal end of the uterine horns. Fetuses with craniofacial hematomas were found in the proximal one-third of the uterine horn, resorbed fetuses, and fetuses with submucous palatal clefts in the middle one-third of the uterine horns and dead fetuses and fetuses with exencephalies, cleft lips, and secondary palatal clefts were localized in the distal one-third of the uterine horns. In comparing the effect of drug, dosage, and time on the development of craniofacial malformations in the CD-1 mouse fetus, CMZ was the least teratogenic and embryotoxic of the three anticonvulsant drugs employed in this study.

Abnormalities, Drug-Induced↗
PubMed1992

Characterisation of dystrophin in fetuses at risk for Duchenne muscular dystrophy.

Dystrophin, the product of the Duchenne muscular dystrophy (DMD) gene, was studied in muscle from 16 human fetuses at risk for the disease. Eleven high risk (greater than 95% probability) and 5 low-risk (less than 25% probability) fetuses were studied with antibodies raised to different regions of the protein. All low-risk fetuses showed a similar pattern to that of normal fetuses of a comparable age: using Western blot analysis, a protein was detected of similar size and abundance to that of normal fetuses (i.e. smaller molecular weight than that of adult muscle); immunocytochemistry showed uniform sarcolemmal staining in fetuses older than 18 weeks gestation and differential staining of myotubes at different stages of development (distinguished by size) in younger fetuses (less than 15 weeks gestation). In contrast, Western blot analysis of high-risk fetuses detected low levels of dystrophin in 4 cases; 7 fetuses had no detectable protein. Immunocytochemistry with some dystrophin antibodies showed weak staining of the sarcolemma and around central nuclei in younger fetuses; in older fetuses there was little sarcolemmal staining with any antibody other than occasional positive fibres. These results indicate that careful study of dystrophin in fetuses at risk for DMD can be used to establish the clinical phenotype and provide additional information for future family counselling.

Blotting, Western↗
PubMed2003

Phenotypic and molecular characterization of bovine Campylobacter fetus strains isolated in Brazil.

The objective of the present study was to characterize the phenotypic and molecular aspects of Campylobacter fetus strains isolated from bovine herds with reproductive problems. Thirty-one Brazilian field isolates, together with one reference strain of each subspecies of C. fetus, were analyzed. The strains were submitted to phenotypic identification followed by subspecies characterization using the polymerase chain reaction (PCR) and numeric evaluation of restriction fragment length polymorphism (RFLP) separated by pulsed-field gel electrophoresis (PFGE). Phenotypically, 4 isolates (12.1%) were classified as C. fetus subsp. fetus, and 29 isolates (87.9%) were classified as C. fetus subsp. venerealis. However, according to molecular analysis, only 1 isolate (3.0%) was classified as C. fetus subsp. fetus (the reference strain), whereas 32 isolates (97.0%) were considered C. fetus subsp. venerealis. SalI digestion of C. fetus genomic DNA, obtained from the 33 strains, yielded 7-10 DNA fragments ranging in size from 40 to 373kb, with 12 distinct patterns. Furthermore, the numeric analysis by neighbor-joining of the DNA from the 33 strains resulted in a dendrogram in which 2 distinct groups were identified. It was concluded that phenotypic characterization of C. fetus subspecies might lead to erroneous classification of field isolates. Although RFLP-PFGE is a powerful and reliable technique to characterize C. fetus, it has the inconvenience of being time consuming and laborious. Whereas PCR, besides providing rapid results, was found to be reliable and convenient for the characterization of field isolates of C. fetus.

Animals↗
PubMed1997

Can twin fetuses be numerically clustered characterizing fetal cardiovascular system function?

To clarify whether twin fetuses could be clustered quantitatively observing in utero cardiovascular system function, 71 twin-paired fetuses between 24 and 40 weeks' gestation were subjected. Cluster analysis was performed using four variables; end-diastolic dimension and fractional shortening in the right ventricle (EDD, FS), resistance index in the umbilical artery (RIUA) and urine production rate (UPR). Three different groups were revealed. In Cluster 1 (C1), larger fetuses showed a significant increase in both EDD and UPR, and a significant decrease in FS, while smaller fetuses had a significant increase in RIUA and a decrease in UPR. In Cluster 2 (C2), smaller fetuses showed a significant increase in RIUA. Cluster 3 (C3) showed no significant deviations in any variable when referring to singleton pregnancies. C1 had a higher perinatal mortality rate than either C2 or C3, with the cause of death being cardiac failure in larger fetuses and renal failure in smaller fetuses. The frequencies of discordancy, hemoglobin difference above 5 g/dl and monochorionic placenta in C1 were also higher than fetuses in C3. C2 also showed higher frequencies of discordancy and small-for-gestational age than C3 fetuses. In C2 and C3, respiratory insufficiency was found to be the cause of neonatal death. The results revealed that C1 consists of twins with both larger and smaller fetuses displaying cardiac failure with an increase in renal perfusion and a decrease in renal and placental perfusion, respectively, and C2 consists of twins with smaller fetuses having both placental insufficiency and intrauterine growth retardation. C3 consists of twins with both lager and smaller fetuses having normal circulation, when compared to singleton pregnancy.

Birth Weight↗
PubMed2002

Ultrasound evaluation of aortic valve anatomy in the fetus.

OBJECTIVE: To assess the feasibility of ultrasound identification of aortic valve anatomy in the fetus, with particular emphasis on the detection of bicuspid aortic valve. METHODS: This study was a prospective analysis of 21 fetuses with prenatally diagnosed congenital left heart obstructive lesions and 45 normal fetuses undergoing routine ultrasound evaluated at a tertiary referral center. These fetuses underwent detailed echocardiography, including the study of the aortic valve on a targeted short-axis view of the right ventricle. Necropsies or postnatal echocardiograms were available for confirmation of the diagnosis in all cases. RESULTS: Aortic cusps and commissures were satisfactorily visualized in 38/45 (84%) normal fetuses and in 18/21 (86%) fetuses with congenital heart disease. The aortic valve was correctly defined as bicuspid in one normal fetus and in six fetuses with congenital heart disease. In two fetuses with a positive family history, the bicuspid aortic valve was isolated. There was one incorrect diagnosis (a unicuspid unicommissural valve diagnosed prenatally as a bicuspid aortic valve in a fetus with severe aortic stenosis) and one false-positive diagnosis in a fetus diagnosed with a coarctation and a bicuspid aortic valve late in the third trimester of pregnancy and in which both anomalies were not confirmed at neonatal echocardiography. CONCLUSIONS: This study demonstrated that aortic valve anatomy can be satisfactorily assessed in fetuses with and without left heart obstructive lesions. We believe that a detailed search for a bicuspid aortic valve should be attempted in all patients referred for a positive family history of congenital heart disease, in general, and of left ventricle outflow tract obstruction or bicuspid aortic valve, in particular. In fact, the presence of an asymptomatic bicuspid aortic valve has been demonstrated to represent an important factor predisposing to the development of bacterial endocarditis and dissecting aortic aneurysm late in adult life. Therefore, an early detection of such an anomaly may contribute to ensure a longer symptom-free lifespan of individuals with the most common cardiac anomaly at birth.

Aortic Coarctation↗
PubMed1995

The effects of thyroid hormones on oxygen and glucose metabolism in the sheep fetus during late gestation.

1. The effects of thyroid hormones on fetal metabolism during late gestation were examined by measuring the rates of glucose and oxygen utilization rates in chronically catheterized sheep fetuses made hypothyroid by either fetal thyroidectomy (TX) or hypophysectomy (HX). The values were compared with those in intact fetuses and in thyroxine (T4)-treated TX and HX fetuses. 2. Umbilical O2 uptake expressed on a weight-specific basis was reduced by 20-30% in the hypothyroid fetuses and was restored to normal values when plasma T4 levels were maintained in the TX and HX fetuses by exogenous T4 administration. 3. The low O2 consumption rates of the untreated hypothyroid fetuses were accompanied by fetal growth retardation, an abnormal blood gas status, and in the TX fetuses, by significant reductions in the rates of glucose oxidation, CO2 production from glucose carbon and O2 utilization for glucose oxidation. 4. When T4 levels were maintained in the TX fetuses, these metabolic rates and fetal blood gas status were restored to their normal values. Replacement of T4 also sustained growth in TX but not in HX fetuses. 5. When the data from all fetuses were combined irrespective of treatment, there were significant positive correlations between plasma levels of T4 (but not triiodothyronine (T3)) and the rates of umbilical O2 uptake, glucose oxidation, CO2 production from glucose carbon and O2 utilization for glucose oxidation in the individual fetuses. 6. These findings demonstrate that T4 is a physiological regulator of O2 utilization by the sheep fetus close to term.

Animals↗
PubMed1998

Hypothalamo-pituitary disconnection of the late-gestation ovine fetus results in profound changes in cortisol secretion that are not reflected in commensurate changes in adrenocorticotropin secretion.

A prepartum increase in fetal glucocorticoid concentrations is essential for the perinatal transition to extrauterine life for many mammalian species. In the case of the sheep, this increase in cortisol is also the trigger for parturition, and depends upon an intact hypothalamo-pituitary unit. Fetal sheep that have undergone hypothalamo-pituitary disconnection (HPD) fail to have a prepartum cortisol surge or initiate labor, despite apparently normal fetal ACTH concentrations in late gestation. We have investigated whether a defect exists in the regulation of pulsatile neurohormone secretion in the pituitaryadrenal axis of the HPD sheep fetus, by comparing immunoreactive (ir) ACTH and cortisol secretory dynamics in intact and HPD fetuses at 126 and 145 days of gestation (normal gestation length, 147 days). The fetal surgery was conducted at 115 days of gestation. Blood samples were collected at 5-min intervals for 2 h on each experimental day, and the resulting irACTH and cortisol concentrations were analyzed by multiple-parameter deconvolution and cross-correlation analysis. Basal irACTH secretion was less (P < 0.01) in HPD fetuses than intact fetuses at 126 days, but it had recovered by 145 days. There were no differences in irACTH half-life or the number or duration of irACTH secretory bursts between the two groups of fetuses or the two gestational ages (GAs). The size of the irACTH secretory bursts was not affected by the operation, but it increased with GA to a similar extent in both groups of fetuses (P < 0.01). In keeping with the observations for irACTH secretion, there was no effect of age or the operation on cortisol half-life or on the number or duration of cortisol secretory bursts. In contrast, there were dramatic age-related increases (P < 0.01) in the basal cortisol secretion rate and the size of the cortisol secretory bursts in the intact, but not the HPD, fetuses. Cross-correlation analysis revealed a significant (P < 0.01) concordance between irACTH and cortisol secretion in only the intact fetuses at 126 days; this was not apparent in the intact fetuses at 145 days, or in the young or old HPD fetuses. These findings confirm a major defect in cortisol secretion in the late-gestation HPD fetus but suggest that this is not caused by defects in irACTH secretion. Together with other observations, these data suggest that ACTH may not be the sole, or primary, regulator of adrenal cortisol secretion in the late-gestation ovine fetus.

Adrenocorticotropic Hormone↗
PubMed1998

The Campylobacter fetus S layer is not essential for initial interaction with HEp-2 cells.

In vitro adherence assays were used to determine whether the S layer mediated interactions between Campylobacter fetus subsp. venerealis strains and HEp-2 cells. At multiplicity of infection ratios ranging from 0.1:1 through 100:1, quantitation of bacterial adherence by light microscopy revealed that S layer deficient isogenic C. fetus 809K and C. fetus 810K were not less efficient in their attachment to HEp-2 cells; either S layer deficient C. fetus strains interacted with HEp-2 cells in greater numbers than the corresponding wild-type parent strains 809 and 810 or there was no significant difference in adherence levels between wild-type and mutant strains. Adherence of C. fetus strains to HEp-2 cells increased most during the first 2 h of a 22-h incubation period with only a slight increase in C. fetus cell numbers occurring subsequent to 2 h. At each assay point throughout this 22-h time period, equivalent numbers of wild-type and S layer deficient C. fetus strains were observed associated with HEp-2 cells. Prior to 2 h, adherence levels of all C. fetus strains exceeded those of Escherichia coli AB264 and Salmonella typhimurium SL1344. And, unlike S. typhimurium, C. fetus did not undergo significant replication following initial adherence to HEp-2 cells. Campylobacter fetus did not adhere to HEp-2 cells in a localized or aggregative pattern but were randomly distributed over individual HEp-2 cells and at no time during the assay with C. fetus were changes in HEp-2 cell morphology apparent. These data suggest that the S layer is not essential for mediating initial interactions between C. fetus and HEp-2 cells.

Bacterial Adhesion↗
PubMed2000

First trimester umbilical artery pulsatility index in fetuses presenting enlarged nuchal translucency.

The aim of this prospective study was to evaluate an umbilical artery pulsatility index (UAPI) in first trimester fetuses who present enlarged nuchal translucency (NT) measurements. UAPI was measured in 121 single fetuses with NT > or =95th centile, from 10+3 to 13+6 weeks (crown-rump length (CRL) > or =38 mm - < or =84 mm). In these fetuses there were 20 trisomy 21, and six other chromosomal abnormalities (three trisomy 18 and three monosomy X). Eighty-nine cases had normal karyotype and delivered a baby without evidence of congenital malformations. Five fetuses with normal karyotype assessed antenatally were excluded from the comparison, because of evidence of congenital malformation. A fetus with normal karyotype that was spontaneously miscarried at 14 weeks' after chorionic villus sampling was also excluded. UAPI of fetuses with enlarged NT was compared with those of 65 singleton fetuses with normal NT and normal karyotype, which were used to establish our terms of reference (5th centile, median and 95th centile). UAPI of 7/20 (35%) Down syndrome and 42/89 (47%) normal karyotype fetuses presenting enlarged NT were above the median, and respectively 2/20 (10%) and 14/89 (15.7%) were above 95th centile of normal NT and normal karyotype fetuses. No significant differences were demonstrated in the UAPI values amongst normal karyotype fetuses with normal NT or normal karyotype fetuses with an enlarged NT or trisomy 21 fetuses with an enlarged NT.

Adult↗
PubMed2003

Venous Doppler ultrasound in 146 fetuses with congenital heart disease.

OBJECTIVE: To assess the influence of isolated congenital heart disease (CHD) on fetal venous Doppler blood flow velocity waveforms. METHODS: Doppler flow velocimetry was performed in the inferior vena cava and ductus venosus in 146 consecutive fetuses with antenatally diagnosed CHD. Gestational age ranged between 19 and 39 weeks. Fetuses with isolated CHD without non-immune hydrops fetalis (NIHF) (Group A, n = 89) were separated from seven fetuses showing isolated CHD with NIHF (Group B) and 50 cases complicated by chromosomal or other extracardiac malformations, intrauterine growth restriction or non-cardiogenic NIHF (Group C). The control group comprised 109 healthy fetuses of uncomplicated pregnancies. Individual peak velocity index for veins (PVIV) measurements were converted into their Z-scores (delta values) for statistical analysis. RESULTS: There was no statistical difference between fetuses with isolated CHD (Group A) and controls, for the delta PVIV of neither the ductus venosus nor the inferior vena cava. Statistical analysis revealed significant differences between non-isolated CHD fetuses (Group C) and controls for both vessels. However, in a separate analysis of isolated right heart malformations compared with the remaining isolated heart malformations (Groups A and B), a significant difference was observed for the ductus venosus, but not the inferior vena cava. There was an overall survival of 62%. In Group A, 58% of fetuses survived despite increased PVIV and 22% of fetuses with normal venous Doppler had an adverse outcome. All fetuses with cardiogenic NIHF (Group B) died. CONCLUSION: Doppler studies of the ductus venosus and inferior vena cava in fetuses with isolated CHD do not present sufficient alterations to be a reliable marker for screening purposes for CHD in mid-second- and third-trimester fetuses. Furthermore, venous Doppler did not predict fetal outcome in cases of isolated CHD. Abnormal venous Doppler results were mainly attributable to myocardial dysfunction and also to severe right heart obstruction even in the absence of congestive heart failure. Therefore, venous Doppler studies are clinically helpful in indirectly monitoring cardiac function in fetuses with cardiac malformations.

Blood Flow Velocity↗
PubMed1981

Effects on rat fetuses of intrauterine injections of insulin.

The effects on rat fetuses of a single intrauterine injection of long-acting insulin with respect to length, body and organ weights, total lipids, phospholipids, cholesterol, neutral fat, total nitrogen and water content were investigated. At the age of 498 hours the fetuses were injected in utero with 2 IU of long-acting insulin or a control solution. Twenty-four hours after the injections the insulin-treated fetuses weighed about 10 per cent more than the control fetuses, 5.32 +/- 0.05 g (75 fetuses) and 4.85 +/- 0.05 (73 fetuses) respectively (p less than 0.001). The body lengths were 54.1 +/- 0.2 mm and 52.9 +/- 0.2 mm respectively (p less than 0.001). The insulin-treated fetuses had higher organ weights and higher content of total lipids, phospholipids and neutral fat. The amount of total lipids was higher in insulin-treated fetuses even after taking into account differences in body weight, suggesting that the insulin-treated fetuses were obese. The finding of significantly lower water content in insulin-treated fetuses at equal body weight is consistent with the higher fat content. There was no increase in total nitrogen or length in the fetuses in the insulin-treated group compared to control fetuses at equal body weight indicating that the administered insulin mobilized maternal proteins and that protein, as well as length, increased proportionately to overweight. For quantitative analysis of morphological and biochemical variables dependent upon body weight, as in this investigation, multivariate analysis is indispensable.

Animals↗
PubMed1998

Morphological classification of nuchal skin in human fetuses with trisomy 21, 18, and 13 at 12-18 weeks and in a trisomy 16 mouse.

An increase in the nuchal translucency that can be detected at 10-14 weeks of gestation by ultrasound forms the basis for a screening test for chromosomal abnormality. Several mechanisms leading to this increase in skin thickness have been proposed, including changes of the extracellular matrix, cardiac defects and abnormalities of the large vessels. This study examines the composition of the extracellular matrix of the skin in gestational age-matched fetuses with trisomy 21, 18 and 13 from 12-18 weeks. Immunohistochemistry was applied with monoclonal and polyclonal antibodies against collagen type I, III, IV, V and VI and against laminin and fibronectin. Collagen type VI gene expression was further studied by in situ hybridization to detect differences in expression patterns of COL6A1, COL6A3 and COL1A1 between normal fetuses and those with trisomy 21. The ultrastructure of tissue samples was studied by transmission electron microscopy (TEM) and additionally by immunogold TEM. Further, we examined the morphology of the skin in an animal model for Down's syndrome, the murine trisomy 16, by light and TEM. The dermis of trisomy 21 fetuses was richer in collagen type VI than that of normal fetuses and other trisomies, and COL6A1, located on chromosome 21, was expressed in a wider area than COL6A3, which is located on chromosome 2. Collagen type I was less abundant in the skin of trisomy 18 fetuses, while the skin of all three trisomies contained a dense network of collagen type III and V in comparison with normal fetuses. Collagen type IV, of which two genes are located on chromosome 13, was expressed in the basement membranes of the skin in all fetuses and additionally in the dermal fibroblasts only of trisomy 13 fetuses. Likewise, laminin was present in all basement membranes of normal and trisomic fetuses as well as in dermal fibroblasts of fetuses with trisomy 18. LAMA1 and LAMA3 genes are located on chromosome 18. Dermal cysts were found in the skin of trisomy 18 and 13, but not in trisomy 21 and normal fetuses. Ultrastructural findings showed that an extracellular precipitate containing glycosaminoglycans was regularly present in the skin of trisomy 21 fetuses and murine trisomy 16 embryos. In conclusion, this study suggests that the skin edema in fetal trisomies is characterized by specific alterations of the extracellular matrix that may be attributed to gene dosage effects as a result of a genetic imbalance due to the condition of fetal trisomy.

Animals↗
PubMed1997

Serum beta 2-microglobulin in fetuses with urinary tract anomalies.

OBJECTIVE: Our purpose was to establish a reference range of fetal serum beta 2-microglobulin, an index of glomerular filtration rate, and to compare the values obtained in fetuses with urinary tract anomalies with this range. STUDY DESIGN: Serum beta 2-microglobulin was measured in 53 control fetuses at 18 to 39 weeks' gestation and in 14 fetuses with urinary tract anomalies, 9 of which had simultaneous urine sampling. RESULTS: In controls fetal serum beta 2-microglobulin had a mean value of 3.4 mg/L (95% data intervals 2.0 to 4.9) and did not correlate with gestational age. In the 14 fetuses with urinary tract anomalies beta 2-microglobulin levels were increased overall compared with controls (median Z score 1.7, range -0.1 to 9.2), and this was also the case in the five fetuses with unilateral renal disorders (median Z score 1.7, range -0.1 to 3.8) and in a fetus who underwent vesicoamniotic shunting and had normal renal function at birth. Serum beta 2-microglobulin was normal in 4 fetuses with bilateral urinary tract obstruction and normal function at postnatal follow-up and also in 1 of 5 fetuses with renal failure. In fetuses with bilateral uropathy urinary sodium correlated with serum beta 2-microglobulin levels. CONCLUSIONS: Increased values of serum beta 2-microglobulin in fetuses with urinary tract anomalies indicate an impaired glomerular filtration rate. The finding of raised concentrations in fetuses with unilateral damage suggests that the compensatory role of the normal kidney is not complete during intrauterine life. Larger series are required to ascertain whether fetal blood sampling is warranted in the antenatal investigation of renal function, especially in view of the close correlation between urinary sodium and serum beta 2-microglobulin levels in fetuses with bilateral obstruction.

Fetal Blood↗