Transplantation of Major ABO-Incompatible Bone Marrow Depleted of Red Cells by Hydroxyethyl Starch

Vox Sanguinis ◽  
1985 ◽  
Vol 48 (2) ◽  
pp. 89-104 ◽  
Author(s):  
Phyllis I. Warkentin ◽  
Joanne M. Hilden ◽  
John H. Kersey ◽  
Norma K.C. Ramsay ◽  
Jeffrey McCullough
Keyword(s):  
Bone Marrow ◽  
Hydroxyethyl Starch ◽  
Red Cells

Transplantation of Major ABO-Incompatible Bone Marrow Depleted of Red Cells by Hydroxyethyl Starch

Vox Sanguinis ◽  
1985 ◽  
Vol 48 (2) ◽  
pp. 89-104 ◽  
Author(s):  
Phyllis I. Warkentin ◽  
Joanne M. Hilden ◽  
John K. Kersey ◽  
Norma K.C. Ramsay ◽  
Jeffrey McCullough
Keyword(s):  
Bone Marrow ◽  
Hydroxyethyl Starch ◽  
Red Cells

scholarly journals Determinants of Erythrocyte Size in Chronic Liver Disease

Blood ◽  
1969 ◽  
Vol 34 (6) ◽  
pp. 739-746 ◽  
Author(s):  
THOMAS M. KILBRIDGE ◽  
PAUL HELLER
Keyword(s):  
Bone Marrow ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Peripheral Blood ◽  
Hepatic Cirrhosis ◽  
Alcoholic Cirrhosis ◽  
Clinical Findings ◽  
Red Cells ◽  
Red Cell ◽  
Cell Volumes

Abstract Serial determinations of red cell volumes were made with an electronic sizing device in 30 patients with hepatic cirrhosis. Variations in red cell volumes were correlated with other hematologic and clinical findings. The results of these studies suggest that volume macrocytosis in patients with alcoholic cirrhosis is either due to megaloblastosis of the bone marrow or to an accelerated influx of young red cells into the peripheral blood.

Hematologic Toxicity of High-Dose Iodine-131–Metaiodobenzylguanidine Therapy for Advanced Neuroblastoma

2004 ◽  
Vol 22 (12) ◽  
pp. 2452-2460 ◽  
Author(s):  
Steven G. DuBois ◽  
Julia Messina ◽  
John M. Maris ◽  
John Huberty ◽  
David V. Glidden ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Radiation Dose ◽  
Red Cells ◽  
Whole Body ◽  
High Dose ◽  
Hematologic Toxicity ◽  
Severe Thrombocytopenia ◽  
Hematopoietic Stem ◽  
Iodine 131 ◽  
Mibg Therapy

Purpose Iodine-131–metaiodobenzylguanidine (131I-MIBG) has been shown to be active against refractory neuroblastoma. The primary toxicity of 131I-MIBG is myelosuppression, which might necessitate autologous hematopoietic stem-cell transplantation (AHSCT). The goal of this study was to determine risk factors for myelosuppression and the need for AHSCT after 131I-MIBG treatment. Patients and Methods Fifty-three patients with refractory or relapsed neuroblastoma were treated with 18 mCi/kg 131I-MIBG on a phase I/II protocol. The median whole-body radiation dose was 2.92 Gy. Results Almost all patients required at least one platelet (96%) or red cell (91%) transfusion and most patients (79%) developed neutropenia (< 0.5 × 103/μL). Patients reached platelet nadir earlier than neutrophil nadir (P < .0001). Earlier platelet nadir correlated with bone marrow tumor, more extensive bone involvement, higher whole-body radiation dose, and longer time from diagnosis to 131I-MIBG therapy (P ≤ .04). In patients who did not require AHSCT, bone marrow disease predicted longer periods of neutropenia and platelet transfusion dependence (P ≤ .03). Nineteen patients (36%) received AHSCT for prolonged myelosuppression. Of patients who received AHSCT, 100% recovered neutrophils, 73% recovered red cells, and 60% recovered platelets. Failure to recover red cells or platelets correlated with higher whole-body radiation dose (P ≤ .04). Conclusion These results demonstrate the substantial hematotoxicity associated with high-dose 131I-MIBG therapy, with severe thrombocytopenia an early and nearly universal finding. Bone marrow tumor at time of treatment was the most useful predictor of hematotoxicity, whereas whole-body radiation dose was the most useful predictor of failure to recover platelets after AHSCT.

scholarly journals CELLS INVOLVED IN THE IMMUNE RESPONSE

1969 ◽  
Vol 129 (4) ◽  
pp. 757-774 ◽  
Author(s):  
Nabih I. Abdou ◽  
Maxwell Richter
Keyword(s):  
Bone Marrow ◽  
Immune Response ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Bone Marrow Cells ◽  
Allogeneic Bone Marrow ◽  
Red Cells ◽  
Allogeneic Bone ◽  
Sheep Red Blood Cells ◽  
Sheep Red Cells

Irradiated rabbits given allogeneic bone marrow cells from normal adult donors responded to an injection of sheep red blood cells by forming circulating antibodies. Their spleen cells were also capable of forming many plaques using the hemolysis in gel technique, and were also capable of undergoing blastogenesis and mitosis and of incorporating tritiated thymidine upon exposure to the specific antigen in vitro. However, irradiated rabbits injected with allogeneic bone marrow obtained from rabbits injected with sheep red blood cells 24 hr prior to sacrifice (primed donors) were incapable of mounting an immune response after stimulation with sheep red cells. This loss of reactivity by the bone marrow from primed donors is specific for the antigen injected, since the immune response of the irradiated recipients to a non-cross-reacting antigen, the horse red blood cell, is unimpaired. Treatment of the bone marrow donors with high-titered specific antiserum to sheep red cells for 24 hr prior to sacrifice did not result in any diminished ability of their bone marrow cells to transfer antibody-forming capacity to sheep red blood cells. The significance of these results, with respect to the origin of the antigen-reactive and antibody-forming cells in the rabbit, is discussed.

scholarly journals The Effect of Anemic Anoxia on the Cellular Development of Nucleated Red Cells

Blood ◽  
1959 ◽  
Vol 14 (4) ◽  
pp. 386-398 ◽  
Author(s):  
ALLAN J. ERSLEV ◽  
Elva Ruiz
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Nitrogen Mustard ◽  
Mitotic Division ◽  
Red Cells ◽  
Red Cell ◽  
Cell Production ◽  
Cellular Development

Abstract The action of an anoxic stimulus on red cell production was studied in rabbits bled 20 ml./Kg., kept anemic for 20 hours and then reinfused with the previously removed blood. This 20-hour period of anemic anoxia was followed by a characteristic reticulocyte response, a response which was modified by nitrogen mustard or colchicine administered immediately after the 20-hour period of anemia, but was not influenced by anoxia or hyperoxia in the postanemic period. When mitotic division was arrested by colchicine during the 20-hour period of anemic anoxia, the onset of the reticulocyte response, though delayed by 1 to 2 days, was otherwise of characteristic magnitude. These observations indicate that (1) the anoxic stimulus operates in the bone marrow by accelerating the differentiation of stem cells into pronormoblasts, and that thereafter (2) the maturation and multiplication of differentiated nucleated red cells proceed at fixed rates independent of the anoxic stimulus.

scholarly journals Idiopathic Dyserythropoietic Jaundice

Blood ◽  
1964 ◽  
Vol 24 (1) ◽  
pp. 1-18 ◽  
Author(s):  
SIEGFRIED BERENDSOHN ◽  
JAMES LOWMAN ◽  
DOROTHY SUNDBERG ◽  
C. J. WATSON
Keyword(s):  
Bone Marrow ◽  
Life Span ◽  
Peripheral Blood ◽  
Red Cells ◽  
Ordinary Sense ◽  
Unique Form ◽  
Unconjugated Hyperbilirubinemia ◽  
Hemoglobin Synthesis ◽  
Plasma Iron ◽  
Normal Erythrocyte

Abstract 1. The term "dyserythropoietic jaundice" is used to designate a peculiar abnormality characterized by marked overproduction of bilirubin and associated with unconjugated hyperbilirubinemia and great excesses of fecal urobilinogen. Labeling with N15 glycine revealed that these excesses were mainly unrelated to destruction of mature circulating red cells, which had only a slightly shortened life span. 2. The hyperplastic, normoblastic bone marrow exhibited considerable phagocytosis of red cells and normoblasts and marked hemosiderosis with many iron-laden phagocytes. Siderocytes were relatively rare in the peripheral blood, which also exhibited consistent reticulocytosis, 3-10 per cent, but normal erythrocyte porphyrin concentrations. There was increased plasma iron turnover but decreased appearance of Fe59 in the circulating red cells. 3. The possibility is considered that there is a basic abnormality in hemoglobin synthesis in the normoblasts, with excessive production of hemoglobin or heme which is then converted to bilirubin either within the normoblast or after excretion into the blood. The observed phagocytosis of normoblasts and erythrocytes may be a secondary rather than basic disturbance of the disease. 4. This case appears to represent a unique form of chronic jaundice due to a remarkable overproduction of bilirubin without evidence of hemolysis in the ordinary sense. The extent to which this is related to intramedullary destruction of young red cells or to a basic abnormality in hemoglobin synthesis in the normoblasts, as above, cannot be determined. It is considered less likely that the overproduction is due to a true shunt—that is, bilirubin formation from porphyrin precursors. The marked dyserythropoiesis suggests that the overproduction of bilirubin was medullary rather than hepatic, although the latter is not excluded.

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