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PubMed2004

Clinical significance of peripheral blood erythroblastosis after hematopoietic stem cell transplantation.

Erythroblasts (EBL) are normally not observed in peripheral blood, but may be found in patients suffering from a variety of severe diseases. The detection of EBL in peripheral blood has been shown to be associated with a poor prognosis. However, the clinical significance of peripheral erythroblastosis after hematopoietic stem cell transplantation (HSCT) has not been evaluated. We retrospectively analyzed the records of 161 patients who underwent HSCT at our hospital from June 1995 to October 2001. EBL at any level were detected in 94% of the patients. Forty-four and 11 patients experienced erythroblastosis exceeding 200 and 1,000/ul, respectively. The erythroblast count was higher in patients who died than in the survivors (geometric mean value 184 vs. 100/ul, P=0.01). High-level erythroblastosis ( >1,000/ul) within 180 days after HSCT was associated with an extremely poor prognosis (median survival 22.5 days). Among the possible confounding factors, the use of total body irradiation (RR 2.35, 95% CI 1.22 - 4.54, P=0.011) and the disease status before transplantation (RR 2.51, 95% CI 1.15 - 5.49, P=0.021) were independent significant factors for erythroblastosis after HSCT. As for post-transplant events, a high EBL concentration was frequently preceded by graft-vs.-host disease, thrombotic microangiopathy, hypoxia, and hematological relapse.

Adult↗

PubMed2005

Role of erythropoietin receptor signaling in Friend virus-induced erythroblastosis and polycythemia.

Friend virus is an acutely oncogenic retrovirus that causes erythroblastosis and polycythemia in mice. Previous studies suggested that the Friend virus oncoprotein, gp55, constitutively activates the erythropoietin receptor (EPOR), causing uncontrolled erythroid proliferation. Those studies showed that gp55 confers growth factor independence on an interleukin-3 (IL-3)-dependent cell line (Ba/F3) when the EPOR is coexpressed. Subsequently, we showed that a truncated form of the stem-cell kinase receptor (sf-STK) is required for susceptibility to Friend disease. Given the requirement for sf-STK, we sought to establish the in vivo significance of gp55-mediated activation of the EPOR. We found that the cytoplasmic tyrosine residues of the EPOR, and signal transducer and activator of transcription-5 (STAT5), which acts through these sites, are not required for Friend virus-induced erythroblastosis. The EPOR itself was required for the development of erythroblastosis but not for gp55-mediated erythroid proliferation. Interestingly, the murine EPOR, which is required for gp55-mediated Ba/F3-cell proliferation, was dispensable for erythroblastosis in vivo. Finally, gp55-mediated activation of the EPOR and STAT5 are required for Friend virus-induced polycythemia. These results suggest that Friend virus activates both sf-STK and the EPOR to cause deregulated erythroid proliferation and differentiation.

Animals↗

PubMed1986

There is evidence that amniotic fluid arginine vasopressin is a marker for foetal stress in rhesus erythroblastosis.

In response to different stress stimuli the foetal neurohypophysis releases arginine vasopressin (AVP). Part of the AVP is cleared from circulation by urinary excretion into the amniotic fluid (AF). Increased AF AVP levels may therefore indicate foetal stress, all the more because AF AVP solely is of foetal origin. We therefore studied AF AVP levels in 13 patients with rhesus erythroblastosis from 22 to 34 weeks of gestation. Twenty-eight patients from 14 to 34 weeks of gestation served as controls. The AVP levels were measured by RIA. Spectral absorption curves were performed and delta/E values determined at 450 nm. Mean AF AVP levels in controls were 2.39 pg/ml and were not normally distributed. There was no significant change in AF AVP levels with different gestational age. If in rhesus erythroblastosis patients the delta/E value was low (n = 7; x = 0.048 +/- 0.007 SE), the AF AVP values were not increased. If the delta/E values were within zone III (n = 6; x = 0.22 +/- 0.035 SE), indicating severe haemolysis, the AF AVP levels were significantly elevated (4.7 pg/ml +/- 0.51 SE; P = 0.001). Linear regression analysis showed a significant correlation between delta/E and AF AVP values (P = 0.05; y = 1.94 +/- 10.88 x). We conclude that there is evidence for the role of AF AVP as a marker for foetal stress in rhesus erythroblastosis.

Amniotic Fluid↗

PubMed1975

Rh erythroblastosis fetalis 1975.

Great advances have been made in the management of Rh erythroblastosis fetalis in the past two decades. Perinatal mortality has been reduced from 16.4% to 3.2%. However, perinatal mortality can only be reduced to zero if Rh erythroblastosis can be eradicated by prevention of Rh isoimmunization. Although prevention of Rh immunization by Rh immune globulin prophylaxis is now a reality, it does not appear that Rh immunization will be completely prevented with a single postdelivery injection. Antenatal treatment plus screening by the Kleihauer technique for massive transplacental hemorrhage may be necessary before complete suppression can be achieved. Low protein Rh immune globulin, and ultimately column-produced, very low protein, highly purified Rh immune globulin for intravenous use may prove to be the safest, most economical, and effective material for Rh prevention and total eradication of Rh erythroblastosis fetalis.

Amniocentesis↗

PubMedDate not supplied

Intracranial hemorrhage in neonates with erythroblastosis fetalis: sonographic and CT findings.

Cranial sonography revealed cerebral hemorrhage in three of seven neonates with erythroblastosis fetalis. Among the three infants with hemorrhage, one was 28 weeks gestational age and experienced germinal matrix hemorrhage with ventricular extension, a finding typical of cerebroventricular hemorrhage in the premature population. The other two infants with intracranial hemorrhage were more gestationally mature, and extensive intraparenchymal cerebral hemorrhages were found at sonography. These hematomas were peripheral in location and one was multifocal. Computed tomography (CT) further revealed hemorrhages in both neonates to be multifocal and in close proximity to the pia-arachnoid. In one case, the hemorrhage appeared to extend centripetally and rupture into the ventricular system. The high incidence, severity, and unusual appearance of intracranial hemorrhages in neonates with erythroblastosis fetalis has not been previously emphasized in the radiologic literature. In severe cases, children with erythroblastosis fetalis should be closely observed for intracranial hemorrhage by either sonography or CT, regardless of gestational age.

Cerebral Hemorrhage↗

PubMed1983

Site-specific mutagenesis of avian erythroblastosis virus: erb-B is required for oncogenicity.

Avian erythroblastosis virus (AEV) induces both erythroblastosis and fibrosarcomas in susceptible birds. Two domains within its replication-defective genome, erb-A and erb-B, have been implicated in AEV-mediated oncogenesis. An efficient transfection system for generating infectious, transforming virus from molecular clones of AEV and RAV-1 (helper virus) was combined with the techniques of site-specific mutagenesis to investigate the contribution of erb-B to the two forms of oncogenesis induced by AEV. Deletion and frameshift mutations were constructed in the erb-B locus of cloned AEV DNA in vitro. Infectious retroviruses harboring these mutations were recovered and their ability to transform fibroblasts in vitro or induce erythroleukemia in vivo was assessed. The presence of mutant viral genomes in chick embryo fibroblasts or erythroblasts of infected birds was confirmed by suitable biochemical analyses. Expression of viral genes in cells infected with AEV mutants was examined by immunoprecipitation with antisera to erb-A and erb-B proteins. It was found that the product of erb-B is necessary for transformation of fibroblasts and induction of erythroblastosis by AEV, although a small portion of this protein at the carboxy terminus is dispensable.

Alpharetrovirus↗

PubMed1979

Mutant avian erythroblastosis virus with restricted target cell specificity.

Avian erythroblastosis virus (AEV) induces a fatal erythroblastosis within 2 weeks of intravenous injection in chicks in virtually 100% of cases. In chicks injected intramuscularly, sarcomas frequently develop at the site of injection before the animals die from erythroblastosis. In vitro, AEV transforms both erythroblasts, derived from bone marrow cultures, and fibroblasts. These effects have been shown to be a general property of AEV and not of separate leukaemia- and sarcoma-inducing forms of the virus. AEV is defective for replication and can be propagated only in the prewence of helper virus. Its transformation specificity is independent of the helper virus used. It is not clear whether AEV has two different genes controlling transformation of the two types of target cell or whether it has only one gene coding for both. To investigate this question, we looked for mutants of AEV unable to transform one of the two types of target cell. We now describe such a mutant, which is defective for erythroblast transformation but which can still transform fibroblasts.

Alpharetrovirus↗

PubMed1984

Cellular homologs of the avian erythroblastosis virus erb-A and erb-B genes are syntenic in mouse but asyntenic in man.

Avian erythroblastosis virus, a retrovirus that causes erythroblastosis and sarcomas in infected birds, possesses two host cell-derived genes [viral (v) erb-A and erb-B]. Although v-erb-B seems to be responsible for oncogenic transformation, v-erb-A might have an enhancing effect on transformation. In chickens, the natural host for avian erythroblastosis virus, cellular (c) erb-A and erb-B genes appear to be unlinked, but their chromosomal locations in other species are unknown. To ascertain the chromosomal location of c-erb genes in man and mouse, we analyzed interspecies somatic cell and microcell hybrids by Southern filter hybridization techniques using specific v-erb-A and v-erb-B probes. We found c-erb-A sequences on human chromosome 17 (17p11----qter) and located c-erb-B on human chromosome 7 (7pter----q22). In contrast, both c-erb-A and c-erb-B reside on mouse chromosome 11.

Alpharetrovirus↗

PubMed1980

Transfection by DNAs of avian erythroblastosis virus and avian myelocytomatosis virus strain MC29.

Chicken embryo fibroblasts and NIH 3T3 mouse cells were transformable by DNAs of chicken cells infected with avian myelocytomatosis virus strain MC29 or with avian erythroblastosis virus. Transfection of chicken cells appeared to require replication of MC29 or avian erythroblastosis virus in the presence of a nontransforming helper virus. In contrast, NIH 3T3 cells transformed by MC29 or avian erythroblastosis virus DNA contained only replication-defective transforming virus genomes.

Alpharetrovirus↗

PubMed1990

Disproportionate septal hypertrophy associated with erythroblastosis fetalis.

We retrospectively reviewed clinical and echocardiographic data on 10 newborns with erythroblastosis fetalis who were admitted to our nurseries between 1984 and 1988 and who required a double-volume exchange transfusion and neonatal intensive care. Echocardiograms were performed in the first 48 hours of life. In 5 patients, disproportionate septal hypertrophy was demonstrated; 1 additional patient had biventricular hypertrophy with a thickened septum but not disproportionate septal hypertrophy. The mean septal: left ventricular free-wall ratio for the group (n = 10) was 1.37. No correlation was apparent between the occurrence of disproportionate septal hypertrophy and newborn glucose, bilirubin, or hematocrit values. When analyzed separately, the 4 patients who did not receive intrauterine blood transfusions had a ratio of 1.73 +/- 0.21 (mean +/- SEM); this was significantly greater than the ratio in the 6 patients who were transfused in utero (1.13 +/- 0.24). In patients who underwent transfusions, there was no correlation between the number of transfusions and the septal:left ventricular ratio. This study reports a significant but previously unrecognized cardiac hypertrophy with disproportionate septal hypertrophy in patients with erythroblastosis fetalis. Our data suggest a sparing effect of intrauterine fetal transfusions. The mechanism by which these transfusions may affect the hypertrophic development of the myocardium remains to be determined.

Cardiomyopathy, Hypertrophic↗

PubMed1999

Treatment of fetal erythroblastosis by intravascular transfusions: outcome at 6 years.

OBJECTIVE: To assess 6 years' neurologic outcome of a complete cohort of survivors of intrauterine intravascular transfusions. METHODS: From January 1986 to December 1991, 136 intravascular transfusions were performed in 43 fetuses presenting with signs of severe erythroblastosis. Before the initial transfusion, 11 of 43 fetuses had some degree of hydrops fetalis, and hemoglobin values ranged between 1.5 and 10.7 g/dL. Neurologic outcome of a complete cohort of 35 long-time survivors was assessed for up to 6 years by reviewing the hospital charts and questionnaires sent to the family physicians or pediatricians. RESULTS: Long-time follow-up was available in all survivors with hydrops at initial transfusion (seven of seven) and in 23 of 28 survivors without hydrops. Only one of 35 survivors had mild psychomotoric disabilities up to 1 year of age, but was free of sensorineural problems on further examination. In a second case, delayed speech development was observed. Fetuses presenting with hydrops fetalis before initial transfusion tended to have a higher perinatal mortality and had a significantly higher rate of preterm delivery (P = .03). However, moderate or severe neurologic impairment was never observed, even when severe cases with hydrops fetalis or extremely low hemoglobin levels were included. CONCLUSION: Treatment of severe fetal erythroblastosis by intrauterine intravascular transfusions is associated with a favorable neurologic long-time outcome.

Blood Group Antigens↗

PubMedDate not supplied

Care of the neonate with erythroblastosis fetalis.

Erythroblastosis fetalis, hemolytic disease of the newborn, occurs when an isoimmunized mother produces antibodies that cross the placenta and cause hemolysis of fetal red blood cells. This hemolysis can be accompanied by severe anemia, ascites, pleural and pericardial effusions, congestive heart failure, and neurological damage with resultant perinatal mortality. Rh isoimmunization in pregnancy still occurs in spite of the advent of Rh immune globulin. This article describes the complex management and nursing implications associated with caring for the neonate with erythroblastosis fetalis.

Anemia, Hemolytic↗

PubMed1978

Haemorrhagic infarction of the myocardium in a newborn with haemoglobin H disease and erythroblastosis.

Extensive haemorrhagic myocardial infarction developed in a newborn, apparently as a result of anoxia due to erythroblastosis fetalis, associated with haemoglobin H disease. Acute massive myocardial infarction in the neonatal period is rare and usually is associated with congenital malformation of the heart or its blood supply. Neonatal myocardial infarction in the anatomically normal heart with normal coronary vessels, has been described in only 8 patients (1). The communication describes a newborn with acute haemorrhagic myocardial infarction due to anoxia believed to be caused by the combined effect of erythroblastosis fetalis and haemoglobin H disease.

Erythroblastosis, Fetal↗

PubMedDate not supplied

Erythroblastosis fetalis produced by Kell immunization: dental findings.

Erythroblastosis fetalis is a severe hemolytic disease in the newborn that originates in utero because of a maternal-fetal blood incompatibility. An unusual case of erythroblastosis fetalis caused by an irregular antibody of the Kell blood group is presented. The dental findings are compared to those found with Rh(D) incompatibility.

Dental Enamel Hypoplasia↗

PubMed1989

Nursing care of the infant with erythroblastosis fetalis.

Care of the infant with erythroblastosis fetalis is most challenging for the neonatal intensive care nurse. The physiological changes that occur in utero continue to present at birth. The pathology and clinical manifestations, medical treatment, and nursing management of the infant with erythroblastosis fetalis are discussed to assist neonatal intensive care nurses in providing quality care.

Erythroblastosis, Fetal↗

PubMed1987

Cardiac output in a fetus with erythroblastosis fetalis: assessment using pulsed Doppler.

Pulsed Doppler studies of left and right ventricular outputs were obtained over time in a hydropic fetus with erythroblastosis fetalis. Despite severe anemia, cardiac outputs were within the normal range and remained normal after in utero percutaneous intravascular transfusions, which reversed the hydrops. The measurement of cardiac output in utero provides direct evidence that high-output failure due to anemia is not the mechanism for hydrops in erythroblastosis fetalis.

Adult↗

PubMed1985

[Rhesus erythroblastosis, monitoring and treatment].

From 1975-1984 92 pregnancies with suspicion of a morbus hemolyticus fetalis were monitored at the University Hospital of Freiburg, Department of Obstetrics and Gynecology. Most of the patients had antibodies against the rhesusfactor D. Amniocentesis was carried out regularly; the bilirubin level and protein content of the amniotic fluid were measured using chemical methods and the bilirubin/protein ratio was determined. The results obtained correlated well with the values of spectrophotometrically measured bilirubin, which reliably indicated the severity of the hemolytic disease. A serious erythroblastosis was observed in 17 cases. Four children died before any treatment was initiated. In 13 children 37 intrauterine transfusions (IUT) were performed. The survival rate of the children with IUT's was 69%, in nonhydropic children it was 82%. The mortality risk of the IUT was low. Children with IUT's often showed complications in the perinatal period, which were due to the premature birth and the erythroblastosis.

Amniocentesis↗

PubMed1977

[Treatment of severe Rhesus erythroblastosis].

Report about the management of cases of severe Rhesus erythroblastosis. One case is specially discussed because of it's actuality. This was a patient with severe Rh-sensitization (OOD at 450 mm from the beginning of the 30th week of gestation in zone III according to Liley). Because of the haemolytic disease and the chronic fetal distress the Caesarean section was already performed in the 32nd week of gestation after Betamethason treatment of the mother. The Lecithin-Sphingomyelin (L/S) ratio in the amniotic fluid as a criterium of fetal lung maturity raised almost twicefold (from 0.9 to 1.6) after Cortison treatment. The intensive care (assisted ventilation with PEEP, correction of the acidosis and transfusion of packed red cells) of the severely anaemic (Hb 3.5 g%, Hk 15 vol.%) and hydropic newborn was already started in the delivery room. The newborn developed no RDS and was discharged healthy. With reference to this and other cases the management of severe Rh-sensitization before the 34th week of gestation is discussed. Premature infants are mainly susceptable to the development of a Respiratory Distress syndrome (RDS). After antepartum Cortison treatment for prevention of an RDS the date of confinement should be arranged earlier. The value of an early Caesarian section after antepartum Glucocorticoid treatment as compared to the application of intrauterine transfusions in cases of severe erythroblastosis is discussed. It is also reported about recent methods of treatment of severe conditions of hydrops fetalis.

Austria↗