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)

A 28-year-old man developed AML 18 months after a diagnosis of non-Hodgkin's lymphoma, diffuse small cell type, clinical stage IIA. Induction therapy for the lymphoma consisted 60Co 4000 rads bilaterally to the cervical areas and 2000 rads to the right cervical area. Complete remission was attained. Nineteen courses of combination chemotherapy with Vincristine (VCR), 6-meraptopurine (6 MP), cyclophosphamide (CY) and predonisolone (pred) was added (Total dose: VCR; 26.5 mg, 6 MP; 3320 mg, CY; 3350 mg, pred; 4310 mg). Seven days after the final chemotherapeutic treatment he developed AML with DIC. Leukemic cells were peroxidase and specific esterase (naphthol AS-D chloroacetate) positive. Induction therapy for the AML consisting of DCMP (Daunomycin, Cytosine arabinosid, 6 MP and pred) and VCR (vindesine, CY and pred) was unsuccessful. The patient died of cranial hemorrhage 3 month after the diagnosis of acute leukemia. Autopsy revealed no recurrence of non-Hodgkin's lymphoma in the lymph nodes, bone marrow, spleen and liver. Seven other cases reported in the Japanese literature are reviewed.
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PMID:[Post therapeutic myeloblastic leukemia in non-Hodgkin's lymphoma]. 659 32

The frequency, nature, and management of chemotherapy-associated oral hemorrhages were studied in 1,093 adult inpatients undergoing treatment for acute leukemia or the blastic phase of chronic leukemia. Of this number, 163 (14.9%) manifested gross bleeding from the mouth during the course of treatment. The most common oral bleeding sites were the lips, tongue, and gingiva. Thrombocytopenia was the underlying cause in 88% of the cases, disseminated intravascular coagulation in 6%, and combinations of thrombocytopenia and hypofibrinogenemia and of thrombocytopenia and vitamin K deficiency in 5.5% and 0.6%, respectively. The vast majority of the patients with mouth bleeding had platelet counts below 40,000/mm3. Approximately 50% had indirect evidence of a coagulation factor deficiency in the blood. The oral hemorrhages were best managed by transfusions of HLA-compatible fresh platelets and fresh frozen plasma, together with topically applied clot-promoting agents, until hemostatic control was restored.
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PMID:Chemotherapy-associated oral hemorrhages in adults with acute leukemia. 661 Jan 54

Hemorrhagic infarction of the basal ganglia was observed in 2 young adult patients with acute leukemia who presented with progressive hemiparesis combined with severe mental alterations. In case 1 (AML) lethal infarction due to thrombosis of both internal cerebral veins occurred during induction therapy for relapsed leukemia; in case 2 (cALL) a devastating stroke probably due to deep cerebral venous thrombosis happened during the third remission. Neither of them had hyperleukocytosis, signs of infection, disseminated intravascular coagulation or CNS leukemia. We discuss long-term glucocorticoid therapy (case 1) and combined prophylactic CNS treatment (case 2) as possible risk factors for cerebrovascular thrombosis in acute leukemia.
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PMID:Hemorrhagic infarction of the basal ganglia. An unusual complication of acute leukemia. 664 5

The transfusion records of 189 patients with acute leukemia were analyzed to correlate lymphocytotoxic antibody (LCTAb) levels with response to a series of random-donor platelet transfusions (Tx). Twenty-one patients were studied twice at times of different LCTAb levels. All transfusions were given when patients were clinically stable without disseminated intravascular coagulation, bleeding, temperature greater than 101 degrees F, or splenomegaly. The mean 1-hr and 24-hr corrected count increments (CCI) for all patients with negative LCTAb were 16,100 and 12,000, and values for patients with positive LCTAb were 5,600 and 2,600 (P less than 0.0005). Thirteen patients had intermediate LCTAb (10-20%) and a variable response to Tx. Of the 137 patients with negative LCTAb levels 106 (77%) had good mean CCI of greater than 10,000 at 1 hr and greater than 7,500 at 24 hr following transfusion. In contrast of 60 patients with positive LCTAb (greater than 20% cytotoxicity), 53 (88%) had poor CCI of less than 10,000 at 1 hr and less than 7,500 at 24 hr after transfusion. Only 4 patients with positive LCTAb had a good response to random donor platelets at both 1 and 24 hrs. Eighteen patients had negative LCTAb with a high 1-hr and low 24-hr CCI. Thirteen of these had a history of positive LCTAb and in 9 there was an anamnestic rise following transfusion. Nine of 137 patients had negative LCTAb with low 1-hr and 24-hr CCI. LCTAb is highly predictive of response to random donor platelets. Cytotoxicity to greater than 20% of tested lymphocytes virtually precludes a good CCI at 1 and 24 hr.
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PMID:Lymphocytotoxic antibody is a predictor of response to random donor platelet transfusion. 685 34

Three patients with acute leukemia, disseminated intravascular coagulation, and a specific acquired chromosome abnormality [t (15;17)] were found by transmission electron microscopy to have the typical distribution of granules seen in promyelocytes. However, the average granule sizes were 120, 170, and 180 nm, respectively, for the three patients, significantly less than the 250-nm resolution of light microscopy. We regard the leukemia in these three patients as comprising a distinct clinical, ultrastructural, and cytogenetic entity that we have chosen to call "microgranular" acute promyelocytic leukemia.
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PMID:"Microgranular" acute promyelocytic leukemia: a distinct clinical, ultrastructural, and cytogenetic entity. 692 5

Bone marrow necrosis (BMN), defined morphologically by destruction of hematopoietic tissue, including the stroma, with preservation of the bone, is a rare syndrome. The conditions in which it is seen include sickle cell disease, acute leukemia, metastatic neoplasia, and bacterial infection, particularly when hypovolemia and septic shock are present. BMN is also associated with disseminated intravascular coagulation (DIC) following irradiation and antineoplastic therapy. The antiphospolipid syndrome (APS) is characterized by antibodies directed against the antiphospolipid substrate. Because this substrate is prominently involved in the coagulation cascade and widely distributed on cell walls, patients present with venous or arterial thromboses, recurrent abortion, thrombocytopenia, and Coombs' positive hemolytic anemia, typically with raised anticardiolipin antibodies or a diagnostic lupus anticoagulant test. BMN does not appear to have been previously recognized in this context. We report what we believe to be the first such case and suggest that the high titers of antibodies present may have played a central role in its pathogenesis.
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PMID:Extensive bone marrow necrosis associated with antiphospholipid antibodies. 777 73

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

When compared to values recorded in the 32 healthy control subjects, plasma protein C activity was found to be significantly decreased in the 29 patients with acute leukemia and especially in those considered to be in a critical condition. On the other hand, plasma antithrombin III activity did not significantly differ from the values noted in control subjects. The concomitantly occurring high plasma fibrinogen levels and low serum cholinesterase activity were highly suggestive for a switch of hepatic protein synthesis towards the production of acute phase proteins. It is therefore considered that in the absence of a consumption coagulopathy, changes affecting plasma protein C and antithrombin III should be related to a modified pattern of hepatic protein synthesis.
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PMID:Plasma protein C and antithrombin III in patients with acute leukemia. 786 37

Recently it has been shown that tissue factor (TF), an important trigger for initiating blood coagulation, is present in the circulating plasma. In order to assess the clinical implications of TF in plasma, plasma concentration of TF was quantitated in 65 patients with disseminated intravascular coagulation (DIC). The mean concentration of plasma TF was elevated in patients with DIC at presentation as compared with healthy subjects (446 +/- SD 536 pg/ml vs. 138 +/- 51 pg/ml, P < 0.001). Abnormally high levels were found only in 46.2% of the patients, predominantly in patients with non-hematological solid tumors and acute leukemia. Plasma TF did not correlate with hemostatic markers of DIC such as thrombin-antithrombin III complex, prothrombin fragment 1 + 2, plasma-alpha 2-plasmin inhibitor complex, FDP, D-dimer, or fibrinogen. Serial determinations of plasma TF demonstrated that plasma TF changes roughly in parallel with the course of DIC in most patients with elevated TF at presentation of DIC. These findings suggest that plasma TF is potentially valuable for monitoring the progress of DIC in a limited population of patients.
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PMID:Tissue factor in plasma of patients with disseminated intravascular coagulation. 803 86

BACKGROUND. Hypofibrinogenemia and increased fibrin(ogen) degradation products in acute leukemia have been attributed to intravascular thrombin generation triggered by leukemic cells. However, the strict relationship between fibrinogen catabolism and turnover of fibrinopeptide A (FPA), which is a sensitive and specific marker of thrombin activity, has not been evaluated in acute leukemia (AL) with or without disseminated intravascular coagulation (DIC) to see whether mechanisms other than thrombin activity could be responsible for fibrinogen consumption. We report here the 125I-fibrinogen kinetics and FPA measurements in 19 patients with AL, 6 of them with DIC. METHODS AND RESULTS. Radiolabelled fibrinogen kinetics were studied in all the patients concomitantly with the start of chemotherapy. Fibrinopeptide A was measured by a radioimmunoassay at time of diagnosis and during chemotherapy. The kinetics of disappearance of radiolabelled fibrinogen where biphasic, with a rapid phase in the first 1-3 days of chemotherapy and a subsequent slow phase associated with the reduction or disappearance of blast cells. Patients with DIC had a significantly shorter half-life and turnover than patients without DIC. The latter group had significant shortening of these parameters in comparison to normal subjects. The thrombin-dependent catabolic rate of fibrinogen, calculated from the mean level of FPA during the first phase of disappearance curve and by assuming 2 moles of FPA generated per mole of fibrinogen, was similar in patients without DIC and in normal subjects, whereas patients with DIC had a significantly higher catabolic rate, even though the increase was not sufficient to account for all the turnover of fibrinogen. No relationship was observed between fibrinogen turnover and FPA turnover.
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PMID:Fibrinogen survival and fibrinopeptide A in acute leukemia. 803 60


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