Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty-seven patients in initial phase of acute promyelocytic leukemia (APL) were treated in the same department with heparin infusion, platelet transfusions, and two related induction regimens both including cytosine arabinoside and daunorubicin. Clinical and biological findings at presentation were studied. The complete remission (CR) rate was 53%. Twenty-seven patients (47%) died during the initial course of the disease, either before day 5 (early death [ED], n = 7) or after day 5 (death in aplasia [DA], n = 20). Most ED was due to intracerebral hemorrhage (6/7), especially when large hemorrhages had been seen on fundus oculi examination. Most DA was due to multivisceral failure (9/20). No correlation was found between initial disseminated intravascular coagulation (DIC) and death. However, the worsening of coagulation parameters during induction therapy, with or without initial DIC, significantly increased the occurrence of renal and respiratory failure which were particularly frequent during the first month. The median duration of survival was short (3.5 months) and the median duration of CR (11 months) was similar to that of other acute myeloid leukemias treated with the same regimens. The possible causes of the high mortality observed during the initial courses of APL and the possible benefit of a more graduate induction chemotherapy are discussed.
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PMID:Acute promyelocytic leukemia in 57 previously untreated patients. 385 65

Three patients, diagnosed as acute promyelocytic leukemia and disseminated intravascular coagulation (DIC), were treated with THP-ADM in combination with heparin and intensive platelet transfusion. Two of the three patients achieved complete remission. The remaining one patient also responded favorably to the therapy and achieved marrow aplasia, and significant improvement of coagulopathy was observed after chemotherapy. However, he suddenly died of intractable congestive cardiac disturbance ten days after the completion of THP-ADM induction therapy. The mechanism of this unique delayed anthracycline-associated cardiotoxicity was discussed.
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PMID:THP-ADM in the treatment of acute promyelocytic leukemia. 386 Oct 2

Disseminated intravascular coagulation (DIC) is a frequent occurrence in acute promyelocytic leukemia (APL), especially after onset of chemotherapy. We have used a human promyelocytic leukemic established cell line (HL-60) and various other human leukemic cells to investigate the effect of cytotoxic drugs on generation of procoagulant activity (PCA). The results indicate that, unlike normal human peripheral blood monocytes and certain other cell types where PCA induction requires active mRNA and protein synthesis, in HL-60 cells, compounds such as actinomycin D, puromycin, and cytosine arabinoside and a variety of other cytotoxic agents, induced generation of a potent PCA. Although different in its mechanism of induction, this HL-60 cell PCA was similar, and may be identical, to mononuclear cell tissue factor. The PCA induction was rapid and preceded the lytic effect of the drugs. It was first detected on the outer cell surface but, following prolonged exposure to the drugs, upon lysis of the cells, it was also found in the extracellular medium. This in vitro effect mimics the development of DIC in patients with APL. The system may, therefore, serve as a model for the study of the cellular and molecular events associated with PCA generation by malignant promyelocytes and DIC occurrence in patients with APL and other malignancies.
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PMID:In vitro generation of procoagulant activity by leukemic promyelocytes in response to cytotoxic drugs. 390 16

Acute promyelocytic leukemia is characterized by bone marrow infiltration with hypergranular promyelocytes, often with Auer bodies. Clinically it is characterized by a hemorrhagic syndrome caused by a disseminated intravascular coagulation. Karyotypic studies have shown a frequent translocation t(15;17). Improved prognosis resulted from chemotherapy with DAT and treatment with heparin.
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PMID:[Acute promyelocytic leukemia. Review of the literature]. 609 Sep 91

In the past several years there has been increasing recognition of the microgranular variant of acute promyelocytic leukemia (APL). This variant is easily mistaken for other types of acute non-lymphocytic leukemia. Its recognition is important because it carries the same high risk of disseminated intravascular coagulation as typical APL. An important clue to the correct diagnosis is the recognition of small numbers of characteristic cells containing multiple Auer rods. This report presents a case in which such Auer-body-containing cells were demonstrable in the marrow only after staining for chloroacetate esterase. They were not apparent with Wright's stain or Sudan black B. The case also highlights the occurrence of variant APL in children and adolescents.
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PMID:Microgranular acute promyelocytic leukemia--a case with multiple Auer rods demonstrable only after staining for chloroacetate esterase. 618 68

A successful embolization for life-threatening uterine hemorrhage is described in a patient with acute promyelocytic leukemia and disseminated intravascular coagulation. On admission the patient was in the 6th week of gestation with incomplete abortion and uterine hemorrhage. In addition to combination chemotherapy and anticoagulant therapy, dilatation and curettage were also performed. After the operation the uterine hemorrhage was progressively increased in amount and was not responsive to usual measures. Embolization of bilateral uterine arteries using Gelfoam was performed with a dramatic improvement of the hemorrhage.
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PMID:Successful embolization for uterine hemorrhage in a patient with acute promyelocytic leukemia. 640 73

Two patients diagnosed as having acute promyelocytic leukemia (APL) and disseminated intravascular coagulation (DIC) were closely followed from the day of admission until completion of the first course of chemotherapy with serial coagulation studies including plasma levels of functional antithrombin III activity (AT III) by fluorometric analysis and anti-activated Factor X activity (anti-Xa) by coagulation assay. Both patients were treated with intravenous heparin and the presence of heparin in plasma was followed by the thrombin time. Consistently normal levels of AT III (greater than 80%) were found despite evidence of intravascular coagulation. However, plasma levels of anti-Xa were often low (less than 70%) and increased only in the presence of heparin. The significance of these results in relationship to heparin therapy for disseminated intravascular coagulation of APL is discussed.
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PMID:Antithrombin III and anti-activated factor X activity in patients with acute promyelocytic leukemia and disseminated intravascular coagulation treated with heparin. 657

Protein C, a newly identified inhibitor of blood coagulation, was measured immunologically in 58 patients with untreated acute leukemias and compared with that of normal subjects. On the average, slightly lower values were found. However, the 17 patients with overt laboratory pictures of decompensated disseminated intravascular coagulation (DIC), including 11 cases with acute promyelocytic leukemia, had protein C concentrations no lower than those of the remaining 41 patients without DIC. Antithrombin III activity and antigen were normal and, like protein C, not lowered in DIC. The concentrations of both proteins were closely correlated with changes in the indexes for liver synthetic function. A subgroup of 13 patients with hyperleukocytic leukemias had lower protein C and antithrombin III, in line with the more compromised synthetic function of their livers. Our findings indicate that liver impairment rather than DIC is the main cause of the changes in the two naturally occurring inhibitors of blood coagulation.
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PMID:Liver dysfunction rather than intravascular coagulation as the main cause of low protein C and antithrombin III in acute leukemia. 658 88

Six patients with disseminated intravascular coagulation (DIC) in association with acute promyelocytic leukemia (APL) were studied with sensitive radioimmunoassays that are able to quantitate the extent of thrombin generation within the human circulation. The levels of prothrombin activation fragment, F1 + 2, and thrombin-antithrombin complex (TAT) were obtained at clinical presentation and were then followed serially in several patients during induction chemotherapy. The antileukemic therapy often resulted in a rise in the plasma levels of these molecular species. Simultaneous measurements of fibrinopeptide A (FPA) were also obtained, and the concentrations of this polypeptide were correlated with the levels of F1 + 2 and TAT in patients who were not receiving heparin. Nine individuals with other morphological subtypes of acute nonlymphocytic leukemia (ANLL) were investigated and were usually found to have increased levels of F1 + 2, TAT, and FPA at clinical presentation. However, the magnitude of the elevations was considerably greater and the correlation between TAT and FPA levels was stronger in APL than in ANLL. These studies provide direct evidence that patients with APL, as well as ANLL, generate excessive amounts of thrombin within their vascular system. Furthermore, the data suggest that the concentrations of F1 + 2, compared with the levels of FPA, may be a more sensitive indicator of hemostatic system hyperactivity in individuals with DIC.
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PMID:Thrombin generation in acute promyelocytic leukemia. 659 7

Two patients with acute promyelocytic leukemia and severe bleeding associated with hypofibrinogenemia were studied. The markedly shortened whole blood clot lysis time and dilute clot lysis time suggested that the defect was an increase in fibrinolysis. Although disseminated intravascular coagulation could not be totally excluded as an alternative mechanism, excessive fibrinolysis was confirmed as the pathogenic cause by the prompt response to the administration of tranexamic acid. The low circulating plasminogen, alpha 2 plasmin inhibitor level and the presence of alpha 2 plasmin inhibitor-protease complex in both patients suggested that the increased fibrinolysis probably resulted from the liberation of plasminogen activator from the promyelocyte.
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PMID:Hypofibrinogenemia due to increased fibrinolysis in two patients with acute promyelocytic leukemia. 659 15


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