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PubMed1992

Failure of microchromatographic measurement of fetal hemoglobin in beta zero thalassemia-hereditary persistence of fetal hemoglobin.

We report microchromatographic measurement of fetal hemoglobin (HbF) proportions in a 36-year-old African-American multigravida woman. At 34 weeks she delivered a 630-g male infant who subsequently did well. Hemoglobin electrophoresis of the hemolysate revealed nearly 100% HbF without HbA, an extremely unusual naturally occurring sample. Family studies revealed a combination of hereditary persistence of fetal hemoglobin (HPFH) and beta zero-thalassemia minor. Southern blot technique confirmed heterozygous alpha 2 thalassemia and HPFH but failed to identify the beta thalassemic lesion. The absence of HbA and the very high amounts of HbF led us to measure HbF by several methods to confirm the accuracy of microchromatography of HbF at values approaching 100%. HPLC revealed a 14% F1 suggestive of microchromatographic underestimation due to glycated HbF. We conclude that cation-exchange microchromatography and the Betke method of alkali denaturation underestimate HbF values as they approach 100% and do not recommend these procedures in this rare situation.

Adult↗
PubMed1982

Mouse hemoglobin during gestation. Absence of fetal hemoglobin.

A "fetal hemoglobin' has been reported to exist during mouse gestation, Investigations using CMC chromatography, starch gel electrophoresis or isoelectric focusing have shown a hemoglobin band from fetal tissues, and blood was obtained which was different from the adult hemoglobin and designated a "fetal hemoglobin'. In the current study isoelectric focusing was used to study the hemoglobins existing in the tissues and blood during fetal and neonatal development and the results suggest there is no "fetal hemoglobin' present during gestation. It appears that the hemoglobin designated as "fetal' in our laboratory was a methemoglobin formed by an incomplete reaction of KCN with the hemoglobin. The additional hemoglobin bands which were obtained from fetal liver or neonatal spleen tissues appeared to be a modified adult hemoglobin.

Animals↗
PubMed1979

On the chromatographic heterogeneity of human fetal hemoglobin.

Minor fetal hemoglobins in red cell hemolysates of newborn and adults with elevated levels of Hb F have been separated and quantitated by Biorex 70 column chromatography. In addition to Hb F1, other minor hemoglobin zones eluting before F1, pre-F1, and after F1, post-f1 have been observed. The relative amounts of the two pre-F1 zones and F1 are higher in the red cells of adults with 97--100% Hb F (homozygous hereditary persistence of fetal hemoglobin, homozygous deltabeta-thalassemia and homozygous beta0-thalassemia) than in the red cells of an adult with homozygous beta+-thalassemia with 66% Hb F, a child with a trisomy-D-13 having 38% Hb F, and in two newborn. Hb F was glycosylated in vitro with [14C]glucose or [14C] glucose 6-phosphate, and was acetylated using chicken reticulocyte lysate or a crude acetyltransferase preparation isolated from the same lysate with [14C]acetyl-CoA as substrate. Chromatographic analyses indicated that the Hb F1 zone can be formed both by glycosylation and acetylation of Hb F, and that pre-F1 zones can be products of the reaction of Hb F with phosphorylated glycolytic intermediates. Biosynthesis of minor hemoglobins in reticulocytes was studied with [14C]leucine in the presence and absence of cycloheximide and by pulse-chase. The resulting data indicate that Hb F1 synthesis is dependent upon Hb F synthesis and that the posttranslational modification may take place at an early stage in Hb F synthesis.

Acetylation↗
PubMed1980

Cellular mechanisms for increased fetal hemoglobin production in culture. Evidence for continuous commitment to fetal hemoglobin production during burst formation.

Using microscopic immunodiffusion assays and microdensitometric analysis of pericellular immunoprecipitate, the percentage of nucleated erythrocytes containing fetal hemoglobin (FNRBC) and the mean picograms of fetal or adult hemoglobin per nucleated erythrocyte (picograms HbF/NRBC, picograms HbA/NRBC) were assayed in 14-d-old colonies (bursts) derived from peripheral blood erythroid progenitors. In the peripheral blood of 11 normal adults only 2.2+/-0.5% (mean+/-SE) erythrocytes contained HbF whereas pooled bursts from the same subjects revealed a 13-fold increase in the percentage of FNRBC (29.6+/-3.9%). In culture both the picograms HbF/NRBC (5.2+/-0.4) and the picograms HbA/NRBC (27.7+/-1.5) are increased approximately 20% above the mean in vivo levels in NRBC from normal bone marrow aspirates. Analysis of each of 58 bursts from one subject demonstrated that FNRBC are present in all bursts and range from 5.0 to 95.0% of the total NRBC per burst. The percent FNRBC in each burst was neither correlated with picograms HbF/NRBC per burst nor with picograms HbA/NRBC per burst. Individual subcolonies from one burst in each of two subjects demonstrated between 3 and 81% FNRBC. These findings indicate that first, the increase in HbF production in culture is primarily due to increased production of the number of cells containing HbF, not to increased picograms HbF/NRBC. Second, all 14-d bursts contain some FNRBC. Third, just as seen in vivo, the picograms HbF/cell and the number of cells that contain HbF are independently regulated in culture. Fourth, commitment to produce HbF in vitro continues after subcolony formation in 14-d-old bursts. Augmentation of HbF production in culture therefore closely resembles that seen in acute erythroid stimulation in vivo.

Adult↗
PubMed1990

Hereditary persistence of fetal hemoglobin presenting as fetal-maternal hemorrhage.

This report describes a case of hereditary persistence of fetal hemoglobin (HPFH) presenting initially as a marginal placental abruption in a primiparous woman at 27 weeks gestation. Persistent but erratic elevation of percent hemoglobin F positive cells, as determined by a modified Kleihauer-Betke method, complicated the remainder of her pregnancy. The clinical impression of placental abruption with possible extension could not be documented by ultrasound or examination of the placenta at delivery. Hemoglobin electrophoresis followed by quantitative fetal hemoglobin first suggested the diagnosis of HPFH, which was confirmed seven months postpartum. Furthermore, the magnitude of percent positive F-cells could be profoundly altered by subtle changes in pH of the acid elution reagent. This case demonstrates that positive acid elution tests for maternal-fetal transfusion may be caused by elevated maternal hemoglobin F. Erratic results, elevated quantitative hemoglobin-F and sensitivity to reagent pH should alert the pathologist to this diagnosis and alter clinical management.

Diagnosis, Differential↗
PubMed1986

Differential prooxidative effect of adult and fetal hemoglobin.

Human fetal hemoglobin assayed in a peroxidizing system shows an increased prooxidative effect when compared to human adult hemoglobin. This effect is related only to the oxyhemoglobin form since both fetal and adult methemoglobins did not show any prooxidative effect. The prooxidative effect of the oxyhemoglobin form is ascribed to its increased sensitivity to form superoxide free radicals when transformed to the methemoglobin form. It is proposed that the structure of the heme pocket of fetal oxyhemoglobin enhances free radical release when compared to adult oxyhemoglobin. This difference may be important in some hematological disorders presented by the newborn.

Female↗
PubMed2005

Role of intergenic human gamma-delta-globin sequences in human hemoglobin switching and reactivation of fetal hemoglobin in adult erythroid cells.

The details of the molecular events regulating normal human hemoglobin switching and reactivation of fetal hemoglobin in adult hematopoietic cells are unclear. The potential role of sequences between the human gamma- and delta-globin genes (intergenic gamma-delta sequences) in this process has been in question until the recent finding that two patients homozygous for the Corfu deletion, involving the loss of 7.2 kb of the intergenic gamma-delta region upstream of the delta gene, have 88% and 90% fetal hemoglobin, only mild anemia, and no transfusion requirements. These results provide the first strong evidence in humans that the gamma-delta intergenic sequences alone have a role in the reactivation of fetal hemoglobin in adult-type cells, and perhaps are involved in normal hemoglobin switching as well. The polypyrimidine (PYR) complex is a hematopoietic cell-specific and stage-specific chromatin remodeling complex that binds upstream of the human delta-globin gene within the Corfu deletion. Deletion of the PYR binding site has been shown to delay human gamma-to-beta globin switching. The PYR complex is present in adult human hematopoietic cells and absent in fetal-embryonic cells: properties of a globin-switching complex. Taken together, the data from patients with the Corfu deletion and the PYR complex results suggest that intergenic gamma-delta sequences are involved in human gamma-to-beta globin switching and reactivation of fetal hemoglobin in adult cells.

Adult↗
PubMed1994

Hypoxemia and increased fetal hemoglobin synthesis.

Fetal hemoglobin (HbF) synthesis in children with congenital cyanotic heart disease was compared that in normal children. Children with hypoxemia had higher levels of hemoglobin, total HbF, and HbF synthesis. In these children there was also an inverse correlation between HbF synthesis and oxygen content, as well as between HbF synthesis and hemoglobin concentration. Thus hypoxemia increases HbF synthesis.

Child↗
PubMed2003

A signaling mechanism for growth-related expression of fetal hemoglobin.

Increases in fetal hemoglobin have been identified after birth in several clinical settings associated with stressed or malignant erythropoiesis. To better understand the relationship between the expression of this fetal protein and growth, donated human erythroid progenitor cells were cultured in the presence of erythropoietin (EPO) plus the growth-modifying cytokine stem cell factor (SCF), and several growth-related signaling pathways were interrogated. Only the MEK1/2 inhibitor (PD98059) demonstrated significant effects on fetal hemoglobin. In the absence of PD98059, levels of fetal hemoglobin averaged 27.4% +/- 7.9% in EPO+SCF compared with 1.26% +/- 1.7% in EPO alone (P =.02). A linear dose response in levels of fetal hemoglobin to PD98059 was detected (0.16 microM = 27.13%, 0.8 microM = 19.6%, 4 microM = 12.2%, 20 microM = 1.54%). Western blot analyses revealed that SCF was required for phosphorylation of MEK and p44MAPK in this setting, and quantitative polymerase chain reaction demonstrated a significant increase in gamma-globin mRNA. Particular perturbations of growth-related signaling may also function to activate tissue-specific genes normally expressed during fetal development. This concept may be relevant for the development of new treatment rationales for beta hemoglobinopathies.

Antigens, CD34↗
PubMed1976

Oxygen equilibrium characteristics of adult and fetal hemoglobin of Japanese monkey (Macaca fuscata).

Adult hemoglobin and fetal hemoglobin were obtained from Japanese monkey (Macaca fuscata) and their oxygen equilibrium characteristics were studied. (1) The oxygen affinity of fetal hemoglobin was higher than that of adult hemoglobin both in the presence and absence of 2,3-diphosphoglycerate. The presence of diphosphoglycerate lowers the oxygen affinity of adult hemoglobin much greater than does that of HbF and the diphosphoglycerate levels of red cells of adult and newborn monkeys are about the same. (2) The intensity of the Bohr effect, as expressed by -deltalogP50/deltapH, at pH 7.4 was in the order of fetal hemoglobin-diphosphoglycerate greater than adult hemoglobin-diphosphoglycerate greater than fetal hemoglobin greater than adult hemoglobin.

Animals↗
PubMed1984

Fetal hemoglobin synthesis in erythroid cultures in hereditary persistence of fetal hemoglobin and beta o-thalassemia.

To determine whether hemoglobin regulation is normal in diseases affecting beta-globin gene expression, globin synthesis was examined in members of a family of a patient with hereditary persistence of fetal hemoglobin/beta o-thalassemia (HPFH/beta o-thal). The HPFH defect is the Ghanian type II, with a deletion from psi beta 1 to at least 20 kb 3' to beta. The beta o-thal gene has the haplotype II restriction enzyme pattern and has the beta 39 nonsense mutation. Erythroid colonies from blood BFU-E were radiolabeled, and globin chains were separated by gel electrophoresis. Colonies from the beta o-thal heterozygote had non-alpha/alpha ratios more balanced than in the reticulocytes. Gamma synthesis was 11% of non-alpha, which is higher than in reticulocytes, but within the range seen in normal adult colonies. Both HPFH heterozygotes produced 20%-30% gamma in erythroid colonies as well as reticulocytes, although non-alpha/alpha was more balanced in the colonies. The HPFH/beta o-thal patient produced 100% gamma in reticulocytes and in colonies. G gamma and gamma-synthetic proportions were not correlated at the individual colony level in the heterozygotes, suggesting that they had "adult" and not "fetal" progenitor cells. The Hb expression of these adult progenitors is presumably modulated normally in vivo in beta o-thal, but the normal decrease in HbF production does not occur in gene deletion HPFH.

Cells, Cultured↗