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)

Three children with ALL having poor prognostic features developed clinical and laboratory evidence of disseminated intravascular coagulation (DIC). Two developed a bleeding diathesis associated temporally with a rapid drop in blast cell counts during induction therapy with L-asparaginase, prednisone, and vincristine. One of these children died of massive cerebral hemorrhage. The third patient developed episodes of superficial thrombophlebitis associated with relapses and rising blast cell counts which responded to chemotherapy and treatment with heparin. The unusual association of ALL with DIC and the fact that all 3 patients had multiple poor prognostic signs have led us to monitor carefully the coagulation system and withhold L-asparaginase in patients with massive disease until the white cell count and organomegaly have responded to prednisone and vincristine. The more common association of DIC with non-lymphocytic leukemia and recent reports of the presence of the Ph' chromosome in children with leukemia morphologically resembling ALL suggest that chromosomal evaluation be done in selected leukemic patients.
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PMID:Disseminated intravascular coagulation in childhood acute lymphocytic leukemia with poor prognostic features. 27 70

Biological symptoms of D.I.C. were investigated in 43 patients with acute leukemia. Ten of them were found to be positive either at the onset or at the relapse of the disease and in some cases D.I.C. was triggered by chemotherapy. Among the ten positive cases 3 patients had an acute promyelocytic leukemia, 4 had an acute lymphoblastic leukemia, 2 a myeloblastic and 1 a monoblastic leukemia. D.I.C. was found either in patients with an hypercellular form of the disease or in patients with a normal or low white cell count. Symptoms of D.I.C. in acute leukemia must be systematicaly sought at the onset and during treatment by chemotherapy and treated with heparin and platelet transfusions as it is now admitted for acute promyelocytic leukemia.
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PMID:[Disseminated intravascular coagulation (D.I.C.) and fibrinolysis in patients with acute leukemia (author's transl)]. 28 87

The frequency and the severity of disseminated intravascular coagulation (DIC) and of metabolic complications during the induction treatment were studied in 62 cases of acute lymphocytic leukemia with initial white blood cell count over 100 000/cu mm. Transient DIC were noted in 20,5% of cases. Metabolic complications were frequent: hyper-uricemia noted in 62% of cases was not the chief problem. Hyperazotemia was noted in 33% of cases and hyperkaliemia in 26% of cases. Hypocalcemia, noted in 34% of cases, was always associated with hyperphosphoremia. Blood glucose was low in 4 cases and increased in 7 cases out of 39.
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PMID:[Acute lymphoblastic leukemia with hyperleucocytosis: an urgent problem during initial treatment (author's transl)]. 28 98

Biological symptoms of D.I.C. were investigated in 43 patients with acute leukemia. Ten of them were found to be positive either at the onset or at the relapse of the disease and in some cases D.I.C. was triggered by chemotherapy. Among the ten positive cases 3 patients had an acute promyelocytic leukemia, 4 had an acute lymphoblastic leukemia, 2 a myeloblastic and 1 a monoblastic leukemia. D.I.C. was found either in patients with an hypercellular form of the disease or in patients with a normal or low white cell count. Symptoms of D.I.C. in acute leukemia must be systematically sought at the onset and during treatment by chemotherapy and treated with heparin and platelet transfusions as it is now admitted for acute promyelocytic leukemia.
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PMID:[Disseminated intravascular coagulation (D.I.C.) and fibrinolysis in patients with acute leukemia (author's transl)]. 75 51

Three patients with acute lymphoblastic leukemia and one with lymphosarcoma cell leukemia developed transient hypofibrinogenemia during a course of treatment with vincristine and prednisone. There was no evidence of overt, disseminated intravascular coagulation or significant liver impairment. Fibrinogen survival using homologous-125-I-labelled fibrinogen was measured in two patients; it was moderately shortened in both, perhaps indicating subclinical intravascular coagulation. Rapid lysis of leukemic cells might have been responsible for activating coagulation and fibrinolysis in vivo. These four patients, however, were not different in any clinical or laboratory parameter from nine others with lymphoblastic leukemia similarly treated and investigated without observing any defect in their fibrinogen. There were no bleeding complications and the fibrinogen level became normal within 13 to 30 days.
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PMID:Hypofibrinogenemia associated with vincristine and prednisone therapy in lymphoblastic leukemia. 105 92

We previously studied fibrinolysis and fibrinogenolysis by analyzing fragments of fibrin/fibrinogen degradation products (FDP) employing sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting. In this report, we characterized the fragments of FDP in four patients with disseminated intravascular coagulation (DIC), that were caused by various diseases. In the patients suffering from acute lymphoblastic leukemia (case 1) and acute suppurative cholangitis (case 3), DD and DY/X fragments resulting from fibrinolysis accounted for the most part of the FDP fragments. In case 3, D fragments resulting from fibrinogenolysis were also observed to much less extent. In a DIC associated with acute myeloblastic leukemia (case 2), both fibrinolysis and fibrinogenolysis were increased and resulted in high levels of D, Y and DY/X fragments, concomitant with moderate levels of DD and high molecular weight (HMW) fragments in the patient's sera. The increased fibrinogenolysis in this case was attributed to accelerated activation of plasmin. In a DIC patient of case 4, who underwent an operation due to hepatocellular carcinoma, marked increase in DY/X and HMW fragments and slight increase in DD fragment were observed on the day of operation. Hyperfibrinolysis documented in case 4 was explained by both increased production of thrombin and moderately accelerated activation of plasmin. Both qualitative and quantitative changes in the fragments of FDP during the courses of treatment in two cases of DIC were also noted. In summary, each underlying disease expresses characteristic pattern of FDP fragments in DIC.
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PMID:[Studies on the fragments of FDP in 4 patients with DIC]. 130 14

We determined the incidence and complications of disseminated intravascular coagulation (DIC) at presentation and during remission induction of previously untreated adults with acute lymphoblastic leukemia (ALL) or de novo Philadelphia chromosome-positive ALL (PCALL) seen at Memorial Hospital between January 1, 1978 and December 31, 1989. DIC was diagnosed in the presence of (1) low fibrinogen (less than or equal to 160 mg/dL), (2) prolonged prothrombin time (PT) and falling fibrinogen, or (3) prolonged PT and positive fibrin split products (FSP). L-Asparaginase was not used during remission induction. Among adequately screened patients with ALL, DIC was detected in 7 of 58 (12%) before initiation of chemotherapy and in 35 of 45 (78%) during remission induction. DIC was not simply the result of infection because clinical and laboratory signs of infection were absent in 16 patients, whereas only 2 of the 22 febrile patients with DIC had positive cultures. Among the 38 patients with DIC at presentation or during remission induction, serious complications were seen in 13 in temporal association with DIC (pulmonary embolus in one, sagittal sinus thrombosis in three, and serious hemorrhage in nine) and were major factors in the deaths of three patients. Among the 10 patients with thorough screening but no evidence of DIC there was only one hemorrhage during the same time interval. In patients with PCALL, DIC was detected in 9% at presentation and in 80% during remission induction. We conclude that DIC is rare at presentation but common during remission induction of adult ALL and PCALL and may be associated with significant thrombotic and hemorrhagic complications. We suggest daily screening for DIC during the first 14 days of remission induction. The treatment of DIC in ALL and PCALL should be a subject of future clinical studies.
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PMID:High incidence of disseminated intravascular coagulation during remission induction of adult patients with acute lymphoblastic leukemia. 768 21

A 48-year-old female received serial combination chemotherapy including L-asparaginase (L-ASP) for acute lymphoblastic leukemia. After administration of L-ASP, the prothrombin time and activated partial thromboplastin time were prolonged, while fibrinogen and antithrombin III levels markedly decreased, so she was given fresh frozen plasma (FFP). But subsequently, she developed cerebral infarction in the left parietal region and further hemorrhagic infarction in the right parietal region, and died. Autopsy revealed superior sagittal sinus thrombosis and bilateral cerebral infarction, but no obvious thrombus in other organs. Coagulopathy following L-ASP therapy is well-known. In this case, the coagulation studies at the first attack showed that the plasma protein levels of coagulation and fibrinolysis factors decreased in spite of administration of FFP. Fibrin-fibrinogen degradation products (FDP) slightly increased. However there were no significant abnormalities in the platelet count, nor soluble fibrin monomer, which suggested no evidence of disseminated intravascular coagulation. Thus, these findings suggest that L-ASP might be associated with the pathogenesis of thrombosis in this case.
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PMID:[Superior sagittal sinus thrombosis following L-asparaginase therapy of acute lymphoblastic leukemia]. 157 39

Disturbed erythrocytic rheology revealed in ALL patients with hypocoagulative shifts is suggested to trigger DIC syndrome. Combined treatment enhanced erythrocytic aggregation, viscosity and reduced deformability. Nevertheless, the patients improved, hemorrhagic complications attenuated, hemostasis underwent positive changes. The shifts are thought a defense reaction. A correlation exists between rheologic abnormalities and ALL severity.
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PMID:[Rheologic properties of erythrocytes of the hemostatic system in patients with acute lymphoblastic leukemia]. 180 Feb 36

Patients with acute leukemia undergoing remission induction chemotherapy occasionally develop venous thrombosis despite severe thrombocytopenia and in the absence of disseminated intravascular coagulation. This observation prompted us to study the levels of the naturally occurring anticoagulant proteins C and S prospectively in patients undergoing remission induction chemotherapy for acute leukemia. Plasma samples from 50 adult patients with acute leukemia (34 AML, 16 ALL) were analyzed for protein C antigen, functional protein C, immunologic total and free protein S as well as levels of C4b binding protein (C4bBP). Plasma levels of immunologic protein C were significantly lower in patients with active acute myelocytic leukemia (mean = 77.9) than in controls (mean = 123.6) or patients in remission (mean = 132). Functional protein C levels were also significantly lower in AML patients with active disease (mean = 58.5) than controls (mean = 95.5) or patients in remission (mean = 98.5). Patients with acute lymphocytic leukemia (ALL) had normal levels of immunologic and functional protein C. Although total protein S levels were normal in all patients studied, levels of free protein S were significantly decreased in patients with active AML (mean = 29.3) compared with patients in remission (mean = 42.0) or controls (mean = 42.4). In contrast, patients with ALL, both with active disease and in remission had normal free protein S levels. This decrease in free protein S seen in active AML was not associated with liver disease, white cell count or an increase in C4bBP. These findings provide a possible explanation for the occasional occurrence of venous thrombosis in patients with acute myelocytic leukemia.
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PMID:Protein C and S levels in acute leukemia. 183 Apr 52


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