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)

Magnetic resonance (MR) of bone marrow was studied in two cases of acute leukemia which showed bone marrow necrosis. Case 1:A 24-year-old female was admitted because of sternum pain and bleeding tendency. She was diagnosed AML based on the peripheral blood picture. Bone marrow biopsy revealed the presence of bone marrow necrosis. T1 weighted imaging of MR showed low signal intensity in all vertebral marrow. Fatty marrow was demonstrated after achieving complete remission and the MR imaging of bone marrow changed to show high intensity, suggesting fat deposition. Case 2: A 19-year-old female suffered from chest pain and lumbago, and was diagnosed as ALL. DIC and bone marrow necrosis were confirmed during chemotherapy for remission induction. T1 weighted imaging showed the mosaic pattern of low and high signal intensity. She achieved complete remission and bone marrow clot revealed the presence of fatty marrow. Most areas of low signal intensity of T1 weighted imaging changed to those of high signal intensity. These observations suggest that necrotized bone marrow seemed to change to fatty marrow along with achieving remission. MR imaging study of bone marrow is useful for evaluating hematopoiesis in hematologic disorders.
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PMID:[Magnetic resonance imaging (MRI) of bone marrow necrosis]. 786 14

The association of cancer with clinical abnormalities of blood coagulation, including superficial thrombophlebitis, deep vein thrombosis (DVT), and disseminated intravascular coagulation (DIC) is well-known, particularly in patients with solid tumors and acute promyelocytic leukemia (APL). Less commonly appreciated is the potential for the development of venous thromboembolic disease (TED) in patients with acute lymphocytic leukemia (ALL). Multiple mechanisms have been implicated for the activation of coagulation in these patients, with an emphasis on the contribution made by the procoagulant properties of the tumor cells themselves. We present two cases of patients with pre-B cell ALL, both of whom developed recurrent TED as the presenting manifestation of their leukemia and/or heralding relapse. The blast cells from one of the patients were studied for the presence of procoagulant activity (PCA) and by Northern blot analysis for tissue factor (TF) messenger RNA (mRNA). Neither PCA nor TF mRNA could be identified in highly purified populations of the lymphoblast cells. We conclude that recurrent TED can be a manifestation of ALL and that mechanisms other than the release of tumor cell procoagulants should be sought to explain the pathogenesis of thrombosis in some patients.
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PMID:Recurrent venous thrombosis as the presenting manifestation of acute lymphocytic leukemia: leukemic cell procoagulant activity is not responsible for the hypercoagulable state. 796 91

Tissue factor activity of intact cell and cell lysate, and the presence of tissue factor antigen on cell surface, were examined in leukemic cells from patients with acute myelogenous leukemia (AML, M1-M5) or acute lymphoblastic leukemia (ALL-L1), and in mononuclear cells from normal donors. Leukemic cells from AML or ALL had significantly more tissue factor activity not only on intact cells but also in cell lysate than mononuclear cells from normal donors (p < 0.001). Tissue factor activities of the intact leukemic cells and lysate from AML patients with DIC were significantly higher than those without DIC (p < 0.001). The relationship between the percent of positive cells for tissue factor and the presence of DIC at the time of diagnosis of acute leukemia was observed. The patients with DIC showed the higher percentage of tissue factor-positive cells than those without (p < 0.01). The development of DIC following chemotherapy was recognized in 2 out of 7 AML-MI patients and 2 out of 4 ALL-L1 patients who had relatively high tissue factor activities of cell lysate. The release of tissue factor from cytoplasm induced by chemotherapy would be another mechanism for the development of DIC. The report suggests the possibility of the prediction for DIC by the flowcytometric assay of tissue factor antigen.
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PMID:The expression of tissue factor antigen and activity on the surface of leukemic cells. 842 86

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

In order to establish the frequency and clinical complications of DIC during remission induction of untreated adults with acute lymphoblastic leukemia, we retrospectively reviewed the records of 125 consecutive patients treated with vincristine, doxorubicin, and dexamethasone but without L-asparaginase. DIC, defined as hypofibrinogenemia in the presence of elevated fibrin-fibrinogen degradation products, was detected at presentation in 10% of 99 and during remission induction in 67% of 58 patients who were screened for DIC. Elevated levels of D-dimers (DD) were seen in all eight patients with DIC in whom they were measured. All cases of DIC were diagnosed by the ninth day of induction and were associated with infection in 15 of 39 patients. DIC did not cause any deaths but was temporally associated with two thromboses and four hemorrhages in six of the 16 patients with fibrinogen levels < 100 mg/dl but with only one hemorrhage among 23 patients (4%) with fibrinogen levels > 100 mg/dl (P < 0.01). Heparin was not administered to any patient, whereas platelets were administered to all to maintain platelet counts > 20 x 10(9)/l. Fresh frozen plasma (FFP) and/or cryoprecipitate were administered 26 patients resulting in a contemporaneous correction of the coagulopathy and in control of hemorrhages and thromboses. We conclude that DIC is rare at presentation but common during induction of adult ALL and is frequently associated with clinical complications when fibrinogen levels are < 100 mg/dl. We recommend daily testing of fibrinogen, PT, and DD during the first 10 days of induction, and for the patients with DIC platelet transfusions to maintain counts > 20 x 10(9)/l, and when fibrinogen levels fall below 100 mg/dl transfusions of FFP and/or cryoprecipitate. Additional studies are needed to determine the optimal management of the DIC during remission induction of adult acute lymphoblastic leukemia.
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PMID:Disseminated intravascular coagulation in adult acute lymphoblastic leukemia: frequent complications with fibrinogen levels less than 100 mg/dl. 890 74

It is well established that in acute lymphoblastic leukemia (ALL) patients L-asparaginase (L-Ase) provokes thrombotic events reducing coagulation inhibitors in both adults and children. A tight correlation between thrombotic and hemorrhagic complications and ALL has also been hypothesized because of the high incidence of disseminated intravascular coagulation (DIC) found during the early period of chemotherapeutic treatment apart from L-Ase. All the authors reporting on this subject, however, consider the remission induction phase of treatment the most risky, if not exclusive, for the development of a thrombotic event, in particular if it includes the administration of L-Ase. We report here two cases of ALL patients who experienced a cerebral sinus thrombosis in a later phase of treatment, demonstrating that the thrombotic risk is surely exacerbated by chemotherapy but is not exclusive to the remission induction period.
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PMID:Thrombotic events are not exclusive to the remission induction period in patients with acute lymphoblastic leukemia: a report of two cases of cerebral sinus thrombosis. 936 81

An 18-year-old female with CNS relapse of acute lymphoblastic leukemia after previous complete remission of the disease underwent chemotherapy. Due to the therapy she suffered from profound suppression of bone marrow with consecutive thrombocytopenia and leukopenia. Despite prophylactic treatment, severe septicemia occurred with septic shock, hemolysis and disseminated intravascular coagulation (DIC). As the clinical course became uncontrollable by means of conventional therapy, including broad-spectrum antibiotics, substitution of fresh frozen plasma, antithrombin III and heparin therapy, plasma exchange was used as a rescue therapy. This method succeeded in effective replacement of clotting factors and normalization of coagulation, in removal of fibrinogen degradation products and probably of toxins and shock mediators. The patient recovered from shock.
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PMID:Plasmapheresis in severe septic shock with disseminated intravascular coagulation. 942 19

A high frequency of disseminated intravascular coagulation (DIC) in adult acute lymphoblastic leukemia (ALL) has been reported; however, its clinical relevance and characteristics have not been fully determined. We studied 67 adults with newly diagnosed ALL between 1982 and 1996 to clarify these questions. DIC was diagnosed in ten of 64 patients (16%) who underwent coagulation study at presentation and in 14 of 40 patients (35%) screened for DIC within 7 days after starting remission induction therapy. Overall, 24 of 67 patients (36%) had DIC during this period. Hemorrhagic symptoms were generally mild, while two patients required red blood cell transfusions. Patients who developed DIC had higher white blood cell counts and more frequently a palpable spleen than those who did not. There was no difference in age, French-American-British subtype, karyotype, immunophenotype, lactate dehydrogenase level, percentage of blasts in bone marrow, or frequency of lymphadenopathy or hepatomegaly between patients who had DIC and those who did not. Fibrinolysis tended to be milder in DIC complicating ALL than in that complicating acute promyelocytic leukemia; however, there was no difference in other coagulation parameters between these two subtypes. An etiological link between CD34 expression in common ALL patients and DIC was suggested.
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PMID:Disseminated intravascular coagulation in acute lymphoblastic leukemia at presentation and in early phase of remission induction therapy. 969 14

To know the clinical characteristics and the prognostic factors of hyperleukocytic acute leukemia, we reviewed 244 patients with acute leukemia associated with hyperleukocytosis. Restrospective analysis and control study were used. Hyperleukocytosis occured in 8.5% of patients with acute leukemia. Hyperleukocytosis in ALL was more common than that in AML. Among AML with hyperleukocytosis, M5 subtype was the most. Hepatomegaly, splenomegaly, lymphadenopathy, DIC and CNSL were more frequent in hyperleukocytosis group. The complete remission rate was 41.4% for patients with hyperleukocytosis versus 54.2% for patients with non-hyperleukocytosis. The early mortality rate was significantly increased in hyperleukocytic patients (23.8%) as compared to the nonhyperleukocytic group (11.1%). Intracranial hemorrhage was the main cause of early death. The high risk factors of early death were: hemoglobin < or = 40 g/L, blood platelet < or = 30 x 10(9)/L, DIC, infection, CNSL at presentation. Acute leukemia with hyperleukocytosis has poor prognosis. Especially, acute myeloid leukemia with hyperleukocytosis must be taken seriously because of high early mortality rate.
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PMID:[244 patients with hyperleukocytic acute leukemia. Shanghai Leukemia Cooperation Group]. 1043 59

Coagulation disorders are often the reason for fatal bleeding in acute promyelocytic leukemia. Their occurrence as well as pathogenesis and prognostic significance in other subtypes of acute myelogenous leukemia and acute lymphoblastic leukemia is less known. Tests were carried out in 70 patients including 49 with AML and 21 with ALL. In all patients thrombin-antithrombin complexes (TAT), D-dimer (DD) and plasmin-antiplasmin complexes (PAP), antithrombin III activity, fibrinogen/fibrin degradation products, APTT and PT were determined. The tests were performed on diagnosis and after cytostatic treatment. The level of TAT, DD and PAP was elevated in 83% of the patients on diagnosis and in 90% after treatment. The highest values were observed in AML M3 patients. Among leukemic patients with normal levels of TAT, DD and PAP at diagnosis, cytostatic treatment had a negligible effect on the level of these markers. During remission the levels of these markers returned to the normal values while in patients without remission they were either elevated or returned to normal values. No correlation between the levels of activation markers and remission rate was reported. DIC was diagnosed in 13 patients including three after chemotherapy. The DIC was acute or subacute in AML and chronic in ALL patients. In the majority of acute leukemia patients there were already changes on diagnosis indicating coagulation activation. Except for AML M3, these usually had a subclinical course. The TAT, DD and PAP tests are not reliable markers of remission in acute leukemias.
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PMID:Assessment of coagulation disorders in patients with acute leukemia before and after cytostatic treatment. 1061 52


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