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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 consecutive patients with acute promyelocytic leukaemia who presented with severe haemorrhagic syndromes were studied and the findings contrasted with those of two patients with classical defibrination after electroshock or complicated labour. The leukaemic patients showed no depletion of fibrinogen. There was no evidence of disordered thrombin generation by either intrinsic or extrinsic pathway sufficient to account for their haemorrhage. All, however, showed strikingly enhanced fibrinolytic activity, which could have accounted for bleeding. This fibrinolytic disorder was characterized by free u-PA in the plasma and differed from that seen after classical defibrination, where free t-PA was observed. U-PA was found also in malignant promyelocytes, which may be the source of u-PA activity in the patients' plasma. Bleeding in promyelocytic leukaemia may be primarily a fibrinolytic disorder.
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PMID:The bleeding disorder in acute promyelocytic leukaemia: fibrinolysis due to u-PA rather than defibrination. 249 42

A case of acute leukemia with atypical malignant cells is reported. The clinical picture and coagulation studies were consistent with a disseminated intravascular coagulation syndrome. Morphologically, the leukemic cells from the peripheral blood and bone marrow showed azurophilic granules. More than 80% of cells were hypergranulated, resembling the macrogranular type of promyelocytes. Ultrastructural studies and the pattern of endogenous peroxidase were consistent with the microgranular type of promyelocytes in about 20% of the leukemic cells. Auer bodies were present in both types of atypical promyelocytes. Cytochemically, the whole malignant population exhibited intense peroxidase activity. Studies with monoclonal antibodies showed that about 45% of the proliferating cells expressed T-cell markers T3, T4, T8 and T11, but the cells were not reactive with OKM1 monoclonal antibodies. The chemotherapy for acute promyelocytic leukemia was inefficient, and the prompt disappearance of the blood abnormalities was observed only when chemotherapy for acute lymphoblastic leukemia was started. Therefore, it seems that in some cases of leukemia with hybrid types of malignant cells the morphological features determine the clinical picture, while the patient's response to the therapy is conditioned mainly by the cell surface phenotype.
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PMID:Acute promyelocytic leukemia with T-cell markers and particular response to treatment. Report of a case. 249 88

The association of acute leukemia (AL) and disseminated intravascular coagulation (DIC) in 89 patients with a de novo diagnosis of AL made in our center during the last 8 years was retrospectively evaluated. DIC was demonstrated in 14 patients (15.7%) (7 AML-M3, 1 AML-M3, 1 AML-M2, 1 AML-M4, 2 AML-M5, and 2 ALL-L1). In 5 of them ICD was diagnosed after the beginning of chemotherapy. The factors predisposing to the development of DIC were: 1) the type of AL (p less than 0.01), as 70% of AML-M3 had DIC; 2) the intensity of granulation in leukemia cells (p less than 0.004); 3) the presence of Auer's rods and/or splinters in these cells, and 4) the presence of hemorrhagic diathesis (p less than 0.007). Eight of the 14 patients with DIC received heparin at a prophylactic dosage. No significant differences in the clinical course were in the group of patients with DIC who received heparin and in those who did not, excepting that in the former the platelet requirements were higher (p less than 0.005). Mortality rate during the first month was higher in the group of AL with DIC than in AL without DIC (p less than 0.025). Long term mortality was similar in both groups. The control of hemostasis is fundamental in AL, even in those patients without DIC at the time of diagnosis. The administration of blood derivatives has a high priority in AL with DIC. The role of heparin is still controversial.
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PMID:[Association of acute leukemia with disseminated intravascular coagulation in adults. Analysis of 14 cases]. 260 8

A case of acute myeloblastic leukemia associated with multiple intracerebral hematomas is presented. A 19-year-old woman with a two week's history of mild fever suddenly lost consciousness, and was afflicted right severe hemiparesis, left mild hemiparesis and motor aphasia. A CT scan revealed bilateral thalamic hyperdense lesions and paraventricular small hematoma in the right hemisphere. Hematology showed marked leukocytosis (450,000/mm3), mild anemia and no coagulopathy including disseminated intravascular coagulation syndrome. Cytology showed myeloblasts with positive stain in peroxidase and negative in esterase both in cerebrospinal fluid and blood. These findings indicated M 1 type, myeloblastic leukemia without maturation, according to FAB (French-American-British Co-operative group) classification. CT scan on the second day demonstrated expansion of the hematoma in the right thalamus, and nine brand-new small hematomas in different locations. The patient deteriorated into brain death soon after this examination. The pathology of this case was supposed to be "hyperleukocytosis", which is defined as a leukocyte count greater than 100,000/mm3. Severe leukostasis due both to dense leukocytes and lack of mobility of the myeloblast brought about an increase in permeability because of local impairment of nutrition to the walls of the vessels. As a result, the following histological changes occurred: 1) cellular exudation into Virchow-Robin space, 2) the appearance of leukemic nodule, admixtures of leukemic cells and erythrocytes, 3) mechanical compression of the capillaries and venules by the enlarging mass of the leukemic nodules. CT scan showed these characteristics as follows: 1) multiplicity, 2) small-size, 3) cerebral hemisphere, especially in white matter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of acute myeloblastic leukemia associated with multiple intracerebral hematomas]. 269 89

Fibrinopeptide A (FPA) was systematically investigated in 74 patients with acute leukaemia at different stages of the disease (50 with non-lymphocytic leukaemia, ANLL; 24 with lymphocytic leukaemia, ALL). At diagnosis, 75% of the cases had high FPA levels (86% in ANLL and 54% in ALL) with significantly higher levels in ANLL than in ALL (13.4 vs 4.4 ng/ml; p less than 0.001). Patients with DIC (20 cases in ANLL and 1 case in ALL) had significantly higher levels (p less than 0.001). FPA levels were neither correlated with fibrinogen or FDP levels nor with blast cell count. During chemotherapy, median FPA did not show significant changes whereas, at the end of therapy, a return toward normality was generally observed both in ALL and ANLL apart from the group of patients with acute promyelocytic leukaemia. Among the 24 patients who entered post-remission follow-up (13 ANLL and 11 ALL), 10 cases out of the 11 relapsing (6/6 with ANLL and 4/5 with ALL) had increased FPA 1 to 2 months before the ascertainment of the relapse. However, 16% and 9% of the samples obtained on different occasions, respectively from ANLL and ALL cases in maintained first remission, showed FPA above the normal limit. This study demonstrates that subclinical activation of blood coagulation, as indicated by high FPA level, is common both in lymphocytic and non-lymphocytic leukemia and suggests that this phenomenon is related to disease activity.
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PMID:Clinical significance of fibrinopeptide A in acute lymphocytic and non-lymphocytic leukaemia. 276 77

We present the case of a young man with acute monocytic leukemia (French-American-British classification:M5) and systemic hyperfibrinolysis with severe bleeding. Although fibrinolysis is usually mild and secondary to disseminated intravascular coagulation, its role as a primary and dominant factor in rare cases of leukemia warrants that its presence be sought as a cause of abnormal bleeding. Decreased serum plasminogen and increased serum plasmin determined by synthetic substrate assay and a negative protamine paracoagulation test are crucial findings. Use of high-dose epsilon-aminocaproic acid was effective in treating this complication. A transient increase in fibrinolytic activity coincident with the early effect of antileukemic treatment suggested that plasminogen activator and/or fibrinolytic protease substances were released from leukemic cells. Fibrinolytic activity subsequently disappeared with reduction in the population of leukemic cells.
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PMID:Primary fibrinolysis in acute monocytic leukemia. 276 88

A 24 year-old female was admitted because of hypermenorrhea and petechiae. The peripheral blood tests on admission were consistent with acute promyelocytic leukemia complicated with DIC. BHAC-DMP therapy was started along with platelet transfusions and heparin administration. On the day 9 of admission, on the contrary to the improvement of hematological data, the patient suffered from severe headache and nausea. The neurological examination revealed anisocoria. Right side chronic subdural hematoma was a diagnosis made by emergency CT scan and was treated with drainage of the hematoma. Post-operatively, the patient did well, and achieved complete remission on the day 43 of admission. Since intracranial hemorrhages due to DIC complicated with leukemia are often fatal, those patients are usually treated conservatively. However, as shown in this case report, some cases might have an indication for the neurosurgical operation. It is important to check conditions carefully whether the patient has an indication for the operation.
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PMID:[Successful treatment by a drainage of subdural hematoma in a case of intracranial hemorrhage due to DIC complicated with acute promyelocytic leukemia]. 279 98

An 18-year-old male patient who had suffered from polyuria, nocturia and easy fatigability since childhood is described. A germ cell tumor in the suprahypophyseal region was diagnosed at the age of 13 years, and was treated by cranial irradiation. Growth retardation and other signs of hypophyseal deficiency successively occurred, and human growth hormone was administered for two years and five months from the age of 16 years until acute lymphoblastic leukemia developed. Adriamycin, vincristine and prednisolone therapy induced complete remission, but the patient died of disseminated intravascular coagulation two months later. The relationship between the occurrence of leukemia and administration of growth hormone is discussed.
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PMID:Occurrence of acute lymphoblastic leukemia in a boy treated with growth hormone for growth retardation after irradiation to the brain tumor. 283 38

Plasma D-dimer was measured and compared with serum fibrinogen/fibrin degradation product levels (FDPs) in patients with disseminated intravascular coagulation (DIC) and other conditions associated with a hypercoagulable state. D-dimer (N less than 200 ng/ml) was elevated in all 43 patients with DIC, in 48 of 59 patients with liver disease, in 22 of 27 patients with acute leukaemia at presentation, in 17 of 23 patients with malignant disease, in 29 of 39 women in the third trimester of a complicated pregnancy, in 17 of 18 patients with deep venous thrombosis and in only four of 27 patients with acute myocardial infarction. There was a significant correlation between plasma D-dimer and serum FDP levels (P less than 0.01) as follows; DIC: r = 0.58, liver disease: r = 0.57, acute leukaemia: r = 0.84, malignancy: r = 0.87. The frequent elevation of D-dimer observed in liver disease, acute leukaemia, malignancy and complicated pregnancy indicates that a hypercoagulable state is a common occurrence in these conditions although in liver disease elevated levels resulting from a failure of normal clearance mechanisms cannot be excluded. The close relationship between D-dimer and FDP levels suggests that serum FDPs predominantly arise from the interaction of plasmin with crosslinked fibrin rather than with fibrinogen in the conditions in which these were compared.
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PMID:Plasma D-dimer levels and their relationship to serum fibrinogen/fibrin degradation products in hypercoagulable states. 291 30

Monoblasts from 7 patients with acute monoblastic leukaemia produced significantly less procoagulant activity (PCA) in response to endotoxin (mean 0.7 U/10(6) monocytes, range 0.4-1.4) than monocytes from 6 patients with chronic myelomonocytic leukaemia (mean 6.0 U/10(6) monocytes, range 1.25-10.7) and 15 normal subjects (mean 8.9 U/10(6) monocytes, range 3.1-21.2). However, when expressed as the quantity of monocyte-related PCA generated per millilitre of blood, there was no significant difference between patients with acute monoblastic or chronic myelomonocytic leukaemias, though both types of patients generated significantly higher amounts of PCA than normal subjects or patients in haematological remission. The relationship of these findings to the occurrence of disseminated intravascular coagulation is discussed.
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PMID:A quantitative study of monocyte procoagulant activity in acute monoblastic and chronic myelomonocytic leukaemias. 311 6


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