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)

A total of 23 leukaphereses were performed on five normal, healthy donors for the purpose of providing granulocyte transfusions to septic leukemia patients with granulocytopenia. Dexamethasone 7.25 to 7.50 mg was given orally 10 to 12 hours prior to each donation, and an average of 304 ml of hydroxyethyl starch (HES) was given intravenously during each procedure. During the period of observation for each donor, there was no significant change of total leukocyte and platelet counts, total bilirubin, alkaline phosphatse, LDH, SGOT, creatinine, BUN, and uric acid determinations. Changes in the concentrations of serum protein, albumin, cholesterol, and glucose were thought to be due to hemodilution. Partial thromboplastin and prothrombin times remained within normal limits following collection procedures. Hemoglobin levels decreased transiently following the first three leukaphereses in all donors, but fell progressively to 11.8 gm/dl in one donor undergoing seven procedures in a 35-day period. Dexamethasone and HES in these doses can be given safely to multiply leukapheresed donors.
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PMID:The safety of dexamethasone and hydroxyethyl starch in the multiply leukapheresed donor. 5 93

Factors and inhibitors of coagulation and fibrinolysis were investigated on admission in 57 patients with acute leukaemia and they were correlated to the occurrence of haemorrhage. Coagulation disturbances were found in 98%. Seventeen of the patients with haemorrhagic symptoms had major bleeding. Severe thrombocytopenia (< 20 x 10(9)/l) was found in 16%. Patients with major bleedings had significantly lower concentrations of prothrombin complex, fibrinogen, protein C and platelets. Low levels of antiplasmin and fibrinogen were characteristic of 'bleeders' with promyelocytic and lymphoblastic leukaemia. We found a positive correlation between vWF:Ag and leukaemic cell count especially in lymphoblastic leukaemia (ks = 0.72). Reduced levels of antithrombin indicated a poorer prognosis.
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PMID:Bleeding complications and coagulopathy in acute leukaemia. 140 6

A multicenter study of a recently developed ELISA for the determination of prothrombin fragment F1+2 was performed in order to evaluate analytical and clinical aspects. Mean intra-assay and inter-assay reproducibility were found to be 11.0 and 12.6%, respectively. The measuring range covered by the calibration curve reaches from 0.04 to 10.0 nM/l F1+2. Testing 133 healthy subjects a reference range of 0.37 to 1.11 nM/l F1+2 (2.5-97.5 percentile) with a median of 0.66 nM/l F1+2 was calculated. Minor difficulties with blood sampling (venous occlusion for 2 min) did not affect F1+2 plasma concentrations. Significantly increased F1+2 levels were measured in patients with leukemia (p < 0.0001), severe liver disease (p < 0.005) and after myocardial infarction (p < 0.01). Elevated F1+2 concentration before the beginning of heparin therapy (1.25 nM/l) decreased to 0.77 nM/l (p < 0.0001) after 1 day of therapy. For patients in the stable phase of oral anticoagulant therapy decreasing F1+2 concentrations were measured with increasing INR. F1+2 levels were already significantly reduced in patients with INR < 2.0 (0.56 nM/l; p = 0.0005). Thus F1+2 determination may be helpful in identifying activation processes as well as in monitoring anticoagulant therapy.
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PMID:Multicentric evaluation of a new assay for prothrombin fragment F1+2 determination. 144 72

A variant strain of Rauscher leukemia virus (RLV-A) obtained from a transplantable murine monomyelocytic leukemia causes a disease characterized by frank anemia, wasting, hepatosplenomegaly and erythroblastosis. The involvement of platelets in this disease are reported here. The RLV-A induced a severe thrombocytopenia (25 percent of control level) at the terminal stage of disease. This thrombocytopenia was not associated with disseminated intravascular coagulopathy since the prothrombin times were always within normal limits. The partial thromboplastin time was elevated in the terminal stages of disease and was found to be associated with factor deficiencies, possibly owing to the presence of anti-factor antibodies, in the intrinsic coagulation pathway, especially factor VIII. Further, splenectomy did not abolish the thrombocytopenia, since splenectomized, virally infected animals also developed severe thrombocytopenia (29 percent of control levels). The ensuing splenomegaly during progression of disease was not the cause of the thrombocytopenia. A physiological response to the severe thrombocytopenia was the production of larger size platelets. At terminal stages of the disease, platelet volume increased to 4.2 mu 3 (normal is 3.0 mu 3). An increase in platelet volume was also observed in splenectomized, virally infected animals. Electron microscopy indicated that these circulating platelets contained c-type viral particles. Viral infection was associated with decreased life span of circulating platelets, as measured by 75Se-methionine at mid and terminal stages of the disease. Our results suggest that direct viral infection of platelets and/or megakaryocytes with subsequent cell lysis is a possible cause of the observed thrombocytopenia observed in RLVA-induced disease and may also occur in other retrovirally-induced diseases.
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PMID:Thrombocytopenia in a retrovirally-induced murine erythroleukemia. 145 28

Cytostatic therapy is known to aggravate tumor-induced coagulopathy. Therefore, we have studied the effect of different chemotherapeutic regimens on the activation of coagulation and fibrinolysis in patients with non-Hodgkin's lymphomas or acute leukemias. In non-Hodgkin's lymphoma patients treated with an aggressive protocol (COL-BLAM) and in leukemia patients (TAD-9) fibrinopeptide A, prothrombin fragment (F1 + 2) and thrombin antithrombin III complexes (TAT) increased (Tables 4 and 6), while D-dimer did not deviate significantly. The ratio D-dimer/TAT consequently showed a significant decrease, indicating increased formation of thrombin after release of procoagulant factors, which is not paralleled by an activation of fibrinolysis. Both these groups were also characterized by an increase in uric acid and in C-reactive protein and plasminogen-activator inhibitor, two acute-phase reactants. In contrast, patients with non-Hodgkin's lymphomas treated with a less aggressive protocol (COP) showed no significant changes in hemostatic variables, uric acid, or acute-phase reactants. The release of procoagulant factors relates to the cytostatic sensitivity of the tumor and to a high tumor-cell destruction. Our results further emphasize the need for large-scale studies on antithrombotic prophylaxis in patients undergoing cytostatic treatment.
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PMID:Influence of cytostatic treatment on the coagulation system and fibrinolysis in patients with non-Hodgkin's lymphomas and acute leukemias. 171 7

Little information is available on the prevalence and etiology of the coagulopathy present in some children with acute leukemia at disease presentation. We studied 102 children with newly diagnosed acute leukemia (50 retrospective: Group A; and 52 prospective: Group B) with prothrombin time (PT), partial thromboplastin time (PTT), thrombin time (TT), fibrinogen (FIB), and fibrin degradation products (FDP). All patients in Group B also had assessment of thrombin activation by measurement of the crosslinked fibrin fragment, D-dimer, and of primary fibrinolysis with the B beta 1-42 peptide. Additionally, ten patients from Group B had Factors II, V, VII, and X measured, and eight of these patients had measurement of tissue factor from sonicated bone marrow cells. Thirty-two percent of Group A and 40% of Group B had totally normal coagulation studies, whereas 20% of Group A and 10% of Group B had a severe coagulopathy on disease presentation. A high percentage of both groups had elevated PT (Group A, 52%; Group B, 27%) and increased FDP (Group A, 39%; Group B, 25%). In Group B, 38% of the patients had a positive D-dimer, whereas only 4% of this prospective group had an elevated B beta 1-42 peptide (P less than 0.00001). Nine of ten patients with a positive D-dimer had low levels of one or more of the extrinsic pathway factors. Three of four patients with the highest tissue factor levels were of monocytoid leukemia cell type. These data indicate that the coagulopathy associated with acute leukemia of childhood is usually mediated by thrombin activation.
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PMID:The coagulopathy of childhood leukemia. Thrombin activation or primary fibrinolysis? 238 1

The Cancer and Leukemia Group B (CALGB) conducted a prospective randomized trial to evaluate the role of warfarin and alternating chemotherapy in extensive small-cell lung cancer (SCCL). After stratification for sex and performance status, patients were randomly assigned to receive chemotherapy with methotrexate, doxorubicin (Adriamycin; Adria Laboratories, Columbus, OH), cyclophosphamide, and lomustine (CCNU) (MACC), or MACC plus warfarin (MACC + W), or mitomycin, etoposide, cisplatin, and hexamethylmelamine alternating with MACC (MEPH/MACC). Warfarin was given continuously to maintain a prothrombin time of one and one half to twice the control values. A total of 328 patients were enrolled, and 294 were evaluable. There was a statistically significant advantage in objective response rates (complete [CR] and partial responses [PR], respectively) for MACC + W (17% and 50%) as compared with MACC alone (8% and 43%) or MEPH/MACC (10% and 38%) (P = .012). Both failure-free survival (P = .054 Wilcoxon test) and overall survival (P = .098 Wilcoxon test) were higher on MACC + W (median, 6.6 months and 9.3 months, respectively), as compared with MACC (5.0 months and 7.9 months) and MEPH/MACC (5.0 months and 7.9 months). Toxicity was comparable among the three arms, except for increased hemorrhagic events on MACC + W, which were life-threatening in four patients (4%), and lethal in two others (2%). These data support the role of warfarin in the treatment of SCCL, but do not establish its mechanism of action. Warfarin deserves further studies in SCCL, particularly in patients with limited disease.
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PMID:A randomized trial of anticoagulation with warfarin and of alternating chemotherapy in extensive small-cell lung cancer by the Cancer and Leukemia Group B. 215 91

Recently, the association of granulocytic fragments on blood smear with leukoerythroblastosis in sepsis has been identified in nine patients. Granulocytic fragments were identified by both light and electron microscopy as well as cytochemistry. Leukoerythroblastosis is a poorly defined, uncommon syndrome with leukocytosis, left shift, and nucleated red blood cells (nRBCs) disproportionate to the degree of anemia, which may be associated with leukemia or neoplasia in the bone marrow, acute infection, hemolysis, myelofibrosis, or miscellaneous causes. Here a subgroup with high white blood cells (WBC) and acute infection was studied. The corrected WBC for nine patients was 40 x 10(9) per L with 33 nRBC per 100 WBC; serum C3 and C4 levels before and after the development of leukoerythroblastosis were 0.6 +/- 2 g per L; 0.18 +/- 0.04 g per L pre-leukoerythroblastosis and 0.7 +/- 0.46 g per L; 0.30 +/- 0.27 g per L post-leukoerythroblastosis, respectively, in four patients. The platelet count, prothrombin time (PT), and activated partial prothrombin time (aPTT) were 133 x 10(9) per L, 24.4 sec., and 53.5 sec., respectively, for nine patients. Multiphasic chemistries at the time of leukoerythroblastosis were measured in five patients; abnormal values included calcium of 2.0 +/- 0.4 mmol per L, creatinine of 336 +/- 130 mumol per L, total protein of 45 +/- 17 g per L, albumin of 27 +/- 11 g per L, total bilirubin of 421 +/- 362 mumol per L, uric acid of 499 +/- 264 mumol per L, triglycerides of 4.9 +/- 3.7 mmol per L, and alkaline phosphatase of 3.5 +/- 1.0 mu kat per L.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biochemical values, complement levels, and hemostatic data in septic leukoerythroblastosis. 260 78

Cathepsin G, isolated from human polymorphonuclear leukocytes, was found to effect rapid and specific degradation and biological inactivation of bovine and human prothrombin in the absence of calcium ions with the formation of two peptide fragments from the N-terminal end of the molecule. Polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulphate indicated that the molecular weights of the fragments were 5,000 and 17,500. Proteolysis of prothrombin by cathepsin G was inhibited by calcium ions. Leukocyte proteinases such as cathepsin G may be responsible for haemorrhagic disorders associated with myelocytic leukaemia and septicaemia.
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PMID:The degradation of bovine and human prothrombin by human polymorphonuclear leukocyte cathepsin G. 287 63

115 patients with acute promyelocytic leukaemia (APL) were studied retrospectively to evaluate prognostic factors and assess therapeutic approaches, particularly the use of heparin in the management of disseminated intravascular coagulation (DIC). The remission rate was 86% (30/35 patients) in those who received heparin and 49% (39/80 patients) in those who received no heparin (P = 0.0002). This difference in remission rates was accounted for by a marked decrease in the number of haemorrhagic deaths, especially those due to intracranial haemorrhage (ICH), in the heparin treated group. Other factors associated with a poor remission rate were prothrombin ratio (PTR) greater than 1.3 (P = 0.008), fibrinogen less than 1.5 g/l (P = 0.02) and WCC greater than 2.0 x 10(9)/l (P = 0.03).
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PMID:Beneficial effect of heparin in the management of patients with APL. 316 83


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