Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0023418 (leukemia)
93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recognition and resolution of ABO grouping discrepancies are essential skills in pre-transfusion testing. Discrepancies in ABO grouping can be characterized by inappropriate results in either cell or serum grouping. These unexpected reactions come in two categories: reduced reactivity or extra reactivity detected in initial tests. Weak or missing expression of A or B antigens have been reported in some patients with leukemia, resulting in weak or mix-field agglutination with routine typing reagents. We will discuss the relationship between ABH blood group antigenic status and an acquired disease: anomolous phenotypes observed in hemopoietic disorders. OR.
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PMID:[Alterations of ABH antigens in leukemic patients]. 930 2

We have analyzed the factors associated with engraftment in 216 recipients of T-cell depleted allogeneic HLA identical sibling marrow transplants using Campath 1 monoclonal antihuman lymphocyte (CD52) antibodies. The patient population consisted of 168 patients with hematologic malignancies, 26 with severe aplastic anemia (SAA), and 22 with hemoglobinopathies, half of whom received marrow treated in vitro with Campath-1M (IgM) and half received marrow with Campath-1G (IgG2b isotype). Patients with durable engraftment had fast hematopoietic recovery: SAA patients reached ANC > 0.5 x 10(6)/L on Day 14; those with leukemia attained ANC > 0.5 x 10(6)/L on Days 18, 17, and 15 for ANLL, ALL and CML respectively, while patients with thalasemia reached ANC > 0.5 x 10(6)/L on Day 21. Overall, 24 patients (17 with leukemia, 4 with SAA, and 3 with thalassemia) suffered graft failure: 10 patients (all grafted with Campath-1M) rejected their grafts, while 14 others (9 grafted with Campath-1M, and 5 with 1G isotype) never engrafted (p = 0.009). Multivariate analysis revealed that neither pretransplant protocol, nor stage of disease or type of antibody used, donor sex and ABO match had any impact on engraftment. The variables favorably associated with engraftment were older age (p = 0.030, RR = 1.016) and CFU-GM number (p = 0.013, RR = 1.001). Patients with ANLL or SAA had a better chance to engraft (p = 0.027, RR = 1.400; and p = 0.003, RR = 2.677, respectively) compared to patients with thalassemia (p = 0.001, RR = 0.551). A higher concentration of Campath-1 antibody in vitro and in vivo adversely affected engraftment. Our data show that satisfactory engraftment can be achieved in patients transplanted with Campath-1 treated marrow allografts. However, despite the measures undertaken to prevent rejection, graft failure still poses a problem. Further pretransplant immunosuppression and perhaps more selective T-cell depletion may reduce the increased graft failure in these patients.
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PMID:Engraftment of marrow allografts treated with Campath-1 monoclonal antibodies. 1039 Jan 97

It is not known if donor-recipient ABO blood group incompatibility contributes to graft-versus-leukemia after allogeneic BMT. One hundred and nineteen patients with acute myeloid leukemia in first remission underwent non-T cell-depleted marrow allografts from HLA-identical siblings after TBI and cyclophosphamide (n = 72) or melphalan (n = 47). GVHD prophylaxis comprised cyclosporine alone or cyclosporine-methotrexate. Twenty-two patients relapsed at 3-46 months (median 7): 18 of 76 patients with ABO-matched donors and four of 43 patients with ABO-mismatched donors (actuarial 5-year probabilities 33 +/- 6% vs 12 +/- 6%; P = 0.028). The incidence of acute and chronic GVHD was not affected by ABO mismatch. The following factors were studied in Cox analysis for effect on outcome: gender, age, FAB subtype, ABO mismatch, CR-transplant interval, conditioning, TBI dose, nucleated cell dose, lymphocyte recovery, acute GVHD, and chronic GVHD. Donor-recipient ABO match was the only factor independently associated with a higher risk of relapse (RR = 3.7; 95% Cl, 1.1-12.6; P = 0.04). ABO mismatch was also associated with superior overall and disease-free survivals. We conclude that ABO incompatibility may influence relapse rates and survival favorably after allogeneic BMT. It is not known if this holds true for allogeneic blood stem cell transplants.
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PMID:Does donor-recipient ABO incompatibility protect against relapse after allogeneic bone marrow transplantation in first remission acute myeloid leukemia? 1237 98

Thirty consecutive patients were given non-myeloablative stem cell transplants (NST) and posttransplant chimerism was studied by several methods. In 16 individuals definitive proofs of chimerism have been shown: In 10 cases sex chimerism, in 7 cases chimerism shown by means of microsatellites, in 4 cases ABO chimerism, in two cases Rh chimerism and in one HLA-DR chimerism. In addition, in 9 individuals the disappearance of the molecular marker of the leukemia is an indirect evidence of the chimerism, as well as the presence of graft versus host disease (GVHD) in 17 allografted patients. Only in 6 patients no evidence of chimerism could be shown; all of them died as a result of either persistent or relapsing malignancy. Since the early patterns of chimerism may be predictive of either GVHD or graft loss in NST and, since therapeutic intervention (such as donor lymphocytes infusions) is based in the patterns of chimerism, it is possible that chimerism studies in these types of allografts should be ideally done more frequently than in conventional allotransplants.
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PMID:Follow up of hemopoietic chimerism in individuals given allogeneic hemopoietic stem cell allografts using an immunosuppressive, non-myeloablative conditioning regimen: a prospective study in a single institution. 1238 39

Severe acute graft-vs.-host disease (aGVHD) remains a major cause of transplantation-related mortality. However, because of a graft-vs.-leukaemia effect, a mild (grade I) aGVHD is desirable. As risk factors predisposing for aGVHD are not necessarily the same in children and adults, we have performed a retrospective analysis of risk factors (RFs) for grade II-IV aGVHD in 258 paediatric patients undergoing allogeneic stem cell transplantation at our centre. Thirty-two potential RFs were assessed with univariate analysis in logistic regression. Eleven factors were selected for further evaluation in stepwise elimination multivariate analysis. Three independent RFs were found: (1) donor other than human lekocyte antigen (HLA)-identical sibling [odds ratio (OR) 6.1, p < 0.001); (2) single drug [cyclosporine A (CsA) or methotrexate (Mtx)] graft-vs.-host disease (GVHD) prophylaxis (OR 7.0, p < 0.001); and (3) ABO disparity of any kind (OR 2.4, p = 0.02). The RFs were additive: moderate-to-severe aGVHD was seen in none of the patients without any RFs; in 16% with one RF; in 32% with two RFs and in 67% with all three RFs present. Single drug GVHD prophylaxis (CsA or Mtx), any kind of ABO mismatch, and non-sibling donors are RFs for grade II-IV acute GVHD in paediatric SCT. We encourage the use of combination GVHD prophylaxis in children. ABO mismatch should be considered when choosing between otherwise equally suitable donors.
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PMID:Risk factors for moderate-to-severe acute graft-vs.-host disease after allogeneic stem cell transplantation in children. 1265 54

Allogeneic G-CSF-mobilized blood cell transplantation (BCT), an alternative to allogeneic bone marrow transplantation (BMT), is associated with enhanced engraftment and accelerated hematopoietic recovery. In addition, immune reconstitution and overall alloreactivity after BCT versus BMT differ significantly. Indeed, despite an increased number of donor T cells infused, the incidence of acute graft-versus-host disease (GvHD) after BCT appears to remain identical or lesser than after BMT. On the other hand, a higher risk of chronic GvHD has been reported after BCT. In a SFGM phase III trial, 101 patients with early leukemia and an HLA-matched sibling donor randomly received a BCT or BMT. BCT was associated with a higher number of infused CD34+ cells, accelerated platelet and neutrophil reconstitution, fewer platelet transfusions and similar acute GvHD incidence. However, chronic GvHD occurred more frequently after BCT. With a median follow-up of 20 months, relapse, survival and leukemia-free survival were not different. In the course of this study, immune parameters related to the graft as well as to early reconstitution were prospectively examined. T cells subsets, B cells, NK cells and monocytes numbers were significantly higher in BC grafts (versus BM). T cells in BC grafts were less activated than in BM grafts. Frequency of IFN-gamma, IL-2- and TNF-alpha-secreting cells and single-cell IFN-gamma production potential was reduced in BC graft. One month after BCT, blood T-cell counts were 3-fold higher than after BMT. Moreover, post-BCT T cells were less activated and counts correlated with the number of T cells infused with the graft, which was not the case after BMT. Several acute hemolysis episodes, resulting from anti-A and/or -B donor-derived Ab directed at Ag present on recipient red blood cells (minor ABO mismatch), have been described after BCT. Recipients indeed exhibited significantly increased anti-A and/or -B Ab titers after BCT, particularly in the setting of a "minor" ABO mismatch. Furthermore, the frequency of anti-HLA Ab early after BCT was significantly increased (despite the reduction in platelet transfusion requirements). The higher number of activated B cells and/or CD4 T cells and monocytes in a BCT graft and/or the higher number of circulating CD4 T- and B-cells after BCT could be associated with the enhanced alloAb production. G-CSF-induced TH2 cytokine profile of the T cells present in the graft could also be contributive. Recent studies have determined that BC grafts contained a higher number of type 2 dendritic cells (DC2), themselves associated with high frequencies of TH2 CD4+ cells. Since chronic GvHD is associated with the occurrence of Ab-mediated auto-immune-like syndromes, it is tempting to speculate that a higher incidence of chronic GvHD may result from these findings. In conclusion, BCT results in clinically relevant distinct hematopoietic and immune reconstitution patterns.
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PMID:Blood versus marrow hematopoietic allogeneic graft. 1287 95

We studied the distribution of ABO blood groups in Hodgkin's lymphoma, non-Hodgkin's lymphoma, acute myeloid leukaemia and acute lymphoblastic leukaemia, in children up to the age of 12 years, in a hospital-based retrospective study. Blood group data were recorded from the case records of all the patients in a tertiary care centre with the diagnosis of Hodgkin's lymphoma, non-Hodgkin's lymphoma, acute myeloid leukaemia and acute lymphoblastic leukaemia, during the period 1987-1997. There were 63 Hodgkin's lymphoma, 78 non-Hodgkin's lymphoma, 116 acute myeloid leukaemia and 522 acute lymphoblastic leukaemia patients. We assessed the distribution of ABO blood groups and the difference in the distribution from the source population. In Hodgkin's lymphoma, there were 45.6% [95% confidence interval (CI): 6.8-84.5] more patients with B blood group. In acute lymphoblastic leukaemia, there were 14.3% (95% CI: 3.2-25.2) more patients with O blood group. In Hodgkin's lymphoma and non-Hodgkin's lymphoma patients, there were 56.5% (95% CI: 19.9-85.4) and 52.9% (95% CI: 18.1-82.6) less patients with A blood group, respectively. This shows that the relationship between the ABO blood groups and haematological malignancies merits further investigation in a population-based prospective study. This is the first study of its kind in any Indian population.
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PMID:Distribution of ABO blood groups in acute leukaemias and lymphomas. 1517 95

Platelet transfusions are widely used. Prophylactic transfusions are employed in severely thrombocytopenic patients without evidence of bleeding, but no randomized trial data prove the safety or efficacy of this approach. Randomized trials have demonstrated the equivalence of transfusion triggers of 10,000 and 20,000/microl for prophylactic transfusions. The former threshold is potentially safer for the patient, conservative of donor resources and leads to lower costs, with perhaps a slightly greater risk of minor hemorrhage. Randomized trials have demonstrated the equivalence of pheresis or whole blood-derived platelet transfusions. The former present a lower risk for infectious agents, and the latter are less expensive and a more efficient use of limited donor resources. Randomized trials prove that leukoreduced and ABO identical platelet transfusions reduce the risks of HLA alloimmunization and platelet transfusion refractoriness (both leukoreduction and ABO matching), transfusion reactions (leukoreduction) and CMV transmission (leukoreduction). Leukoreduction and ABO matching of platelet transfusions also have been associated in preliminary observational studies with reduced morbidity and mortality in surgical patients and reduced infections in patients with leukemia. These results require further investigation. Future challenges include (1) determining the best approach to bacterial contamination of platelets, whether by detection methods or pathogen inactivation and (2) determining the threshold for prophylactic platelet transfusions in thrombocytopenic patients undergoing surgery or invasive procedures.
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PMID:Optimizing platelet transfusion therapy. 1518

Reports have shown a worse outcome for donor-recipient pairs mismatched for ABO blood groups in bone marrow transplantation (BMT). These studies, however, included small and heterogeneous study populations, and not all considered bidirectional ABO incompatibility separately. Because the issue remains controversial, we analyzed the effect of ABO mismatch on the overall survival, transplant-related mortality, and occurrence of acute and chronic graft-versus-host disease (GVHD) in a large homogenous group of patients undergoing allogeneic BMT. A total of 3103 patients with early-stage leukemia who underwent transplantation between 1990 and 1998 with bone marrow from an HLA-identical sibling and who were reported to the Center for International Blood and Marrow Transplant Research were studied. The median follow-up was 54 months. A total of 2108 (67.9%) donor-recipient pairs were ABO identical, 451 (14.5%) had a minor mismatch, 430 (13.9%) had a major mismatch, and 114 (3.7%) had a bidirectional ABO mismatch. The groups did not differ significantly in patient or donor characteristics except for more female-to-male sex mismatch in the bidirectional ABO mismatch group (P = .017). In multivariate models of overall survival, transplant-related mortality, and grade II to IV acute GVHD, there were no significant differences among the 4 groups. Bidirectional ABO mismatch was associated with a significantly higher risk of grade III or IV acute GVHD (hazard ratio, 1.869; 95% confidence interval, 1.192-2.93; P = .006). Patients with major ABO mismatch received red blood cell transfusions (P = .001) for a longer timer after transplantation and had a slightly slower neutrophil recovery (P < .001). There was no evidence of a substantial effect of ABO blood group incompatibility on the outcome of conventional BMT among patients with leukemia.
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PMID:ABO blood group barrier in allogeneic bone marrow transplantation revisited. 1633 23

The revised and expanded practice guideline 'Blood transfusion' describes the whole transfusion chain within the hospital for the first time. Despite compatibility tests before transfusion (determination of the ABO and Rhesus blood groups and detection of clinically relevant antibodies (C, c, D, E, e, Fy(a), Fy(b), Jk(a), Jk(b), M, S and s)), transfusion reactions can occur. So that a transfusion reaction can be recognised in time, the patient must be observed intensively for the first 5-10 minutes after the start of any new transfusion and the vital functions must be recorded. In patients with a Hb level of 4-6 mmol/l, the decision whether or not to transfuse should be made dependent on the patient's other characteristics. Thrombocyte transfusion is not indicated in case of thrombopenia due to increased breakdown or pooling. If leukaemia, tumour infiltration or drug toxicity is the underlying cause of thrombopenia, then a platelet count of 10 x 10(9)/l or 20 x 10(9)/l should be the transfusion trigger. Reduction of the number of blood transfusions can be achieved by the administration of epoetin in case of renal insufficiency: transfusion can thus be avoided in more than 70% of the patients concerned. Autotransfusion during surgery with severe blood loss also results in a reduction of the number of allogenic blood transfusions.
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PMID:[The practice guideline 'Blood transfusion' (third integral revision)]. 1635 77


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