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PubMed2002

Cell-free fetal DNA in the maternal circulation does not stem from the transplacental passage of fetal erythroblasts.

Fetal cells, specifically fetal erythroblasts, as well as cell-free fetal DNA are present in the maternal circulation. Both are currently being investigated as a means for the non-invasive risk-free analysis of fetal genetic traits. The origin of this cell-free fetal DNA in the maternal circulation is currently unclear. Since numerous fetal erythroblasts have been demonstrated to exhibit an apoptotic phenotype in the form of fragmented nuclear DNA, it has been proposed that such trafficking fetal cells may be a possible source. This hypothesis is supported by reports of elevated numbers of fetal erythroblast and cell-free fetal DNA concentrations in pregnancies affected by pre-eclampsia or polyhydramnios. To address this question, we have examined fetal erythroblast numbers and cell-free DNA concentrations in the same maternal blood samples. Our study, performed on both normal and pathologically-affected pregnancies, indicates that no correlation exists between these two fetal cellular and molecular species. This is most evident in pregnancies affected by onset of preterm labour, where significant elevations in cell-free fetal DNA concentrations were detected without any concomitant elevation in fetal erythroblast numbers. Our data therefore suggest that an alternative cell type is the source of cell-free fetal DNA. Furthermore, it appears that the release of cell-free fetal DNA from this cell type is affected by pathological placental conditions which are not associated with an increase in fetal cell trafficking.

Blood Cell Count↗
PubMed2003

Maternal growth hormone treatment from day 35 to 80 of gestation alters nutrient partitioning in favor of uteroplacental growth in the overnourished adolescent sheep.

Overnourishing the pregnant adolescent ewe promotes maternal tissue synthesis at the expense of placental growth and leads to a major reduction in lamb birth weight at term. Growth hormone (GH) secretion is attenuated in these overnourished dams and the maternal somatotrophic axis may play a key role in coordinating nutrient usage in the pregnant adolescent. Thus we investigated whether increasing maternal GH during the period of rapid placental proliferation alters nutrient partitioning between the maternal, placental, and fetal tissues as assessed at Day 81 of gestation. Adolescent recipient ewes were implanted with singleton embryos, derived from superovulated dams and a single sire on Day 4 postestrus. Thereafter, the ewes were offered either a high (H) or moderate intake (M) of the same complete diet. From Day 35 to 80 of gestation, ewes were either injected twice daily (s.c. at 0800 and 1800 h) with recombinant bovine GH (bGH, 0.14 mg/kg live weight/day) or remained untreated (n = 8 ewes per group). Maternal concentrations of GH, insulin, insulin-like growth factor (IGF-1), glucose, and non-esterified fatty acids (NEFAs) were higher, and leptin secretion lower, in bGH-treated dams from both nutritional groups. Maternal body weight gain was higher in H versus M groups and was independent of bGH treatment. Treatment with bGH reduced relative perirenal and carcass fat deposition and increased carcass protein content in both H and M dams. Uteroplacental mass (uterus + placentomes + fetal membranes) averaged 1099, 1069, 1112, and 1754 g in M, H, M+GH, and H+GH groups. This significant increase in uteroplacental development in the H+GH group was associated with higher fetal kidney and liver weights and elevated fetal insulin, glucose, and lactate concentrations. Treatment with bGH also induced polyhydramnios in the H group. The transplacental glucose gradient was increased twofold in the H+GH group but placental GLUT- 1 and GLUT-3 expression was unaffected. In conclusion, administration of GH during the period of rapid placental proliferation alters endocrine status and thus nutrient partitioning in the overnourished adolescent dam in favor of uteroplacental and fetal growth. It remains to be established whether these effects are due wholly to alterations in maternal metabolism or if they also reflect an effect of bGH and/or the IGF system at the level of the uteroplacenta.

Animal Nutritional Physiological Phenomena↗
PubMed2001

Inherited primary renal tubular hypokalemic alkalosis: a review of Gitelman and Bartter syndromes.

Inherited hypokalemic metabolic alkalosis, or Bartter syndrome, comprises several closely related disorders of renal tubular electrolyte transport. Recent advances in the field of molecular genetics have demonstrated that there are four genetically distinct abnormalities, which result from mutations in renal electrolyte transporters and channels. Neonatal Bartter syndrome affects neonates and is characterized by polyhydramnios, premature delivery, severe electrolyte derangements, growth retardation, and hypercalciuria leading to nephrocalcinosis. It may be caused by a mutation in the gene encoding the Na-K-2Cl cotransporter (NKCC2) or the outwardly rectifying potassium channel (ROMK), a regulator of NKCC2. Classic Bartter syndrome is due to a mutation in the gene encoding the chloride channel (CLCNKB), also a regulator of NKCC2, and typically presents in infancy or early childhood with failure to thrive. Nephrocalcinosis is typically absent despite hypercalciuria. The hypocalciuric, hypomagnesemic variant of Bartter syndrome (Gitelman syndrome), presents in early adulthood with predominantly musculoskeletal symptoms and is due to mutations in the gene encoding the Na-Cl cotransporter (NCCT). Even though our understanding of these disorders has been greatly advanced by these discoveries, the pathophysiology remains to be completely defined. Genotype-phenotype correlations among the four disorders are quite variable and continue to be studied. A comprehensive review of Bartter and Gitelman syndromes will be provided here.

Alkalosis↗
PubMed2001

Twin-twin transfusion syndrome: etiology, severity and rational management.

The twin-twin transfusion syndrome is a serious complication of monochorionic twin pregnancies. Partly as a result of an inadequate understanding of the pathophysiology of the syndrome, there is a lack of consensus in clinical management. We sought to review the available information on the etiology of twin-twin transfusion syndrome, to identify parameters that contribute to the severity of the syndrome, and propose a rational management plan based on pathophysiology, clinical presentation and the efficacy of therapies. We therefore amalgamated recent advances in twin-twin transfusion syndrome computer modelling and clinical studies, particularly on therapeutic outcomes. We found that the oligo-polyhydramnios sequence that defines twin-twin transfusion syndrome prenatally represents a wide continuum of severity in the imbalance between the fetoplacental circulations of both twins. In severe twin-twin transfusion syndrome cases, in which the circulatory imbalance deteriorates beyond fetal control, fetoscopic laser therapy of all anastomoses along the placental vascular equator is predicted to have significantly better survival rates and fewer neurological sequelae than amnioreduction. In contrast, mild twin-twin transfusion syndrome cases have better outcomes after one or at most a few amnioreductions than laser therapy, as a result of significantly fewer procedure-related risks. In conclusion, optimal individual therapy may possibly achieve an 85% survival rate in twin-twin transfusion syndrome, but requires advancement in non-invasive criteria that predict the severity of the syndrome. Identifying such criteria is a future challenge. For the interim, twin-twin transfusion syndrome diagnosed before 26 weeks' gestation has significantly better survival rates and fewer neurological sequelae after laser therapy than amnioreduction. Twin-twin transfusion syndrome diagnosed after 26 weeks can best be treated by amnioreduction, or delivery. Contrary to previous claims, fetoscopic laser therapy has outgrown its experimental status. Although improvements in technique and technology are likely, laser placental ablation has a firm scientific and clinical basis.

Amniotic Fluid↗
PubMed1990

Antepartum management of twin gestation: ultrasound.

1. The use of ultrasound may improve perinatal outcome in twin pregnancy. 2. Singleton growth curves for FL, BPD, and AC may be used to assess fetal growth prior to 28 weeks gestation. 3. After 28 weeks gestation, specific twin growth curves should be used. However, increased morbidity may be seen when fetal weight falls from the normal singleton predictive curves. 4. Amnionicity and chorionicity frequently can be determined. This should be attempted early in the second trimester so that appropriate monitoring can be offered for the monoamnionic and monochorionic gestations. 5. Serial assessment of fetal growth should be performed. In the authors' institutions, growth scans are performed in twins every 2 weeks after 24 weeks gestation. 6. Evidence on ultrasound examination of discordant growth suggests either fetal growth retardation or TTS. In the presence of a dichorionic placentation, growth retardation of one twin is the usual diagnosis. If placentation is monochorionic, it is difficult to differentiate between growth retardation and TTS. The presence of polyhydramnios, a stuck twin, or fetal hydrops are suggestive of TTS. 7. The value and safety of cordocentesis and the management of twin pregnancy and diagnosis of TTS have not been established. 8. Doppler ultrasound may be useful in the assessment of the IUGR twin fetus. The use of Doppler in the identification of TTS is not yet clear.

Amniocentesis↗
PubMed1997

Physiology of amniotic fluid volume regulation.

Although there are fairly wide variations AFV normally undergoes characteristic changes across gestation in which it increases from 10-20 ml at 10 weeks gestation to average 800 ml at 24 weeks. Little change occurs from then until near term when AFV begins to decrease, and large decreases can occur in postterm pregnancies. Across gestation, 95% of AFVs are within the range of 1/2.57-2.57 times the gestational mean volume and 99% are within the range of 1/3.40-3.40 times the gestational mean. Although there are six pathways in which fluid and solutes can enter and/or leave the amniotic sac, there are only four primary pathways that contribute to AFV during late gestation. These include fetal urine and lung fluid secretion as the two primary sources of fluid, with fetal swallowing and intramembranous absorption as the two primary routes of amniotic water clearance. The intramembranous pathway also appears to be a primary source of amniotic solutes (e.g., sodium and chloride). Although fetal hypoxia has been widely believed to cause oligohydramnios, fetal hypoxic hypoxia and anemic hypoxia both appear to be associated with an increased AFV and polyhydramnios rather than oligohydramnios. It is speculated that the oligohydramnios associated with fetal hypoxia is caused by placental dysfunction in addition to the hypoxia.

Amniotic Fluid↗
PubMed2000

Infection and preterm labor.

There are many conditions, such as non-white race, young maternal age, and uterine malformations, that have been associated with preterm birth that are not amenable to intervention. Maternal cervical and intrauterine infection and inflammation may have a primary causative role in a fraction of the cases of preterm birth and preterm rupture of membranes and may also interact adversely with a variety of maternal (shortened cervix, smoking) and fetal factors (polyhydramnios, multifetal gestation) to decrease the threshold to preterm birth. Further studies are needed to better-define the link between various maternal microbial colonizations and preterm delivery, with the possibility to establish new screening and treatment recommendations. Because of the innumerable causes of preterm birth, a new strategy of targeted treatment of cervical or vaginal infections may lead to only a modest reduction in the incidence of this devastating problem of modern obstetrics.

Chronic Disease↗
PubMed1984

High resolution computed tomography in neonatal nasopharyngeal teratoma.

A case of neonatal teratoma of the nasopharynx associated with polyhydramnios and respiratory distress is presented. Surgical excision was carried out after preoperative evaluation with high resolution CT. Computed tomography is valuable in distinguishing a teratomatous tumor and in searching for intracranial extension and malignant characteristics.

Female↗
PubMed1994

Congenital chloride diarrhea. A study in Arab children.

Congenital chloride diarrhea (CCD) is a common metabolic disorder in Saudi children with an incidence of 1 in 5,500. The present retrospective study from Saudi Arabia, over 7.5 years, presents the clinical, biochemical, and treatment details in 10 children with CCD. The perinatal characteristics of maternal polyhydramnios, prematurity, abdominal distention, and diarrhea were seen in 100% and hyperbilirubinemia in 90% of patients. Hypokalemic hypochloremic metabolic alkalosis was a feature in 50% of the children and acidosis in both neonates. Fecal chloride greater than 100 mmol/L in 100% and fecal chloride greater than the sum of fecal sodium and potassium were found in 55% of patients. The mean age at the time of diagnosis was 10 months and the mean duration of follow-up for the group was 38 months (range 2-89 months). Eight of the nine patients treated with continuous oral electrolyte solution demonstrated "catch-up" physical growth. Mental subnormality, growth retardation, and renal impairment were seen in one patient who failed to comply with the treatment. Cerebral palsy in another child was due to neonatal intraventricular hemorrhage.

Alkalosis↗
PubMed1996

Brainstem tegmental necrosis and olivary hypoplasia: a lethal entity associated with congenital apnea.

Previously, we reported an isolated case of a newborn with central apnea at birth, ventilator-dependence, and combined malformative and destructive brainstem lesions (1). We now report 2 additional cases with similar clinicopathologic features. All 3 patients were male (XY karyotype) and required immediate ventilatory support in the delivery room. Perinatal complications included polyhydramnios and breech presentation. Variable cranial nerve palsies and orofacial and limb anomalies were present. The patients dies within minutes of withdrawal of ventilatory support at 2 to 11 weeks after birth. Significant neuropathologic findings were localized to the caudal pons and medulla, and included tegmental necrosis (neuronal loss, gliosis, mineralization) with involvement of respiratory-related nuclei, and anomalies of rhombic lip derivatives (olivary hypoplasia, arcuate nucleus hyperplasia). Three-dimensional computer reconstructions facilitated clinicoanatomic correlations, and underscored the restriction of the lesions to pontine and medullary rhombomeres and rhombic lip. The histopathology of these cases suggests a malformative process occurring at the end of the first trimester (time of rhombic lip migrations), and a superimposed destructive process (tegmental necrosis) in the second half of gestation. Although the etiology is unknown, the segmental nature of the lesions suggests the possibility of an abnormality in homeobox gene regulation. These cases likely represent a distinct clinicopathologic entity that should be considered in the differential diagnosis of Moebius syndrome and failure to breathe at birth.

Apnea↗
PubMed1992

Congenital sodium diarrhea with a partial defect in jejunal brush border membrane sodium transport, normal rectal transport, and resolving diarrhea.

Defective jejunal sodium/proton exchange causes severe, congenital secretory diarrhea. We report a boy who presented typically in utero, but in whom diarrhea resolved during the first year of life. Pregnancy was complicated by polyhydramnios, and an ultrasound at 31 weeks showed a distended fetal small intestine. The abdomen was grossly distended at birth, and profuse secretory diarrhea began immediately. He subsequently thrived on breast milk and electrolyte supplements. Studies of jejunal brush border sodium/proton exchange at 6 months showed a partial defect. Nonequilibrium rectal dialysis showed rectal sodium and potassium transport to be intact. Diarrhea lessened after 9 months, and the patient subsequently required occasional laxatives. These observations suggest that there is a spectrum of congenital abnormality in this exchanger, and that in children with incomplete defects normal colonic sodium salvage can subsequently mask net small intestinal secretion.

Biological Transport↗
PubMed2004

Neonatal enteropathies: defining the causes of protracted diarrhea of infancy.

The underlying causes of chronic diarrhea beginning early in life are increasingly well defined. Infectious and post-infectious enteropathies and food sensitive/allergic enteropathy account for the majority of cases. Recent attention has focused on characterizing defined entities, which cause protracted diarrhea in infants and young children. Disorders of intestinal ion transport usually present at birth following a pregnancy complicated by polyhydramnios. Intestinal mucosal biopsies show normal architect with intact villus-crypt axis. Neonatal enteropathies, by contrast, are characterized by blunting of the villi. These include microvillus inclusion disease, tufting enteropathy, autoimmune enteropathy and IPEX syndrome - and it is these conditions that are the subject of the current review.

Autoimmune Diseases↗
PubMedDate not supplied

Evaluation of a new real-time blood continuous glucose monitoring system in pregnant women without gestational diabetes. A pilot study.

The incidence of gestational diabetes mellitus (GDM) has reached epidemic proportions in the United States, affecting 200,000 pregnant women annually. Controversies exist regarding whether the glucose levels used to diagnose GDM in pregnancy should be lowered since similar fetal complications are seen in women with GDM as well as in nondiabetic women. Although GDM has been extensively studied, the effects of the earlier stage of glucose intolerance are not well understood. The objectives of this descriptive, comparative, correlational pilot study include assessment of real-time blood glucose concentrations in women (20) with idiopathic macrosomia and/or polyhydramnios but with a normal baseline glucose screening test. This group was compared to pregnant women (20) without idiopathic macrosomia and/or polyhydromnios as confirmed by normal ultrasounds (controls). All subjects had a normal screeing test and/or a 3-hour Glucose Tolerance Test earlier in the pregnancy and wore a continuous glucose monitoring system for 72 hours. No adverse maternal complications were seen. Neonatal complications included macrosomia, shoulder dystocia, and hyperbilirubinemia. There was no significant association between real-time blood glucose levels and adverse maternal or fetal/neonatal complications. There is little evidence available regarding real-time physiologic glycemic levels in pregnant women. The findings of our pilot study provide baseline data for the design of a larger study to compare blood glucose levels and complications in euglycemic women and compare to women with those impaired glucose tolerance.

Adult↗
PubMed1989

Antenatal detection of congenital malformations by routine ultrasonography.

Routine ultrasound examination was performed in 9012 fetuses of a general pregnant population to detect fetal malformations. The examination was done on 3098 fetuses at 18 weeks, and on 5914 fetuses it was repeated at 34 weeks. Ninety-three infants (1.03%) showed 123 major malformations, of which 65 (52.8%) in 54 children were visualized in utero. The sensitivity of detection of malformed fetuses was 58.1% (54 of 93), specificity 99.9%, positive predictive value 91.5%, and negative predictive value 99.6%. Five fetal hydronephroses were the only false-positive cases (0.06%), with apparent spontaneous resolution after birth. Fetal growth retardation, polyhydramnios, or oligohydramnios was observed in 43% of the malformed cases, suggesting the importance of these conditions in ultrasound screening. Abnormality of pregnancy was suspected clinically in only 25.8% of the cases at the time of diagnosis of fetal malformation, emphasizing the necessity for ultrasound examination of all pregnancies.

Congenital Abnormalities↗
PubMed1990

Prenatal diagnosis of fetal tumors by ultrasonography.

Fetal tumors lead to serious illness or even death in the fetal or neonatal period. Problems vary from severe hydrops to underdevelopment of fetal organs. In some instances a tumor may cause mechanical obstruction during the birth process. Polyhydramnios frequently develops. Adequate prenatal diagnosis is of utmost importance. Timely detection of the fetal tumor prevents traumatic birth and postnatal care and treatment can be scheduled. This report is a review of the relevant recent literature and the tumors detected in our ultrasound unit between 1982 and 1988. The ultrasonographic appearance, clinical course, and differential diagnosis of the tumors are discussed.

Female↗
PubMed1991

Management of antenatally diagnosed fetal ovarian cysts.

1. Fetal ovarian cysts are usually unilateral, diagnosed in the third trimester and are uncommon. 2. Average ovarian cyst size is 5 x 5 cm at diagnosis and size does not change throughout the pregnancy. 3. Most cysts are functional in origin and histologically benign, simple cysts. 4. Polyhydramnios is a common finding but associated anomalies are rare. 5. Although large cysts can compress other viscera and torsion or rupture can occur, in utero aspiration has limited value in prenatal management. 6. Vaginal delivery with confirmed fetal pulmonary maturity or at term is appropriate. 7. Soft tissue dystocia is rare. Cesarean delivery should be reserved for obstetrical indications only. 8. The best predictor of neonatal cyst torsion risk is length of the cyst pedicle rather than cyst size. 9. When surgery is indicated a cystectomy, with preservation of maximal ovarian tissue is to be preferred over oophorectomy. 10. Ultrasound-guided aspiration of neonatal ovarian cysts may be an alternative to surgical management.

Delivery, Obstetric↗
PubMed1992

Antenatal diagnosis of pulmonary sequestration: a review.

The prenatal diagnosis of pulmonary sequestration has been demonstrated in 17 published reports, including a new case report presented here. In 11 cases (65 per cent), the definitive diagnosis was not appreciated until after birth, although a fetal mass was recognized on ultrasonographic study in the antenatal period. Seventy-five per cent of cases were thoracic sequestrations, and 25 per cent were abdominal lesions. Fetal hydrops, found in 35 per cent of cases, was universally associated with stillbirth or neonatal death. Polyhydramnios, pleural effusions, mediastinal shifts, pulmonary hypoplasia, and preterm labor were not uncommon findings. The high incidence of related malformations, well described in the postnatal literature, was remarkably absent in this antepartum series. Although the perinatal outcome for abdominal lung sequestrations is reasonably good, the prognosis in cases of thoracic sequestration remains guarded. Aggressive respiratory support after birth will not salvage those infants with underlying severe pulmonary hypoplasia. Early in utero catheter drainage may provide the best treatment for the pleural effusions associated with thoracic sequestrations, although this therapy remains under investigation.

Adult↗
PubMed2005

The outcome of prenatally diagnosed renal tumors.

PURPOSE: We assessed the incidence of perinatal morbidity and evaluated the outcome in children with prenatally diagnosed renal tumors in a retrospective multicenter study. MATERIALS AND METHODS: A review of the records of patients from 20 institutions identified 28 children with prenatally diagnosed renal tumors. Prenatal findings, clinical charts, and radiological, surgical and pathological reports were reviewed in this study. RESULTS: There were 26 congenital mesoblastic nephromas and 2 Wilms tumors. One or more complications were identified in 20 of the 28 cases (71%) during the perinatal period. Polyhydramnios was observed in 11 fetuses (39%), 2 presented with hydrops fetalis and 7 presented in acute fetal distress requiring emergency cesarean section, of which 1 died in utero before delivery. Median gestational age of the 27 neonates born alive was 35 weeks (range 29 to 39), including 13 (46%) who were pre-term (less than 34 weeks of gestation). Complications at birth included hemodynamic instability in 3 newborns, of whom 2 underwent emergency surgery, respiratory distress syndrome in 8 (30%) and hypertension in 6 (22%). Surgical complications occurred in 7 patients (26%), including tumor rupture in 1 and intraoperative bleeding with postoperative death in 1. At a median followup of 42 months (range 2 to 105) 26 of the 27 children were in complete remission. CONCLUSIONS: Fetal renal tumors have an excellent oncological outcome but a high risk of perinatal complications. Prenatal diagnosis should allow planning the delivery at a pediatric tertiary care center to avoid a potentially life threatening condition in neonates in the first hours of life.

Female↗