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PubMed2000

[Feto-maternal immunization and fetal hemolytic disease: invasive diagnostics and therapy in the Warsaw center of serological collision in years 1992-1999].

OBJECTIVE: The objective of this study was the assessment of intrauterine procedures, which are performed during the diagnostic phase and therapy of fetal hemolytic disease in the Warsaw Center of Serological Collision. MATERIALS AND METHODS: The study covered 146 women, who were patients of the Center from 1992 to 1999. Analyzed were the time of commencement of diagnostic and treatment, type of operations, duration of therapy, time and manner of delivery after the past intrauterine procedures, the medical condition of infants born as a result of these deliveries and the necessity for blood treatment in the early neonatal stage. RESULTS: 451 intrauterine procedures were carried out, of which 159 were diagnostic punctures of the umbilical vessel and 292 were fetal transfusions. The diagnostics and treatment was performed between the 19 and 38 week of pregnancy. The number of punctures for each patient ranged from 1 to 4, and 1 to 10 for intrauterine transfusions. The therapy, which on average lasted 42 days, significantly improved the fetal blood morphology results. During the therapy 5 intrauterine demises were noted--3 as a result of advanced fetal hemolytic disease and 2 related to operation complications. The average pregnancy duration in the analyzed group was 36.4 for treated women and 37.4 weeks for diagnosed women. 52.7% of deliveries were vaginal, 47.3% were performed by cesarean section. The general condition of 87% of infants was good. However, 77% of infants required blood treatment during the early neonatal period. CONCLUSIONS: Invasive methods of fetal hemolytic disease diagnostics and intrauterine therapy assure high efficiency in the guiding of serological collision and fetal hemolytic disease conflicted pregnancies. At the same time, these methods are safe and carry a low risk of complications.

Anemia, Hemolytic↗
PubMed2001

Diagnosis, natural history, and outcome of fetal heart disease.

Advances in the prenatal diagnosis of heart disease have improved accuracy in the evaluation of structural heart lesions, dysrhythmia mechanisms, and functional pathology and will lead to better perinatal management and counseling. Additional technical advances will lead to earlier diagnosis, perhaps even during embryonic development. Newer developments, including the transumbilical and transuterine approaches, may make antenatal intervention possible and safer for a larger number of affected pregnancies.

Disease Progression↗
PubMed2005

Neonatal hemochromatosis: fetal liver disease leading to liver failure in the fetus and newborn.

Acute liver failure in the newborn is relatively rare but often fatal. The broadest definition of acute liver failure is failure of the vital functions of the liver occurring within weeks or a few months of the onset of clinical liver disease. Therefore, by definition, any liver failure in the newborn can be construed to be acute liver failure. A second component of the general definition of acute liver failure is the lack of known preexisting liver disease. In the case of neonatal acute liver failure, preexisting disease would by definition be liver disease that affects the fetus. Almost nothing is known about fetal onset liver failure, and there is no literature addressing the subject. This review will address fetal liver disease that leads to liver failure in the fetus or newborn.

Female↗
PubMed2006

Fetal serum beta2-microglobulin as a marker for fetal infectious diseases.

OBJECTIVES: To evaluate whether fetal serum beta2-microglobulin could be used as a marker of fetal cytomegalovirus (CMV) or toxoplasmosis infection. METHODS: beta2-microglobulin was retrospectively assayed in fetal serum collected from 64 patients with maternal infectious seroconversion (toxoplasmosis in 49 cases, CMV in 15). Using a beta2-microglobulin cutoff of 5 mg/L, infection and control groups were compared. RESULTS: Fetal serum beta2-microglobulin was >5 mg/L (5.2-13.5 mg/L) in 12 of the 13 cases with proved fetal toxoplasmosis infection, indicating 90% sensitivity. In the 39 pregnancies with maternal seroconversion but no laboratory signs of fetal infection, fetal serum beta2-microglobulin was <5 mg/L, indicating 100% specificity. Fetal serum was >5 mg/L (6.3-32 mg/L) in 14 of the 15 cases with proved fetal CMV infection, indicating 93.3% sensitivity. Specificity cannot be evaluated because maternal serum is not routinely screened for CMV during pregnancy. CONCLUSIONS: Fetal serum beta2-microglobulin is a reliable marker of fetal CMV or toxoplasmosis infection, which can be used in ambiguous situations. Because this increase is not specific, fetal serum beta2-microglobulin would potentially be raised in other fetal infections.

Biomarkers↗
PubMed1992

Human fetal bilirubin levels and fetal hemolytic disease.

The development of secondary fetal anemia in association with maternal red blood cell alloimmunization requires hemolysis. In specimens obtained at the time of a clinically indicated cordocentesis, total and direct umbilical venous bilirubin was measured and the indirect umbilical venous bilirubin calculated in 43 antigen-positive and 30 control fetuses. Twenty-two (51%) of the antigen-positive fetuses had or subsequently developed severe anemia (hematocrit less than 30%). Umbilical venous total bilirubin (r = 0.47, p = 0.0008) and direct bilirubin (r = 0.520, p = 0.04) levels each rose with gestation. Indirect bilirubin did not vary significantly with gestation. Bilirubin was unrelated to hemoglobin. In contrast to the control fetuses, umbilical venous total bilirubin for antigen-positive fetuses was inversely related to hemoglobin (r = -0.57, p less than 0.0001) independent of gestational age (r = 0.53, p less than 0.0001) (multiple R of hemoglobin and gestational age for umbilical venous total bilirubin = 0.76, p less than 0.0001). Eighteen of 22 (82%) fetuses in whom anemia developed had an umbilical venous total bilirubin greater than or equal to 97.5 percentile compared with only eight of 21 (38%) fetuses in whom anemia did not develop (p = 0.009). In longitudinal study the umbilical venous total bilirubin frequently rose above normal weeks before the development of anemia. An umbilical venous total bilirubin greater than 3 mg/dl represented the warning line. Fifteen of 16 (94%) fetuses in whom either severe antenatal anemia or significant postnatal hyperbilirubinemia developed had an umbilical venous total bilirubin greater than 3 mg/dl. We conclude that the normal placental capacity for the transport of fetal bilirubin is exceeded in the face of enhanced fetal hemolysis. An elevated fetal bilirubin often precedes the development of antenatal anemia. The antigen-positive fetus with an elevated bilirubin is at high risk to develop anemia antenatally.

Bilirubin↗
PubMedDate not supplied

Lattice theory analysis of the relationship of hyaline membrane disease and fetal pneumonia in 96 perinatal autopsies.

A previous study of hyaline membrane disease of the newborn demonstrated that the hyaline membrane was derived from necrotic epithelial cells, and it was suggested that a no flow-reflow episode affecting the pulmonary circulation might account for the cell necrosis. An unexpected statistical finding in that study was a highly significant negative correlation between hyaline membrane disease and chorioamnionitis. Because it seemed to us that fetal infection could be expected to produce the circulatory pathophysiology suggested to produce hyaline membrane disease, we reexamined the issue by reviewing a group of autopsied infants. Data were collected on clinicopathologic variables from 42 stillborn and 54 liveborn infants less than or equal to 12 h of age with lung and placenta slides available for review. Correlations and multivariate regression analysis showed that the inflammatory responses in membranes, cord, and lung are interrelated but that hyaline membrane disease develops independently. However, lattice theory analysis, which represents the pathogenesis of a progressive disease process as edges along a mathematical lattice or hyperdimensional cube, showed that this separation was not absolute. Despite the negative correlation of hyaline membrane disease and fetal pneumonia, there were 10 (10%) patients with both conditions and a total of 19 (20%) with hyaline membrane disease and inflammation of membranes, cord, and/or lung. We suggest that the coexistence of hyaline membrane disease and fetal pneumonia in some patients implies a possible pathogenetic relationship between the two entities. Given the nature of the two processes, it seems likely that the direction of causality is that fetal pneumonia would give rise to the hyaline membrane disease of the newborn.

Autopsy↗
PubMed2004

Frontiers in fetal cardiovascular disease.

This article reviews the state of the art in prenatal cardiovascular imaging, the elucidation of regional vascular flow patterns in the developing fetus and what can be learned from these flow patterns, the new clinical practice systems being that are being implemented to deal with the fetal patient and its family, and the prospects for fetal surgery.

Blood Circulation↗
PubMed1987

Immunologic disease and fetal death.

Both maternal isoimmunization and maternal autoimmune disease are associated with fetal death. For isoimmunization the immunologic nature of fetal death (hydrops fetalis) is beyond question, but many of the details are poorly understood. It would be extremely helpful to know what immunologic factors are responsible for the wide variation in the degree of fetal hemolysis. This information would surely lead to improved management of isoimmunized pregnancies and create new and more successful therapies for fetuses at risk for hemolysis. The immunology of autoimmune-associated fetal death is, for the most part, an enigma. For the fetal deaths associated with SLE and the antiphospholipid antibodies, demise appears to be a consequence of uteroplacental vascular damage. But the observable pathology is nonspecific, and the evidence for a direct immunologic mechanism is sparse. The similarity between the uteroplacental vascular lesions found with these autoimmune conditions and those seen in preeclampsia demands more intensive investigation. For the fetal deaths caused by complete congenital heart block associated with maternal autoantibodies, the evidence for a direct immunologic mechanism is now being established. As with isoimmunization, a more complete understanding of autoimmune-associated fetal death will open new avenues of management and therapy.

Autoantibodies↗
PubMedDate not supplied

Neural transplantation of hNT neurons for Huntington's disease.

Fetal striatal tissue transplants have been shown to restore motor deficits in rat and monkey models of Huntington's disease (HD). In the present study, using rats with unilateral striatal lesions, we compared fetal striatal tissue transplants to transplants of human NT (hNT) neurons. hNT neurons are terminally differentiated cells derived from the human NTera-2 cell line. In vitro, we have found that purified hNT neurons have a biochemical phenotype similar to that of human fetal striatal tissue. Both hNT neurons and fetal striatal tissue express mRNAs for glutamic acid decarboxylase, choline acetyltransferase, and the D1 and D2 dopamine receptors. Grafts of either hNT neurons or fetal striatal tissue into unilateral quinolinic acid-lesioned rat striatum improved methamphetamine-induced circling behavior. Sham controls showed no changes in methamphetamine-induced circling behavior. In the staircase test for skilled forelimb use, both transplant groups showed partial recovery in skilled use of the paw contralateral to the side of lesion, whereas the control animals showed continued deficits. These findings suggest that transplantation of hNT neurons may be an alternative to transplantation of fetal striatal tissue in the treatment of HD.

Animals↗
PubMedDate not supplied

Fetal hemolytic disease due to anti-Rh17 alloimmunization.

OBJECTIVE: To delineate clinical features of a case of fetal hemolytic disease due to anti-Rh17, along with a review of relevant studies published in English and Japanese. METHODS: We present clinical features of a -D-/-D- phenotype woman with anti-Rh17 alloimmunization during pregnancy. Relevant English literature in the MEDLINE database was reviewed, while Japanese studies were searched in the Japana Centra Revuo Medicina database. RESULTS: A Japanese -D-/-D- woman with anti-Rh17 (Hro) was treated during pregnancy. Serial ultrasonography, antibody titers, amniocenteses, and cordocenteses were conducted for perinatal management. Amniocentesis results demonstrated a high delta optical density level of 450 in the amniotic fluid, while cordocentesis revealed alloimmunization between the mother and the fetus as well as fetal hemolytic anemia. Blood flow velocity in the middle cerebral artery indicated a rapid development of fetal anemia. The newborn demonstrated severe anemia and hyperbilirubinemia, which were successfully treated with exchange transfusions. Two cases of prenatally diagnosed fetal hemolytic disease due to anti-Rh17 were found published in English and 5 in Japanese. CONCLUSION: A -D-/-D- phenotype patient with anti-Rh17 was successfully managed during pregnancy and a good outcome for the neonate was achieved. Our results and a review of related literature led to the following suggestions. The first pregnancy in a -D-/-D- woman may be affected, an anamnestic immune response can easily occur during pregnancy, the level of anti-Rh17 titer is indicative of the degree of fetal hemolysis, and appropriate intrauterine intervention is warranted for achievement of a good outcome.

Adult↗
PubMed1994

Direct relationship of fetal carboxyhemoglobin with hemolysis in alloimmunized pregnancies.

Because carbon monoxide (CO) is a byproduct of heme degradation and because placental diffusing capacity of CO is limited, we hypothesized that the concentration of CO transported in fetal blood as carboxyhemoglobin (HbCO) would correlate with the severity of fetal hemolytic disease. Fetal blood was obtained by cordocentesis and HbCO was measured by gas chromatography. The two primary study groups included control fetuses (n = 26) and fetuses of Coombs-positive mothers before in utero transfusion (n = 15). Compared with controls, fetuses with hemolytic disease had higher HbCO levels (0.0111 +/- 0.0014 versus 0.0159 +/- 0.0072 fraction of total Hb, mean +/- SD, p < 0.002). In contrast, HbCO levels in simultaneously sampled maternal blood samples were not different in the control and alloimmune groups [0.0110 +/- 0.0025 (n = 20) versus 0.0115 +/- 0.0021 (n = 11)]. There was a significant inverse correlation observed between fetal HbCO and Hb concentrations in the group with hemolytic disease (r = -0.73, p < 0.002) but not in controls. In fetuses with hemolytic disease, HbCO and bilirubin were highly correlated (r = 0.88, p < 0.0001). Data from four anemic fetuses who were Coombs negative, three of whom had no evidence of hemolysis, indicated normal HbCO and normal plasma bilirubin levels. A fourth fetus with anemia had viral sepsis and elevated HbCO and plasma bilirubin levels. We conclude that elevated HbCO levels detected in fetuses of nonsmoking mothers with erythrocyte alloimmunization are likely the result of accelerated hemolysis.

Bilirubin↗
PubMed1989

[Treatment of fetal hemolytic disease by hemosorption].

Hemosorption was used in the combined treatment of fetal hemolytic disease (FHD) for the first time. It was demonstrated that hemosorption was a method of choice in pregnant females with manifest sensitization and a history of stillbirth resulted from an edematous type of the disease. A decrease (by a factor of 10(2) to 10(6] in the Rh antibody titers in the blood of the pregnant after hemosorption, and reversibility of echocardiographic signs of FHD, and normalized fetal cardiac performance were regarded as a beneficial prognostic sign. The authors suggested that hemosorption should be started at weeks 24-25 of pregnancy in the absence of echographic signs of the disease. The interval between the sessions should not exceed a fortnight. The treatment course should be completed 1-2 weeks prior to the labor. As part of combined treatment, hemosorption contributed to a reduction in mortality rates (from 81 to 41%) from the edematous type of the disease.

Adult↗
PubMed2005

Pathophysiological significance of T-type Ca2+ channels: expression of T-type Ca2+ channels in fetal and diseased heart.

Re-expression of fetal genes has been considered to underlie ionic remodeling in diseased heart. T-type Ca(2+) channels have been reported to be functionally expressed in embryonic hearts. In this review, we summarize developmental changes of T-type Ca(2+) channels in mouse ventricles from 9.5 days postcoitum (dpc) to adulthood, using patch clamp and quantitative PCR. In addition, we introduced T-type Ca(2+) channel expression in hypertrophied ventricles caused by myocardial infarction (MI) and aortic banding (AOB). Substantial T-type Ca(2+) channel current was recorded at both 9.5 and 18 dpc. The currents were inhibited by Ni(2+) at low concentrations. The current was not detectable in the adult stage. Ca(v)3.2 (alpha(1H)) mRNA is expressed dominantly at both 9.5 and 18 dpc. Ca(v)3.1 (alpha(1G)) increases from 9.5 to 18 dpc, but remains at low level compared with Ca(v)3.2. In contrast, Ca(v)3.1 is greater than Ca(v)3.2 at the adult stage. In MI, Ca(v)3.1 mRNA correlates negatively with brain natriuretic peptide (BNP) mRNA, whereas Ca(v)3.2 mRNA correlates positively with BNP mRNA. In AOB, these correlations are weak. We also analyzed the neuron-restrictive silencer factor (NRSF) in these hearts because it is the suppressor of transcription of the fetal cardiac gene program. The negative correlation between NRSF and BNP was stronger in MI than in AOB. Our findings show that Ca(v)3.2 underlies the functional T-type Ca(2+) channel in embryonic heart and suggest that NRSF may regulate Ca(v)3.2 expression in diseased hearts.

Animals↗
PubMed1985

Application of Doppler echocardiography in the assessment of fetal cardiac disease.

Pulsed Doppler echocardiography was used in conjunction with real-time two-dimensional and M-mode ultrasound techniques in 19 fetuses between 28 and 40 weeks of gestation. Of these, nine also had echocardiographic examination performed neonatally. In one fetus with complete heart block, pulsed Doppler echocardiography showed tricuspid regurgitation. The ventricular and atrial rates were accurately determined by M-mode ultrasound; pericardial effusion was noted in the two-dimensional examination. The left ventricular stroke volume, as measured by the Doppler technique, was 13.5 ml, and the minute output was 486 ml/min. In another fetus, Doppler studies assisted two-dimensional echocardiography in detecting pulmonary aneurysm. Neonatal echocardiography confirmed this and also showed the presence of tetralogy of Fallot. In three fetuses with ventricular ectopy, 30% to 50% reduction in the right ventricular stroke volume was recorded by the Doppler technique. This study demonstrates the clinical potential of pulsed Doppler echocardiography in assessing fetal cardiac disorders and justifies further investigation to define its clinical utility.

Cardiac Output↗
PubMed1999

Congenital chylothorax in neonatal thyrotoxicosis.

We report a patient with congenital chylothorax who also had neonatal thyrotoxicosis secondary to maternal Graves' disease. Fetal tachycardia with hydrops was detected at 28 weeks' gestational age. The fetus responded to antithyroid medication in utero but had persistent bilateral pleural effusion. At birth, he had respiratory distress due to massive pleural effusion. Cytologic studies of pleural fluid were consistent with chylothorax. To the best of our knowledge, the association of congenital chylothorax with fetal (neonatal) thyrotoxicosis, has not been reported previously.

Adult↗
PubMed1998

[Computer-assisted analysis of cardiotocographic recordings in the course of fetal hemolytic disease].

OBJECTIVES: The aim of this study was to assess the usefulness of computerized cardiotocography in the diagnostics of fetal hemolytic disease. STUDY DESIGN: 50 invasive diagnostic and therapeutic procedures proceeded by computer assisted CTG recording were analysed. The values of particular parameters of CTG were compared with adequate values obtained in uncomplicated pregnancy. The correlation between both cardiotocographic and hematological parameters was estimated. The common relationship between all analyzed features was examined using multidimensional analysis of variancy. RESULTS: The most significant correlation was determined in case of short-term variation and hematocrite of fetal blood. The five-feature algorhythm, containing short- and long-term variation, number of accelerations, fetal movements and gestational age, was established for the prognosing of the most probable level of fetal hematocrite. CONCLUSION: Computerized cardiotocography seems to be the useful diagnostic method which enable to decrease the number of invasive intrauterine procedures in case of fetal hemolytic disease.

Adolescent↗
PubMed2005

Imaging in cell-based therapy for neurodegenerative diseases.

Fetal cell transplantation for the treatment of Parkinson's and Huntington's diseases has been developed over the past two decades and is now in early clinical testing phase. Direct assessment of the graft's survival, integration into the host brain and impact on neuronal functions requires advanced in vivo neuroimaging techniques. Owing to its high sensitivity, positron emission tomography is today the most widely used tool to evaluate the viability and function of the transplanted tissue in the brain. Nuclear magnetic resonance techniques are opening new possibilities for imaging neurochemical events in the brain. The ultimate goal will be to use the combination of multiple imaging modalities for complete functional monitoring of the repair processes in the central nervous system.

Diagnostic Imaging↗