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Periodic acid Schiff (PAS) positivity in fetal erythroblasts.

The smears of 26 fetal blood samples taken for prenatal diagnosis were stained for the PAS reaction. Twelve out of 26 cases were subsequently found to be normal and 14 were found to be affected by different abnormalities; 83.4% of normal cases and 92.8% of abnormal cases showed moderate positivity to the PAS reaction. A higher percentage of PAS positive erythroblasts was found in the abnormal cases (p less than 0.01). Five cases with a percentage greater than 10% also showed a very high percentage of erythroblasts. No linear correlation was found between PAS positivity and erythroblastosis either in the normal or the abnormal cases, but pooling them resulted in a correlation between PAS positivity and erythroblastosis (r = 0.536; p less than 0.005). PAS positivity was most often diffuse and scored 1+. Since erythroblastosis is considered an indirect sign of fetal liver erythropoiesis, the hepatic environment and its peculiar hemopoiesis could play a role in producing a cohort of PAS positive erythroblasts.

Congenital Abnormalities↗
PubMed1980

[Problems of distinction of normal, arteficial and pathological structures in mature human placental villi. III. Morphometric studies in rhesus incompatibility (author's transl)].

Sections of human placental villi which were up to 80 micrometer in diameter were examined light microscopically and morphometrically. The villi were obtained by taking an aspiration biopsy of the attached placenta from 20 normal patients at term and from eight patients delivered at or before 37 weeks because of varying degrees of rhesus incompatibility. The distribution of three histological types of villi was determined. The intermediate villi from patients with erythroblastosis showed an increase in number and volume matching the severity of the disease. The intermediate villi also showed an increase in the amount of cytotrophoblasts, in the amount of materno-fetal diffusion surface area, in the thickness of syncytium, and in the number of Hofbauer cells. The terminal villi were not affected by erythroblastosis and the mature end villi showed a relative decrease in number. To obtain these results an optimal fixation technique was required.

Biopsy, Needle↗
PubMed1988

The reversal of hydrops fetalis by intravascular intrauterine transfusion in severe isoimmune fetal anemia.

Seventy-two intrauterine intravascular transfusions were performed on 26 patients with severe erythroblastosis fetalis. Twenty of the 26 fetuses were hydropic at the time of referral. Of the 20 hydropic fetuses, 16 (80%) survived. Hydrops was completely reversed in 13 of the 16 fetuses (81%). Total protein of less than 3 gm/dl, albumin less than 2 gm/dl, and a hematocrit level of less than 15% were associated with hydrops fetalis. After hydrops was reversed, total protein greater than 3 gm/dl, albumin greater than 2 gm/dl, along with a sustained hematocrit level of greater than 15%, were found. Only three neonates were born with minimal ascites, two of whom had had intraperitoneal transfusions before intravascular treatments. There were 21 survivors of the total group, giving an overall survival rate of 82%. There was one neonatal death from severe respiratory distress syndrome. Thirty-eight percent of the neonates did not require exchange transfusions in the newborn period. Intrauterine intravascular transfusions appear to be an effective mode of therapy in severe erythroblastosis fetalis and not only increase survival rates but also decrease neonatal morbidity and mortality.

Adult↗
PubMed1992

Fetal plasma erythropoietin concentration in red blood cell-isoimmunized pregnancies.

OBJECTIVE: The aim of this study was to investigate the relationship between fetal anemia, plasma erythropoietin concentration, and erythroblastosis in red blood cell-isoimmunized pregnancies. STUDY DESIGN: Fetal plasma erythropoietin concentration in umbilical venous blood samples from 68 red blood cell-isoimmunized pregnancies at 18 to 35 weeks' gestation was measured. Measurements were compared with the appropriate reference range with gestation, and associations with blood pH, erythroblast count, and hemoglobin concentration were examined. RESULTS: The mean fetal plasma erythropoietin concentration and erythroblast count in red blood cell-isoimmunized pregnancies were significantly increased only in severe fetal anemia (hemoglobin deficit > 7 gm/dl). Furthermore, some severely anemic fetuses were hydropic and acidemic. The degree of increase in plasma erythropoietin was significantly associated with both fetal acidemia and, more strongly, fetal erythroblastosis. CONCLUSION: These findings suggest that in fetuses from red blood cell-isoimmunized pregnancies the ability to prevent tissue hypoxia is present until anemia becomes severe, presumably by an increase in cardiac output and tissue perfusion. In severe anemia tissue hypoxia occurs, and the data indicate that fetuses respond by increasing erythropoietin production from at least 20 weeks' gestation. Furthermore, more accurate assessment of tissue oxygenation may be obtained by measuring the erythroblast count rather than the blood pH.

Anemia↗
PubMed1977

Influence of folic acid on birthweight and growth of the erythroblastotic infant. I. Birthweight.

The birthweights of 100 infants with erythroblastosis were carefully matched as to sex, gestational age, and parity with the birthweights of 200 control infants born during the same period. At all gestational ages the average birthweight of the affected infants was below that of the controls, the average reduction being 227 g. The more severely affected infants tended to be at a lower centile for birthweight than were the mildly affected ones. The relationships between maternal serum folate, cord blood serum folate, and centile for birthweight among affected infants were also studied. There was a strong correlation between low maternal serum folate and the incidence of small-for-dates babies among the affected infants. There was also a strong correlation between maternal and cord blood serum folate values. There was a lack of correlation between maternal serum folate and cord blood haemoglobin. It is concluded that infants with erythroblastosis are lighter than controls and that the reason for this may be a shortage of folic acid available for fetal growth.

Birth Weight↗
PubMed1976

Acetylcholinesterase activity in the erythrocytes of newborn infants with hyperbilirubinemia and asphyxia.

The authors measured erythrocyte acetylcholinesterase (ACHE) activity in 51 physiologic newborn infants, 35 pregnant women and 101 infants with hyperbilirubinemia caused by hemolytic diseases in the ABO and Rh systems, or of other origin (6 children). In total, 374 examinations of erythrocyte ACHE were performed. The normal values of physiologic infants during the first hours of life were 0.162 +/- 0.03, at the age of 3 days 0.104 +/- 0.04. The values in pregnant women were 0.206 +/- 0.07. The ACHE activity was considerably decreased in newborn infants affected by erythroblastosis-ABO, and its mean value, in the case of exsanguinotransfusion indicated by the Polácek scheme, amounted to 0.060 +/- 0.051. It raised after exsanguinotransfusion and was equal to the value of red cells transfused. In newborn infants affected by erythroblastosis-Rh, the value decreased in the cases complicated with asphyxia. Low values of ACHE are sometimes found in certain cases of IRDS or of septicemia. The determination of erythrocyte ACHE activity enables assessing the state of red blood cells.

Acetylcholinesterase↗
PubMed1994

Basal ganglia and thalamic calcification following intrauterine intravascular transfusion.

In recent years intrauterine intravascular transfusion has become the method of choice for the treatment of severe fetal erythroblastosis. Despite the association of the procedure with fetal complications such as bradycardia and overtransfusion, later neonatal neurological consequences have been only rarely reported. A case is described of a neonate who underwent repeated intrauterine intravascular transfusion for treatment of erythroblastosis and who later developed calcification in the thalamus and the basal ganglia. The possible pathogenetic mechanisms are discussed.

Basal Ganglia Diseases↗
PubMed1989

Acute Rh isoimmunization following abdominal trauma associated with late abruption placenta.

Acute exacerbation of Rh isoimmunization following abdominal trauma is a rare complication of pregnancy. The report describes a case of a mild case of erythroblastosis fetalis following maternal exposure to massive fetal-maternal transfusion, occurring after abdominal injury in motoring accident. Abruptio placenta 7 days following the trauma indicated emergency cesarean section, at which a severely affected fetus (erythroblastosis fetalis) was delivered. Late abruption--in the presence of no other risk factor--is considered to call for prolonged surveillance. Any abdominal trauma in a Rh-negative woman should alert one to the possibility of massive transplacental hemorrhage and augmentation of the maternal immune response.

Abdominal Injuries↗
PubMed1985

Kell alloimmunization, hemolytic disease of the newborn, and perinatal management.

The relative frequency of Kell (K:1) antibodies in pregnant women and a series of cases of Kell hemolytic disease of newborns were evaluated to review the strategy of managing potential disease. Among reproductive-aged women, Kell antibodies are about 60% as frequent as Rho (D) antibodies, but Kell disease is only 3% as common as Rho hemolytic disease. The reason is related to frequent transfusion-alloimmunization by Kell antigen and the low frequency of the K:1 gene among fathers. Kell hemolysis is severe in about half of cases. Amniocentesis is indicated in only a few circumstances: previous child with erythroblastosis fetalis, significant increase in maternal Coombs titer, presence of Kell antigen in the father, and after comparison of the relative risks of hemolytic disease and amniocentesis in each patient. Screening for Kell antigen before transfusing premenopausal women would be a means of avoiding erythroblastosis, but the rarity of severe disease does not justify this approach.

Adolescent↗
PubMed1975

[An unusual cause of sensitization against the Rh factor].

A case of Rh-sensitization is reported which was caused by the intra-muscular injection of blood from the patient's husband during the first pregnancy as treatment for hyperemesis gravidarum. The first infant showed a mild erythroblastosis. The second infant suffered of a severe erythroblastosis. The literature is reviewed and the causes of Rhesus sensitization are discussed.

Adult↗
PubMed1976

Hormone independent in vitro erythroid colony formation by mouse bone marrow cells.

B.M. cells of RLV-infected BALB/c mice can proliferate in methylcellulose in the absence of E.P., while normal B.M. cells cannot (12). Not only the more primitive BFU-E shows hormone-independency (18). This phenomenon is in favour of the view that the Rauscher virus induced erythroblastosis is a true neoplasia although transplantation experiments failed so far. The experiments in which transformation in vitro of B.M. cells by RLV is established (19) show that the CFU-E can serve as a target for the virus. Treatment of normal mice with CFA leads to a rapid increase in CFU-E in the bone marrow (18). Splenomegaly of RLV-infected mice is enhanced by CFA-treatment probably due to an increase in targets. Transfection with proviral DNA also can transform the CFU-E of BALB-c mice. This approach allows in vitro studies on the resistence of mouse strains to RLV in vitro. The studies are of interest for the human disease in two aspects. In vitro transformation assays are needed to study the oncogenic potential of putative human leukemia viruses. Furthermore the studies have yielded some new insight in the pathogenesis of virally induced erythroblastosis. This might serve as a model for e.g. acute myeloid leukemia in man.

Anemia↗
PubMed1985

Germ-line chromosomal localization of human C-Erb-A oncogene.

The human germ-line position of c-erb-A, the cellular counterpart of v-erb-A, has been determined by in situ molecular hybridization of a 3H-labeled c-onc gene probe to meiotic pachytene chromosomes. Both v-erb-A and v-erb-B are the v-onc genes that are associated with induction of sarcoma and erythroblastosis in chicken by the avian erythroblastosis virus, a rapidly transforming RNA tumor virus. The position of c-erb-A, determined here to be at 17q21.33-q22, is in the same region of chromosome 17 in which a nonrandom break occurs in the generation of t(15;17), a translocation commonly seen in acute promyelocytic leukemia.

Chromosome Mapping↗
PubMed1990

Biochemical basis of thyroid hormone action in the heart.

Thyroid hormone-induced changes in cardiac function have been recognized for over 150 years; however, the biochemical basis of triiodothyronine (T3) action in the heart has been intensely investigated only during the last two decades. T3-induced changes in cardiac function can result from direct or indirect T3 effects. Direct T3 effects result from T3 action in the heart itself and are mediated by nuclear or extranuclear mechanisms. Extranuclear T3 effects, which occur independent of nuclear T3 receptor binding and increases in protein synthesis, influence primarily the transport of amino acids, sugars, and calcium across the cell membrane. Nuclear T3 effects are mediated by the binding of T3 to specific nuclear receptor proteins, which results in increased transcription of T3-responsive cardiac genes. The T3 receptor is a member of the ligand-activated transcription factor family and is encoded by cellular erythroblastosis A (c-erb A) genes. The c-erb A protein is the cellular homologue of the viral erythroblastosis A (v-erb A) protein, which causes red cell leukemia in chickens. Currently, three T3-binding isoforms of the c-erb protein and two non-T3-binding nuclear proteins that exert positive and negative effects on T3-responsive cardiac genes have been identified. T3 increases the heart transcription of the myosin heavy chain (MHC) alpha gene and decreases the transcription of the MHC beta gene, leading to an increase of myosin V1 and a decrease in myosin V3 isoenzymes. Myosin V1, which is composed of two MHC alpha, has a higher myosin ATPase activity than myosin V3, which contains two MHC beta. The globular head of myosin V1, with its higher ATPase activity, leads to a more rapid movement of the globular head of myosin along the thin filament, resulting in an increased velocity of contraction. T3 also leads to an increase in the speed of diastolic relaxation, which is caused by the more efficient pumping of the calcium ATPase of the sarcoplasmic reticulum (SR). This T3 effect results from T3-induced increases in the level of the mRNA coding for the SR calcium ATPase protein, leading to an increased number of calcium ATPase pump units in the SR. Overall, thyroid hormone leads to an increase in ATP consumption in the heart. In addition, less chemical energy of ATP is used for contractile purposes and more of it goes toward heat production, which causes a decreased efficiency of the contractile process in the hyperthyroid heart.

Heart↗
PubMed1991

Elevated fetal plasma lactate produces polyhydramnios in the sheep.

In human fetuses with hemolytic diseases such as erythroblastosis fetalis, hydrops fetalis or polyhydramnios often develops. The mechanism(s) that produces these fluid imbalances is unknown, although lactate concentrations have been reported to be elevated in hydropic human fetuses with erythroblastosis. In this study we explored the role of lactate in producing fetal fluid imbalances. In seven near-term fetal sheep, we infused 5 mol/L sodium lactate at a rate of 10 mmol/hr for 3 days. Fetal plasma lactate rose by 6.0 +/- 1.0 (mean +/- SE) mmol/L above control. Fetal plasma osmolality and Na+ increased slightly, Cl- decreased, and bicarbonate rose in proportion to the Cl- decrease. Fetal renal lactate excretion was 1.1 +/- 0.3 mmol/hr while Na+ excretion was 10.6 +/- 1.9 mEq/hr. Fetal urine flow increased by 1.9 +/- 0.4 L/day and the urine remained hypotonic relative to fetal plasma throughout the infusion. Amniotic fluid lactate and Na+ rose during the infusion period and remained elevated during a 24-hour recovery period. Amniotic plus allantoic fluid volume at autopsy was 5.3 +/- 0.8 L compared with a normal of 0.5 to 1.0 L. There was little evidence of fetal edema. In summary, a moderate sustained elevation in fetal plasma lactate concentration appears to be a powerful osmotic agent for fetal accumulation of fluid from the maternal compartment over a period of days. This may be the primary mechanism whereby hydrops fetalis or polyhydramnios develops in severely anemic human fetuses.

Animals↗
PubMed1985

Transformation of erythroid cells by Rous sarcoma virus (RSV).

RSV transforms several nonhematopoietic cell types and as reported here also has the capacity to transform hematopoietic cells of the erythroid lineage. In vitro, the three RSV isolates tested induced erythroblast-like colonies in infected bone marrow cells that were distinguishable by size and cell arrangement from those induced by avian erythroblastosis virus (AEV). Also in contrast to AEV-transformed erythroblast cultures, isolated cell colonies induced by RSV required complex growth conditions in liquid medium similar to the in vitro conditions necessary for erythroblasts transformed by the acute leukemia virus E26. Temperature-shift experiments using temperature-sensitive (ts) NY68 RSV revealed that when grown at the nonpermissive temperature (42 degrees), mutant-infected cells became benzidine positive and partially differentiated into erythrocytes. Wild-type (wt) RSV-transformed cells did not undergo similar changes. However, both wt RSV-, and to a greater extent, ts RSV-transformed cultures at the permissive temperature (37 degrees) did contain populations of spontaneously differentiating erythroid cells signifying that the transforming activity of the virus did not fully arrest erythroid maturation. In addition, the RSV-transformed cells did express tyrosine kinase activity. When injected intravenously into birds, RSV induced an erythroblastosis-like disease similar to AEV but also caused fibrosarcomas and leg paralysis. These results show that RSV can alter the pattern of erythroid differentiation in a manner similar to, but distinct from, AEV and indicate that the tyrosine-specific pp60src kinase is involved in erythroid cell transformation. Since the src and erb B proteins share a significant amino acid homology, these data suggest that both may also share a common functional homology.

Alpharetrovirus↗
PubMed1982

Temperature-sensitive changes in the structure of globin chromatin in lines of red cell precursors transformed by ts-AEV.

Chicken bone marrow cells infected in vitro with a temperature-sensitive avian erythroblastosis virus fall to produce hemoglobin at 36 degrees C. When the product or products of the transforming gene (erb) are inactivated by a temperature shift to 42 degrees C in culture, several different cloned lines of cells infected with the temperature-sensitive avian erythroblastosis virus begin to make hemoglobin. This shift in phenotype correlates with an increase in hemoglobin mRNA specific to both adult and embryonic alpha and beta globin. The switch is accompanied by the acquisition of DNAase I-hypersensitive sites in one cell line (clone 2); however, a hypothetically more mature line (clone 3) has already acquired globin DNAase-hypersensitive sites but does not express hemoglobin until the temperature shift. Several (but not all) specific restriction sites associated with both the alpha and beta domains become unmethylated after the switch from 36 degrees C to 42 degrees C. The magnitude of these methylation switches is small compared with changes that occur in these genes during normal avian erythropoiesis. The results suggest that changes in chromosomal structure precede transcription and are not a consequence of transcription. Since (presumptive) precursor cloned lines can be established with some, but not all, of the structural properties of active globin chromatin, it is likely that many of these properties can be independently established and are not obligatorily related.

Alpharetrovirus↗
PubMed1990

Activation of cell growth by binding of Friend spleen focus-forming virus gp55 glycoprotein to the erythropoietin receptor.

Friend spleen focus-forming virus (SFFV) is a defective murine C-type retrovirus which causes a multi-stage erythroleukaemia in mice and erythroblastosis in bone marrow cultures. The SFFV env gene encodes a membrane glycoprotein, gp55, which is located on the cell surface and in the rough endoplasmic reticulum and is essential both for the induction of leukaemia in vivo and erythroblast proliferation in vitro. The mechanism by which gp55 causes increased erythroblastosis and ultimately leukaemia is unknown, but a reasonable suggestion is that gp55 can mimic the action of erythropoietin by binding to its receptor (Epo-R), thereby triggering prolonged proliferation of erythroid cells. To test this possibility, we have co-expressed gp55 and the murine Epo-R in a fibroblast cell line. We show here that in such cells, the SFFV glycoprotein binds directly to Epo-R. Furthermore, when an interleukin-3 (IL-3)-dependent lymphoid cell line was co-infected by SFFV and a virus that carries the Epo-R gene, it could grow without IL-3. We suggest that through direct binding to Epo-R, gp55 can stimulate the receptor and by-pass the normal requirement for Epo, causing prolonged proliferation of infected erythroid cells. This could be the first step of leukaemogenesis induced by Friend virus.

Animals↗
PubMed1999

Transformation by v-Myb.

The v-myb oncogene of the avian myeloblastosis virus (AMV) is unique among known oncogenes in that it causes only acute leukemia in animals and transforms only hematopoietic cells in culture. AMV was discovered in the 1930s as a virus that caused a disease in chickens that is similar to acute myelogenous leukemia in humans (Hall et al., 1941). This avian retrovirus played an important role in the history of cancer research for two reasons. First, AMV was used to demonstrate that all oncogenic viruses did not contain a single cancer-causing principle. In particular, although both Rous sarcoma virus (RSV) and AMV could replicate in cultures of either embryonic fibroblasts or hematopoietic cells, RSV could transform only fibroblasts whereas AMV could transform only hematopoietic cells (Baluda, 1963; Durban and Boettiger, 1981a). Second, chickens infected with AMV develop remarkably high white counts and therefore their peripheral blood contains remarkably large quantities of viral particles (Beard, 1963). For this reason AMV was often used as a prototypic retrovirus in order to study viral assembly and later to produce large amounts of reverse transcriptase for both research and commercial purposes. Following the discovery of the v-src oncogene of RSV and the demonstration that it arose from the normal c-src proto-oncogene, a number of acute leukemia viruses were analysed by similar techniques and found to also contain viral oncogenes of cellular origin (Roussel et al., 1979). In the case of AMV, it was shown that almost the entire retroviral env gene had been replaced by a sequence of cellular origin (initially called mab or amv, but later renamed v-myb) (Duesberg et al., 1980; Souza et al., 1980). Remarkably, sequences contained in this myb oncogene were shared between AMV and the avian E26 leukemia virus, but were not contained in any other acutely transforming retroviruses. In addition, the E26 virus contained a second sequence of cellular origin (ets) that was unique. The E26 leukemia virus was first described in the 1960s and causes an acute erythroblastosis in chickens, more reminiscent of the disease caused by avian erythroblastosis virus (AEV) than by AMV (Ivanov et al., 1962).

Animals↗