Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of ABO and Rhesus (D) blood groups was studied retrospectively in 40 patients with primary myelofibrosis (PMF). Only patients with a leukoerythroblastic peripheral blood, splenomegaly and marrow fibrosis in whom chronic myeloid leukemia and secondary myelofibrosis was absent were included in the study. In 14 patients (35%), PMF was preceded by another myeloproliferative disorder (polycythemia rubra vera, essential thrombocythemia or unclassified myeloproliferative disorder), while 26 patients (65%) represented agnogenic myeloid metaplasia (AMM). Comparison with Hospital and Irish blood group distribution showed a significant increase in blood group B (p less than 0.01) in PMF. This increase remained statistically significant for both the AMM and the non-AMM subgroup of PMF when each subgroup was considered separately. This finding supports previous suggestions that the various myeloproliferative disorders which proceed to myelofibrosis are a closely related group rather than a heterogeneous collection of diseases.
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PMID:Excess of blood group B in primary myelofibrosis. 311 Oct 93

Allogenic bone marrow transplantation was performed in a patient with chronic myelocytic leukemia (Ph+) in a stable phase. A 1,5-year recurrence-free period since the time of transplantation was observed. Transplantation features were as follows: incompatibility of the recipient and donor by ABO-antigens, the development of acute graft versus host disease and transient Ph-positivity.
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PMID:[A case of successful transplantation of allogeneic bone marrow in a patient with myelocytic leukemia]. 330 11

Between February 1971 and October 1980, 34 patients with leukemia or aplastic anemia received bone marrow transplants from HLA-identical siblings whose lymphocytes did not react in a mixed leukocyte culture. The donors of 10 patients were ABO-incompatible, and for five pairs the ABO incompatibility was major. Plasma exchanges followed by a red blood cell exchange transfusion reduced the anti-A titres to 1:4 or less in these patients. The ABO incompatibility had no adverse effect on the results of marrow transplantation. Twenty-two patients, including 16 of the 20 who received their transplant after Jan. 1, 1980, are still living. Seven of the 15 patients with acute leukemia have survived 89 to 466 days, and 4 of the 6 with chronic myelogenous leukemia (CML) have survived 117 to 545 days. Of the 13 patients with aplastic anemia, 11 are alive up to 8 years after transplantation. Marrow transplantation, when possible, is the treatment of choice for young patients with acute leukemia in remission and for patients with aplastic anemia. Marrow transplantation may also prove to be effective in patients with CML.
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PMID:Bone marrow transplantation for leukemia and aplastic anemia: management of ABO incompatibility. 703 2

The use of an ABO-incompatible donor for BMT after total body irradiation (TBI) has no adverse effect on engraftment, incidence of GVHD or survival when donor erythrocytes and plasma are depleted from the infused marrow. The outcome of ABO-incompatible BMT following a non-TBI-containing preparative regimen has not been as well studied. We therefore performed a retrospective review of consecutive patients undergoing allogeneic BMT for myeloid leukemia after treatment with high-dose busulfan and cyclophosphamide (BUCY) between January 1984 and January 1993. Of the 199 evaluable patients, 100 had AML or myelodysplastic syndrome, 30 of which were ABO-incompatible, and 99 had CML, 35 of which were ABO-incompatible. All patients undergoing transplant received erythrocyte and plasma-depleted marrow but 14 major ABO-incompatible patients also underwent plasma exchange before transplant. T cell-depletion and purging techniques were not employed. All records were reviewed for prognostic factors including patient age, sex, diagnosis, remission status at the time of transplant, and incidence and severity of acute and chronic GVHD. Compatible and incompatible patients with myeloid leukemia did not differ with respect to age, sex, remission status of disease at the time of transplant or incidence of GVHD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Survival after ABO-incompatible allogeneic bone marrow transplant after a preparative regimen of busulfan and cyclophosphamide. 774 42

Pure red cell aplasia (PRCA) was found in a male patient with chronic myelocytic leukemia after major ABO incompatible bone marrow transplantation (BMT). He had blood group O, and received BMT from an HLA identical sibling (blood group A). Erythrocyte-depleted marrow was transplanted. Methotrexate for short time and cyclosporine (CyA) were used for graft versus host disease (GVHD) prophylaxis. Engraftment of neutrophils and platelets were observed on day 14 and 22, respectively. The Ph1 chromosome disappeared on day 133. However engraftment of erythrocytes was not observed on day + 280. Bone marrow puncture revealed depletion of erythrocyte precursors. Anti-A isoagglutinin was persisted. There was no evidence of acute or chronic GVHD. Administration of prednisolone, discontinuance of CyA and subcutaneous infusion of recombinant human erythropoietin failed to improve PRCA. Bolus methylprednisolone (m-PSL) therapy started on day 284 resulted in rapid increase in reticulocyte counts within 6 days, which was followed by normal hemoglobin concentrations. We conclude that bolus m-PSL may be one treatment for PRCA after BMT.
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PMID:[Treatment with bolus methylprednisolone for pure red cell aplasia after ABO incompatible bone marrow transplantation in a patient with chronic myelocytic leukemia]. 869 68

A 46-year-old woman with chronic myelogenous leukemia received allogeneic bone marrow transplantation from an unrelated human leukocyte antigen (HLA) matched (but mixed lymphocyte culture (MLC) positive to graft-versus host disease (GvHD) donor. The blood type of the recipient was A type Rh (+) while the donor blood type was B type Rh (+). The patient received busulfan 8 mg/kg, cyclophosphamide 120 mg/kg, and total-body irradiation 10 Gy before bone marrow transplantation. Short-term administration of methotrexate and cyclosporin was given for prophylaxis of GvHD. The mononuclear cells harvested from the donor were concentrated by COBE Spectra before bone marrow transplantation. Although engraftment of transplanted bone marrow in the recipient was confirmed on day 11, the patient suffered from severe anemia on day 10. Since the direct Coombs' test to A type red blood cells was positive, and anti-A antibody titer increased 16-fold, we diagnosed her anemia as hemolytic anemia caused by ABO mismatched transplantation. In addition to hemolytic anemia, she had skin symptoms of acute GvHD grade II, microangiopathic hemolytic anemia, and died of multiple organ failure on day 44. This experience indicated that some allogeneic transplant recipients are at risk of severe hemolytic anemia in the early stage after unrelated ABO mismatched donor and that it is necessary to establish proper treatment and prophylaxis.
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PMID:[Rapid onset of hemolytic anemia after allogeneic bone marrow transplantation from an unrelated ABO major mismatched donor]. 902 56

A patient with CML in accelerated phase received G-CSF-mobilized PBPC from an unrelated HLA genotypically matched donor. The blood groups of the patient and donor were bidirectionally incompatible. Hematologic recovery was rapid with > 500 PMN/microliter on day +9. Starting on day +5 bilirubin levels increased from 1.3 mg/dl up to a maximum of 18 mg/dl on day +14. Clinical signs and laboratory tests supported major hemolysis. Blood typing on day +16 revealed early blood-group change, consistent with donor-derived antibodies produced by passenger-lymphocytes which may have mediated severe hemolysis. The early onset and strong intensity of the hyperbilirubinemia could be a specific feature of ABO-incompatible allogeneic PBPC transplantation which would be difficult to differentiate from GVHD or VOD.
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PMID:Rapid engraftment after allogeneic ABO-incompatible peripheral blood progenitor cell transplantation complicated by severe hemolysis. 902 62

A variety of immunohematological complications may occur after ABO-incompatible BMT. We report a CML patient (blood group O) who received a BMT from an HLA-identical sibling (blood group AB). The transplant was followed by normal myeloid and megakaryocytic engraftment, but erythroblastopenia persisted for more than 200 days after BMT. By bone marrow culture studies, a complement-dependent serum inhibitor of hemopoiesis was detected, suggesting immunological inhibition of erythropoiesis. The patient was resistant to a number of treatments such as intravenous gamma-globulins, prednisolone and high-dose erythropoietin. Full engraftment with normal blood counts and marrow cellularity was achieved after two dose-escalating CD34+-enriched donor lymphocyte infusions (DLI). This experience suggests that CD34+-enriched DLI may be an effective treatment for patients with delayed engraftment or late graft failure due to major ABO-incompatibility.
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PMID:CD34+-enriched donor lymphocyte infusions in a case of pure red cell aplasia and late graft failure after major ABO-incompatible bone marrow transplantation. 975 54

Erythroid engraftment after non-T cell-depleted allogeneic bone marrow transplant (BMT) is reviewed in 112 patients treated for chronic myelogenous leukemia (CML). Twenty-two of 76 evaluable patients were transplanted over a major ABO-mismatch compatibility barrier. These patients showed an increased delay in erythroid engraftment and in time to red blood cell transfusion independence when compared with ABO-identical or minor mismatched recipients. No difference in granulocyte or platelet engraftment was evident. Erythroid engraftment usually occurred spontaneously without specific intervention. One patient was found to have erythroid hypoplasia at day 201 after BMT, despite therapy with intravenous immunoglobulin and high-dose erythropoietin. An anti-A titer of 16,000 was documented. This patient was successfully treated with an aggressive course of 18 plasmapheresis procedures and with donor-type plasma replacement. Delayed erythroid engraftment is common after non-T cell-depleted major ABO-mismatched BMT in CML, but rarely requires intervention other than transfusion support. Rare cases of refractory erythroid aplasia may be treated without additional immunosuppression by aggressive plasma exchange with donor-type plasma.
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PMID:Prolonged erythroid aplasia after major ABO-mismatched transplantation for chronic myelogenous leukemia. 992 13

ABH carbohydrate antigens are cell surface carbohydrates which occur in three allelic forms, namely A, B and O blood groups. It is unknown how the ABO blood group is expressed in hemopoietic stem cells. In an attempt to verify the ABO mRNA expression in hemopoietic precursor cells, mRNAs were isolated from human chronic myeloid leukemia (CML) cell lines which are believed to be at the most immature level of hemopoietic differentiation among hemopoietic malignancies. In particular, K-562 and KOPM-28 cells were used with the reverse transcription-polymerase chain reaction (RT-PCR) technique for amplifying ABO gene transcripts. The amplified ABO cDNAs from two cell lines were characterized by the digestion of Kpn-I restriction enzyme. The blood types were determined by polymerase chain reaction of the specific allele (PASA) method. Both of the human chronic myeloid leukemia cell lines expressed ABO mRNA. The quantity of ABO mRNA in the K-562 cell line is significantly higher than that of the KOPM-28 cell line. The ABO blood type of these two cell lines was type O. Because the CML cell lines are presumed to be at the immature stem cell level of hematopoietic cell differentiation and because it is believed that the cultured cell lines from hematologic malignancy reflect the characteristics of normal corresponding hemopoietic cells, the hemopoietic stem cells should express mRNA of the ABO blood group.
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PMID:Detection of histo-blood group ABO mRNA in human chronic myeloid leukemia cell lines using reverse transcription-polymerase chain reaction (RT-PCR). 1007 69


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