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PubMed1982

A quantitative study on the recovery of rat marrow erythropoietic cells after experimental suppression of erythropoiesis by repeated doses of cyclophosphamide.

Rat erythropoiesis was experimentally depressed by repeated doses of cyclophosphamide (CY) or by restriction of food consumption and the diagnostic value of quantitative haematology examinations of rat marrow erythroid morphology was evaluated. A slight depression of rat erythropoiesis (following a dose of 5 mg/kg/day) as well as a higher one (15 mg/kg/day) and the following recovery were determined by a quantitation of marrow erythroid morphology and by peripheral reticulocyte counts, yet a lower validity of peripheral erythrocyte and marrow relative erythroid cell counts was obtained; erythrocyte counts did not change even after a high depletion of marrow erythroid cells. The restriction of food consumption led to a similar depression of rat marrow erythropoiesis as that observed after CY administration. Our data may suggest that the quantitation of marrow erythroid morphology and peripheral reticulocyte counts are desirable in haematological examinations in preclinical safety evaluations performed on rats provided a new drug administered in repeated doses can be cytotoxic.

Animals↗
PubMed1984

Potential role of parathyroid hormone as an inhibitor of erythropoiesis in the anemia of renal failure.

Patients with varying degrees of renal insufficiency and patients with end-stage renal disease receiving continuous ambulatory peritoneal dialysis or regular hemodialysis therapy were studied to assess the independent relationship between serum parathyroid hormone concentration, and both severity of anemia and degree of serum inhibition of erythropoiesis. In patients with renal insufficiency not receiving dialysis, a significant curvilinear relationship between serum parathyroid hormone and creatinine concentrations was present (r = 65, p less than 0.001). Serum parathyroid hormone (by radioimmunoassay) also correlated with hematocrit level (r = -0.54, p less than 0.001) and degree of serum inhibition of in vitro erythroid progenitor cell growth in fetal mouse liver cultures (r = -0.45, p less than 0.001). However, multiple linear regression analysis revealed that after controlling for the effect of creatinine, m-parathyroid hormone is no longer a significant predictor of hematocrit level or erythroid progenitor cell growth. On the other hand, when a restricted population of patients with creatinine values between 1 and 4 mg/dl was analyzed separately, controlling for the effect of creatinine, there was still a significant correlation between hematocrit level and m-parathyroid hormone, but no such relationship was seen when participants with parathyroid hormone levels of less than or equal to 1000 pg/ml were analyzed. No significant correlation was seen between hematocrit level or inhibition of erythroid colony growth and serum parathyroid hormone concentrations in patients receiving either regular hemodialysis or continuous ambulatory peritoneal dialysis. In 13 patients given regular hemodialysis studied before and after parathyroidectomy, there was no significant change in serum erythropoietin (by radioimmunoassay) or serum inhibition of erythropoiesis, although hematocrit levels increased in six of the 13 patients. The 1-34 human parathyroid hormone, 1-84 bovine parathyroid hormone, and 1,25-dihydroxycholecalciferol had no effect on in vitro erythroid burst-forming unit growth. Parathyroid hormone (8 mu/ml) inhibited and 1,25-dihydroxycholecalciferol (4.0 ng/ml) stimulated erythroid colony-forming unit growth only in the absence of exogenous erythropoietin in culture. In summary, it was not possible to demonstrate a significant relationship between serum parathyroid hormone levels and anemia or inhibition of erythropoiesis in patients with uremia either before starting dialysis or after receiving long-term dialysis treatment.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1983

[Effect of acute viral hepatitis B on erythropoiesis in chronic hemodialyzed patients].

The influence of acute hepatitis B on erythropoiesis has been investigated in 30 chronic hemodialyzed patients (mean age 48.3 years; mean duration of dialysis until first demonstration of Hbs-antigen 6.5 months). After onset of hepatitis the mean hematocrit value increased significantly (p less than 0.005) and in 15 of the 30 dialysis patients this increase was more than 10% of the initial value. In these 15 patients the mean value of the hematocrit increased from 21.7 to 27.7%. This maximum value was observed after 4 months on average, and the favourable effect on erythropoiesis was observed for 7.8 months on average. The groups of patients with and without increase in hematocrit (more than 10% of the initial value) after hepatitis differed significantly (p less than 0.01) in extent of the observed increase in transaminases. The importance of extrarenal, hepatic erythropoietin production for the stimulation of erythropoiesis during hepatitis in chronic hemodialyzed patients is discussed.

Acute Disease↗
PubMed1984

Cyclic erythropoiesis in the S1/S1d mouse.

Previously we reported that when young adult female W/Wv mice are given 0.5 microCi strontium-89 per gram body weight IV, their hematocrit values oscillate from nadirs of 26% to zeniths of 42% with a periodicity of 16 days. We now report that a second strain of congenitally anemic female mice, the S1/ S1d , also exhibit large fluctuations in their hematocrit values following a dose of 0.5 microCi 89Sr/g body weight. The zeniths through which these mice cycled averaged 37% (range 35%-38%) and the nadirs averaged 13% (range 12%-14%). Reticulocytes fluctuated from highs averaging 40% (range 35%-45%) to lows that averaged 3% (range 1%-5%). The periodicity of cycling in these eight mice ranged from 16 to 19 days. The hematocrits of three out of five non-strontium-treated mice were found to cycle spontaneously in the absence of 89Sr-mediated hematopoietic insult, with nadirs averaging 22% and zeniths averaging 39%. Similarly, doses as small as 0.1 microCi 89Sr/g body weight coupled with antecedent phlebotomy induced cyclic erythropoiesis of substantial amplitude (average nadir 16% and average zenith of 39%). Splenectomy in the S1/ S1d mouse eliminates both spontaneous and 89Sr-induced cyclic erythropoiesis. If the spleen is removed prior to radiostrontium treatment, then cyclic erythropoiesis is not observed following a dose of 0.5 microCi 89Sr/g body weight.

Animals↗
PubMed1981

Inhibition of Friend virus (FVP)-induced murine erythropoiesis with prostaglandin (PGF2 alpha): potentiation and inhibition of erythropoietin and prevention of both with PGD2.

An erythropoietin-independent virus-induced murine erythroleukemia (FVP) is used to compare the effects of an erythropoiesis inhibitory factor (EIF) isolated from human urine with the effects of prostaglandin F2 alpha. The consequent inhibition of FVP-induced erythropoiesis suggests that EIF and PGF2 alpha have similar effects on the FVP-induced erythropoiesis in mice, and the effect of PGF2 alpha is indirect. The similarity of the actions of EIF and PGF2 alpha may indicate a potential role for prostaglandins in the physiological control of some types of erythrocytosis.

Animals↗
PubMed1981

Intracellular hemoglobin-a specific marker for erythroid cells in paraffin sections. An immunoperoxidase study of normal, megaloblastic, and dysplastic erythropoiesis, including erythroleukemia and other myeloproliferative disorders.

Intracellular hemoglobin represents an excellent marker for specific characterization of normal, megaloblastic, or dysplastic erythroid cells in paraffin sections. Using an immunoperoxidase indirect sandwich technique for detection of intracellular hemoglobin, erythroid cells at all stages of maturation were readily identified in bone marrow biopsies (58 specimens total) with a) normal erythropoiesis, b) megalobastic erythropoiesis, and c) various myeloproliferative disorders, including erythroleukemia. In other tissues (6 spleens, 2 lymph nodes, 1 liver) with extramedullary hematopoiesis, erythroid cells were similarly defined on the basis of this immunohistochemical method. Initial fixation in Zenker's-acetic acid solution (employed for bone marrow biopsies), B5 solution, or formalin, appeared equally effective in preserving the antigenicity of intracellular human hemoglobin. This sensitive and specific immunoperoxidase technique for erythroid cell characterization is particularly applicable to tissues with abnormal erythropoiesis, in which precise cell identification generally presents a diagnostic problem.

Bone Marrow↗
PubMed1982

Endotoxin-induced suppression of erythropoiesis: the role of erythropoietin and a heme synthesis stimulating factor.

The regulation of erythropoiesis is primarily controlled by erythropoietin (Ep). Recently, however, other factors that both stimulate and inhibit erythropoiesis have been reported. Using an in vitro liquid culture of bone marrow cells, a factor in normal mouse serum was demonstrated that markedly stimulated heme synthesis by marrow erythroid cells. In this study, the role of this heme synthesis stimulating factor (HSF) and Ep in the erythropoietic suppression caused by endotoxin administration to mice was examined. Although HSF levels did not alter appreciably after endotoxin injection, marrow erythroid cells from these animals became unresponsive to the factor. This could be reversed if Ep was added to the culture in vitro or if the hormone was injected into the mice 18 hr prior to harvesting the marrow. This marrow erythroid cell response is identical to that seen in animals in whom Ep levels are markedly reduced, such as that found in exhypoxic polycythemia, and suggest a decrease in the hormone following endotoxin administration. Additional studies demonstrated that when Ep was injected into mice 6 hr after endotoxin administration, an increase in femoral erythroid colony-forming units (CFU-E), proerythroblast number, and 59 Fe incorporation into femoral marrow cells could be demonstrated. These findings, together with the marrow erythroid cell response to the hormone, suggest that the mechanism for suppression of erythropoiesis after endotoxin injection is a reduction in the level of circulating Ep.

Animals↗
PubMed1981

[Megaloblastic erythropoiesis in stem cell leukemias].

Among 62 untreated patients with acute leucaemia the primary appearance of a megaloblastic erythropoiesis in the sternal marrow was found in 21 patients. Age and sex were without importance. Megaloblastic cell changes were found only in those patients, the leucaemia cells of whom were classified as particularly immature and were attributed to the type of stem cells or paraleucoblasts. The megaloblastic erythropoiesis might be an expression of a particularly severe neoplastic change and disturbance of differentiation of the pluripotent stem cell. The behaviour of the primarily already megaloblastically disturbed erythropoiesis in patients with leucaemia under cytostatic therapy is described on two observations of the course, in which cases the change of the findings in the bone-marrow is evident.

Adult↗
PubMed1981

A simple in vitro method for the assessment of ineffective erythropoiesis.

A simple in vitro method has been developed for the assessment of ineffective erythropoiesis by measuring the release of heme from a labeled cohort of erythroblasts in short-term suspension culture. The release of labeled heme was shown to correlate with the death of erythroblasts in culture determined by cell counting. Heme release was markedly increased in conditions where there is known to be excessive ineffective erythropoiesis, while in hematologic disorders where ineffective erythropoiesis is thought to be normal, heme release was within the normal range.

Adult↗
PubMed1980

Mathematical analysis of bone marrow erythropoiesis: application to C3H mouse data.

A mathematical analysis of normal bone marrow erythropoiesis is investigated under the following assumptions: there is no correlation for a cell between its position in cell cycle and its maturation level; the transition between proliferant and quiescent cells along the erythroid line occurs at a critical point in its cell cycle when a certain maturation level is reached; there is no net migration between the bone marrow and other hemopoietic tissues. Relationships are derived between model parameters (cell flows and cell number) and kinetic parameters, namely, the classic proliferation parameters (cell cycle time duration and growth fraction) and the maturation parameters (maturation time duration and amplification coefficient). This model, when applied to normal C3H mouse experimental data, provides a complete description of bone marrow erythropoiesis from pluripotent stem cells up to mature red blood cells. No differentiation from the pluripotent stem cells to the erythroid line is necessary to explain our experimental data. The number of erythroid-committed stem cells is estimated to be 3.4 x 10(5). Their maturation is characterized by eight divisions and a transit duration time of approximately 2.5 days. No ineffective erythropoiesis is found. Moreover, important red blood cell production is found in some other hemopoietic tissues. The 55Fe-labeling experiment of proerythroblasts is interpreted, assuming variability among cells for cell cycle and maturation time durations. For our experimental data, neglecting such a variability jeopardizes parameter estimations for proerythroblast population.

Animals↗
PubMed1980

[Erythropoietin-independent stimulation of erythropoiesis in mice infected with Mycoplasma arthritidis].

It was found previously that M. arthritidis stimulates the endogenous colony formation in sublethally irradiated mice. It was of interest to solve the mechanism of the phenomenon. An attempt was made to show that M. arthritidis promotes the restoration of erythropoiesis in plethoric mice. It is a well known fact that in plethoric mice, the synthesis of endogenous erythropoietin is inhibited as well as the macroscopic erythroid colony formation. It is assumed that early initiation of erythropoiesis in mycoplasma-infected plethoric mice occurs because of either mycoplasma-induced restoration of erythropoietin synthesis or mycoplasma-directed involvement of the precursor cells in further differentiation and proliferation. Use was made of the method of 24-hour 59Fe uptake by the blood and spleen of plethorized mice and of other standard procedures aimed at revealing the erythropoietin activity in plasma of M. arthritidis-infected mice. Repeated attempts to recover the increased erythropoietin synthesis invariably failed. Hence the mycoplasma-induced erythropoiesis in plethorized mice is probably erythropoietin-independent and is consequent on the direct action of mycoplasma on the committed precursor cells.

Animals↗
PubMed1981

Evidence that inhibition of erythropoiesis is important in the anemia of chronic renal failure.

Previous studies have documented that serum from patients with chronic renal failure is capable of inhibiting erythropoiesis in vitro. Few data, however, link this finding with the pathophysiology of the anemia of uremia. To study this, we correlated hematocrits from uremic patients with the degree to which serum from these patients inhibited erythropoiesis, using two different in vitro systems. We studied patients receiving hemodialysis and patients with varying degrees of uremia not receiving dialysis and did serial studies on patients in whom long-term hemodialysis was initiated. Study of patients with varying degrees of renal failure showed that levels of inhibitor developed and increased as renal failure worsened and the hematocrit level fell. Finally, we found a fall in inhibitor level in those patients who had an increase in hematocrit after long-term hemodialysis. We interpret these data as evidence that inhibition of erythropoiesis is involved in the anemia of chronic renal failure.

Anemia↗
PubMed1994

Serum erythropoietin and erythropoiesis in high- and low-fetal hemoglobin beta-thalassemia intermedia patients.

Clinical data suggest that in beta-thalassemia-intermedia patients, higher levels of circulating fetal hemoglobin (HbF) are associated with greater disease severity at comparable degrees of anemia. We assessed the influence of the amount of circulating HbF on serum erythropoietin (s-Epo) levels and on serum transferrin receptor, a measure of erythropoiesis, in 30 beta-thalassemia-intermedia patients. Twenty-four showed more than 40% HbF (21 of whom with beta (0)-thalassemia) and 6 presented lower HbF levels (beta(+)-thalassemia). The two groups of patients did not differ in age (15.3 v 19 years, respectively) or degree of anemia (Hb = 8.8 g/dL in both groups). Log (s-Epo) was correlated inversely with Hb (r = -0.47; P < .01), and directly with HbF (r = .55; P < .001). Multivariate regression analysis showed that Hb and HbF were independently correlated with s-Epo levels. High-HbF patients had greater s-Epo values at the same Hb level than low-HbF patients. Considering that iron-deficiency anemia control patients represented the predicted physiologic response of s-Epo to anemia, the observed/predicted s-Epo ratio in low-HbF thalassemic patients was no different from controls, but was increased in the high-HbF group. High-HbF patients also showed an expansion of erythropoiesis as much as four to nine times the normal value at the same Hb level as low-HbF patients. We conclude that HbF exerts an independent regulatory effect on erythropoietin production and erythropoiesis that is detectable only when HbF levels exceed 40%.

Adolescent↗
PubMed1994

Roles for integrin very late activation antigen-4 in stroma-dependent erythropoiesis.

Adhesion molecules are required for development of hematopoietic stem and progenitor cells in the respective hematopoietic microenvironments. We previously showed that development of the erythroid progenitor cells is dependent on their direct adhesion to the stroma cells established from the erythropoietic organs. In this stroma-dependent erythropoiesis, we examined the role of adhesion molecules in erythropoiesis by blocking antibodies. The development of the erythroid cells on stroma cells was inhibited by anti-very late activation antigen-4 (VLA-4 integrin) antibody, but not by anti-VLA-5 antibody, although the erythroid cells express both VLA-4 and VLA-5. Whereas high levels of expression of vascular cell adhesion molecule-1 (VCAM-1) and fibronectin, ligands for VLA-4, were detected in the stroma cells, the adhesion and development of the erythroid progenitor cells were partly inhibited by the blocking antibody against VCAM-1. VLA-5 and fibronectin could mediate adhesion of the erythroid progenitor cells to the stromal cells, but the adhesion itself may not be sufficient for the stroma-supported erythropoiesis. The stromal cells may support erythroid development by the adhesion through a new ligand molecule(s) for VLA-4 in addition to VCAM-1, and such collaborative interaction may provide adequate signaling for the erythroid progenitor cells in the erythropoietic microenvironment.

Animals↗
PubMed1994

Mutual inhibition of murine erythropoiesis and granulopoiesis during combined erythropoietin, granulocyte colony-stimulating factor, and stem cell factor administration: in vivo interactions and dose-response surfaces.

We investigated the in vivo effects of erythropoietin (EPO) on granulopoiesis and, conversely, the effect of granulocyte colony-stimulating factor (G-CSF) treatment on erythropoiesis. Recombinant human EPO at four different doses in combination with recombinant human G-CSF also at four different doses was simultaneously administered for 7 days to splenectomized mice. In total, 16 different combinations of growth factors were thus tested. G-CSF administration increased granulocyte production as expected, whereas immature colony-forming unit granulocyte-macrophage numbers were decreased. EPO analogously increased late erythroid cell numbers. Both EPO and G-CSF dose-dependently inhibited late cell stages of the opposite lineage, with EPO abrogating G-CSF-stimulated granulopoiesis and, conversely, G-CSF inhibiting EPO-stimulated erythropoiesis. In a subsequent experiment, we tested whether these lineage-competitive effects could be prevented by coadministering stem cell factor (SCF). In these three factor-treated mice, all granuloid and erythroid cell stages increased, thereby reducing the effect of the mutual inhibition. We conclude that EPO-stimulated erythropoiesis and G-CSF-stimulated granulopoiesis inhibited each other at a late level. Simultaneous SCF administration increased the input into both the erythroid and granuloid compartment and thereby compensated the mutual inhibition. This study shows that intricate dose-response relationships exist between various growth factors that should be carefully analyzed before combinations of these factors are used in humans.

Animals↗
PubMedDate not supplied

Modifications of erythropoiesis in myelodysplastic syndromes treated with recombinant erythropoietin as evaluated by soluble transferrin receptor, high fluorescence reticulocytes and hypochromic erythrocytes.

BACKGROUND: The aim of this study was to evaluate changes in erythropoiesis induced in vivo by recombinant erythropoietin (r-EPO) treatment in myelodysplastic syndromes (MDS), by means of some new, non invasive laboratory parameters. PATIENTS AND METHODS: Serum levels of soluble transferrin receptor (STR), a marker of total marrow erythroid activity, and automated detection of high fluorescence reticulocytes (HFR) and hypochromic erythrocytes (HE) (respectively, indexes of effective erythropoiesis and functional iron deficiency) were longitudinally measured in 25 MDS patients treated with r-EPO, and then correlated with conventional clinical and laboratory features. RESULTS: Stimulation of erythropoiesis was documented in 8 patients, whose serum STR levels showed a significant, early (within 16 days) increase during treatment with r-EPO. However, only 3 of these patients demonstrated a concomitant rise in HFR, and these were the only subjects who experienced a significant clinical response. Two of these patients also developed a functional iron deficiency while on treatment, as documented by an increase in HE, despite normal serum iron, transferrin saturation and even very high levels of ferritin. They needed iron supplementation to maintain the response to r-EPO. No variation in STR, HFR or HE occurred in the remaining 17 unresponsive patients during at least two months of treatment. Serum levels of thymidine kinase, as aspecific marker of cellular proliferative activity, paralleled those of STR. No correlation was found between STR, HFR or HE and serum levels of endogenous EPO, hemoglobin or transfusion requirements in MDS patients. CONCLUSIONS: These findings suggest that there is a heterogeneous and complex pattern of erythroid response in MDS patients treated with r-EPO. In addition, our results indicate that STR, HFR and HE may provide useful information for the clinical management of these patients.

Adolescent↗
PubMed1994

Erythropoiesis, but not thrombocytopoiesis, is affected by the presence of a large amount of subcutaneously implanted bone marrow.

The concept that megakaryocytopoiesis is regulated in part by the number of megakaryocytes themselves, separately from its regulation by the number of platelets, is referred to as autoregulation. Its occurrence has been implied from animal models that demonstrate compensated megakaryocytopenia. In that condition, normal platelet production can occur even though numbers of megakaryocytes are substantially reduced, and individual megakaryocytes exhibit changes consistent with their being stimulated. The present experiments were undertaken to determine whether the converse situation, namely suppression of megakaryocytopoiesis by an excess of megakaryocytes, could be created. The experimental model consisted of C57Bl mice in which as many as 10 isogeneic femurs were implanted subcutaneously 10 weeks before analysis. The implanted femurs contained hematopoietic marrow morphologically. They incorporated radioiron, but only about 40% as much as an equal number of normal femurs, so hematopoiesis did not regenerate to the full potential of the implanted marrows. After implantation of nine or 10 femurs, thrombocytopoiesis was normal as judged by platelet counts, mean platelet volumes, numbers of megakaryocytes in tibial marrow, and megakaryocyte sizes. Hematocrits were increased, but plasma erythropoietin levels were normal. The implants showed a 15- to 20-hour incorporation of radioiron of 9.4 +/- 0.5%. Iron incorporation into endogenous bones and spleen was reduced, demonstrating that erythropoiesis was redistributed. The total incorporation of iron into all hematopoietic tissue was slightly increased, but red-cell iron incorporation was normal, implying that there was more ineffective erythropoiesis than normal. Leukocyte counts, differentials, and tibial cellularity were normal. After implantation of three or six femurs, no abnormalities of hematopoiesis were detected, even though the implants incorporated iron in proportion to their number. Thus, erythropoiesis was adjusted by the excess of total marrow caused by nine or 10 subcutaneously implanted femurs. This is about the maximum of implanted marrow that is feasible with this model, and the failure to observe suppression of megakaryocytopoiesis may have been due to an inability to achieve a large enough number of megakaryocytes to elicit a detectable response. Alternatively, autoregulation of megakaryocytes may depend more on the marrow concentration of megakaryocytes than on the total body content.

Animals↗
PubMed1996

Defective iron supply for erythropoiesis and adequate endogenous erythropoietin production in the anemia associated with systemic-onset juvenile chronic arthritis.

Systemic-onset juvenile chronic arthritis (SoJCA) is associated with high levels of circulating interleukin-6 (IL-6) and is frequently complicated by severe microcytic anemia whose pathogenesis is unclear. Therefore, we studied 20 consecutive SoJCA patients with hemoglobin (Hb) levels <12 g/dL, evaluating erythroid progenitor proliferation, endogenous erythropoietin production, body iron status, and iron supply for erythropoiesis. Hb concentrations ranged from 6.5 to 11.9 g/dL. Hb level was directly related to mean corpuscular volume (r = .82, P < .001) and inversely related to circulating transferrin receptor (r = -.81, P < .001) suggesting that the severity of anemia was directly proportional to the degree of iron-deficient erythropoiesis. Serum ferritin ranged from 18 to 1,660 microgram/L and was unrelated to Hb level. Bone marrow iron stores wore markedly reduced in the three children investigated, and they also showed increased serum transferrin receptor and normal-to-high serum ferritin. All 20 patients had elevated IL-6 levels and normal in vitro growth of erythroid progenitors. Endogenous erythropoietin (epo) production was appropriate for the degree of anemia as judged by both the observed to predicted log (serum epo) ratio 10.95 +/- 0.12) and a comparison of the serum epo-Hb regression found in these subjects with that of thalassemia patients. Multiple regression analysis showed that serum transferrin receptor was the parameter most closely related to hemoglobin concentration: variation in circulating transferrin receptor explained 61% of the variation in Hb level (P < .001). In 10 severely anemic patients, amelioration of anemia following intravenous iron administration resulted in normalization of serum transferrin receptor. Defective iron supply to the erythron rather than blunted epo production is the major cause of the microcytic anemia associated with SoJCA. A true body-iron deficiency caused by decreased iron absorption likely complicates long-lasting inflammation in the most anemic children, and this can be recognized by high serum transferrin receptor levels. Although oral iron is of no benefit, intravenous iron saccharate is a safe and effective means for improving iron availability for erythropoiesis and correcting this anemia. Thus, while chronically high endogenous IL-6 levels do not appear to blunt epo production, they are probably responsible for the observed abnormalities in iron metabolism. Anemia of chronic disease encompasses a variety of anemic conditions whose peculiar features may specifically correlate with the type of cytokine(s) predominantly released.

Administration, Oral↗