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

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

In two patients receiving L-asparaginase therapy, severe acute pancreatitis complicated by disseminated intravascular coagulation (DIC) developed. In both cases it was successfully treated with continuous infusion of a synthetic protease inhibitor, nafamostat mesilate. In this report, we briefly discuss the clinical efficacy of the synthetic protease inhibitor in treating such cases.
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PMID:Use of a synthetic protease inhibitor for the treatment of L-asparaginase-induced acute pancreatitis complicated by disseminated intravascular coagulation. 162 61

Hemostatic changes were evaluated in ten patients with acute lymphoblastic leukemia and lymphoma who received chemotherapy with L-asparaginase, vincristine, and prednisolone for 1 week. Following treatment, prothrombin time and activated partial thromboplastin time were significantly prolonged, while a marked decrease in fibrinogen levels was observed. The values for cross-linked fibrin degradation products, however, remained within normal limits during treatment, which excluded the possibility of disseminated intravascular coagulation. The concentrations of coagulation inhibitors (antithrombin III, protein C, and protein S), plasminogen, and alpha 2 antiplasmin also significantly decreased; however, levels of both tissue-type plasminogen activator and plasminogen activator inhibitor, which are synthesized in endothelial cells, increased during the treatment. Although a decrease was observed in concentrations of many coagulation factors, including subunits A and B of factor XIII, the activity and antigenicity of factor VII significantly increased following the treatment. From this study, we concluded that these hemostatic abnormalities caused by the administration of L-asparaginase produced a labile condition that easily inclines to bleeding or thrombosis.
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PMID:Changes in hemostatic and fibrinolytic proteins in patients receiving L-asparaginase therapy. 275

Thirty-seven dogs with malignant lymphoma were treated with either polyethylene glycol conjugated (PEG) asparaginase alone (10-30 IU/kg intraperitoneally [IP] weekly--20 dogs) or PEG-asparaginase combined with one cycle of chemotherapy (vincristine, cyclophosphamide, methotrexate, and prednisone), followed by maintenance PEG-asparaginase (30 IU/kg, IP weekly--17 dogs). In the 20 dogs (eight were chemotherapy resistant) treated with PEG-asparaginase alone, seven had a complete response (CR), seven had a partial response (PR), five had no response (NR), and one was not evaluable (NE). The duration of response (CR + PR) ranged from 14 to 102 days (median, 48 days). In the eight chemotherapy-resistant dogs (seven were previously resistant to L-asparaginase) four had responses (one CR and three PR). In the 17 dogs treated with combined PEG-asparaginase and chemotherapy, 13 had a CR, two had a PR, and two had NR. None of the dogs had had prior chemotherapy, and the duration of response (CR + PR) ranged from 7 to 840+ days, with a median of 126+ days. Four dogs are still on maintenance PEG-asparaginase at 16+, 21+, 26+, and 28+ months. Toxicity consisted of death due to massive tumor breakdown (two dogs), disseminated intravascular coagulation (DIC--one dog), hypersensitivity reaction (one dog), vomiting (three dogs) and soft stools (three dogs). Four normal dogs were given very high doses of PEG-asparaginase (200 IU/kg and 1200 IU/kg) once weekly for two treatments without any significant toxicity. These results indicate that PEG-asparaginase has antitumor activity in dog with spontaneously occurring malignant lymphoma.
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PMID:A preliminary study on the evaluation of asparaginase. Polyethylene glycol conjugate against canine malignant lymphoma. 356 63

During a 4-year period, 26 children with systemic malignancies suffered cerebrovascular accidents. These occurred in 17 patients with lymphoreticular malignancy and nine patients with solid tumors. They were the presenting signs of malignancy in three patients and were the direct cause of death in six. Cerebrovascular accidents were directly related to disseminated intravascular coagulation in eight patients, to chemotherapy in eight patients, to metastatic tumor in three patients, to thrombocytopenia in three patients, and to fungal meningitis in one patient. All patients with disseminated intravascular coagulation had leukemia and at times, cerebrovascular thrombosis predated systemic or laboratory evidence of disseminated intravascular coagulation. This review indicates that four major syndromes are apparent in children with cancer: vascular thrombosis associated with disseminated intravascular coagulation, acute arterial or sagittal sinus thrombosis secondary to L-asparaginase in children with leukemia, acute neurologic dysfunction in patients with osteogenic sarcoma treated with high-dose methotrexate, and obtundation, seizures, and focal neurologic deficits in patients with neuroblastoma metastatic to the torcular region. Although elevated WBC counts and thrombocytopenia occur frequently in children with cancer, in themselves they uncommonly result in strokes. It is concluded that cerebrovascular accidents are a relatively frequent cause of acute neurologic compromise in children with cancer and that certain types of malignancies and their treatment predispose patients to this complication.
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PMID:Cerebrovascular accidents in children with cancer. 386 Jul 96

Twelve dogs with lymphosarcoma and hypercalcemia were treated over a period of 36 months. Signs and laboratory findings were referable to hypercalcemia and azotemia. All dogs were staged, classified histologically, and given cytoreductive chemotherapy, using 5 drugs (vincristine sulfate, cytosine arabinoside, cyclophosphamide, L-asparaginase and prednisone). For azotemia, symptomatic therapy (0.9% NaCl solution and furosemide) was given. Seven dogs responded completely, with marked reduction of lymphadenopathy and return of serum calcium concentration to normal. Median duration of remission in this group was 48 days (range, 14 to 93), and median survival time was 112 days (range, 85 to 153). Five nonresponding dogs had less than 50% reduction in measurable tumor mass, although serum calcium concentration returned to normal. The median survival time for this group was 34 days (range, 23 to 68). Two of the nonresponders died from sepsis and another from disseminated intravascular coagulation. Response to therapy did not appear to be influenced by age, breed, sex, initial calcium concentration, degree of azotemia, or histologic classification.
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PMID:Chemotherapeutic responses in dogs with lymphosarcoma and hypercalcemia. 689 39

Thrombotic events have been reported in acute lymphoblastic leukaemia patients, especially during or after L-asparaginase administration. A so-called L-asparaginase associated coagulopathy has been well recognized, being characterized by a hypercoagulable state (decrease of antithrombin III, plasminogen, protein C, protein S and increase of prothrombin fragment F1 + 2, thrombin-antithrombin complexes and fibrinopeptide A). The aim of this study was to determine whether the supplementation of antithrombin III (AT-III) concentrates could improve the L-asparaginase associated coagulopathy, thereby blocking the activation of the haemostatic system. In 25 adult patients with acute lymphoblastic leukaemia (M 19, F6, mean age 34 years) antithrombin III (AT-III) concentrates were administered at daily doses of 50 U/kg for 10 consecutive days from the beginning of L-asparaginase therapy (6,000 U/m2/day s.c. for 7 days), given according to the GIMEMA ALL 0288 trial. A marked increase of antithrombin III was recorded on days IV-VIII-XI (P < 0.001). No changes in protein C, protein S, plasminogen, alpha 2-antiplasmin, factor VII and platelet count were observed and there was no increase in markers of hypercoagulability. There was no evidence of disseminated intravascular coagulation. In conclusion, AT-III concentrate supplementation during L-asparaginase therapy, by the achievement of high levels of antithrombin III, is associated with a lack of activation of the haemostatic system and appears to overcome the complex coagulopathy associated with L-asparaginase.
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PMID:Antithrombin III infusion suppresses the hypercoagulable state in adult acute lymphoblastic leukaemia patients treated with a low dose of Escherichia coli L-asparaginase. A GIMEMA study. 751 43

Ten percent (214/2,059) of all dogs with cancer at North Carolina State University Veterinary Teaching Hospital had thrombocytopenia. The thrombocytopenia was associated with infectious/inflammatory etiologies in 4%, miscellaneous disorders (therapy, bone marrow failure, disseminated intravascular coagulation) in 35%, and neoplasia without identifiable secondary factors in 61% of cancer-bearing dogs. Classifying these dogs by tumor groups revealed the following proportionate ratios: lymphoid, 29%; carcinoma, 28%; sarcoma, 20%; hemic neoplasia, 7%; multiple, 5%; unclassified, 3%; benign, 3%; brain, 3%; and endocrine, 3%. Dogs with hemangiosarcoma, lymphoma, and melanoma were at increased risk of developing thrombocytopenia. Cytotoxic therapy was the major factor increasing the risk of thrombocytopenia in dogs with melanoma. Golden Retrievers were the only breed recognized with a predisposition to develop thrombocytopenia. If thrombocytopenia is identified in a dog with cancer, we recommend thorough evaluation of the coagulation system before surgery or therapy, and careful consideration of the risks and potential benefits of myelosuppressive or L-asparaginase therapy.
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PMID:Thrombocytopenia associated with neoplasia in dogs. 788 25

During a 3-year period, 6 of 50 children with systemic malignacies developed neurologic complications such as hemiparesis, convulsions and loss of consciousness. The children consisted of 1 boy and 5 girls, from 3 to 12 years old, 3 with acute lymphoblastic leukemia and 3 with malignant lymphoma. Four patients received induction treatment that included intravenous administration of L-asparaginase and/or intrathecal administration of methotrexate. One patient received induction treatment and consolidation treatment that included intravenous administration of L-asparaginase. One patient received induction and consolidation treatment, and the protocol for peripheral blood stem cell transplantation. Laboratory examinations revealed coagulation dysfunction in 3 patients treated with L-asparaginase and 1 patient with disseminated intravascular coagulation (DIC). Magnetic resonance imaging (MRI) was performed on a 1.5-T unit, using spin-echo or fast spin-echo sequences. T1-weighted, T2-weighted, and proton density-weighted images were obtained in the axial and/or coronal plane (section thickness, 4 mm; inter-section gap, 2 mm). MRI was initially performed within 36 hours after the onset in all patients, and follow-up MRIs were performed for 6 months. MRI showed lesions involving the cortex and subcortex in 4 patients with coagulation dysfunction. In 2 of these 4 patients, Gd-enhanced T1-weighted images showed contrast enhancement in the surface of the gyrus, suggesting focal vascular stasis. Serial MRI revealed nearly complete resolution of the lesions. Symptoms were relieved in every case. The lesions on MRI were presumed to be due to venous thrombosis related to the coagulation dysfunction caused by L-asparaginase or DIC. On the other hand, in 2 patients with onset after intrathecal administration of high-dose methotrexate and cytarabine, MRI revealed multiple lesions involving the centrum semiovale and periventricular white matter. No Gd-enhancement of the lesion was detected. This MRI finding was consistent with leukoencephalopathy. As time passed, the symptoms improved completely, and the lesions became better demarcated. MRI is useful for differentiating lesions related to coagulation dysfunction from leukoencephalopathy.
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PMID:[MRI abnormalities of the brain in neurologic complications following treatment of cancer in children]. 875 96


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