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)

Eosinophilic leukaemia was diagnosed in a 13-year-old boy with clinical and haematological signs of acute leukaemia. A positive naphthol-AS-D-chloroacetate esterase reaction was present in 93% of bone marrow eosinophils. This confirms earlier findings for this sub-group of leukaemia in adultsmcharcot-Leyden's crystals were found in bone marrow, and the eosinophils were further characterized by other cytochemical and electronmicroscopic studies. Only short remission periods were achieved, the patient dying 53 weeks after diagnosis. Attacks of cardiac arrhythmias, thought to be due to adriamycin treatment, were probably related to thrombi in the coronary arteries as a result of disseminated intravascular coagulation. It is thought that eosinophilic leukaemia with a positive naphthol-AS-D-chloroacetate esterase reaction is a variant of acute myeloid leukaemia.
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PMID:[Eosinophilic leukaemia with chloroacetate-esterase-positive granules in a child (author's transl)]. 116 79

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

Automated platelet counts in a patient with newly diagnosed AML M5 with extreme leukocytosis were reported as 129, 166 and 121 x 10(9)/1. Routine blood films showed a corresponding number of platelet-sized particles, judged to be platelets. The patient was treated for DIC with low-dose heparin infusion. Platelet transfusions were not given initially. The patient died 14 h after admission from intracerebral haematoma. The origin of the platelet-sized particles seen in routine stained blood films was examined by cytochemical and immunological staining for peroxidase, non-specific esterase, CD 13 and CD 33. About 1/3 of the fragments had the same staining characteristics as the leukaemia cells, indicating leukaemia cell origin. Staining for platelet-specific antigen GpIIIa was positive only in 4% of the platelet-sized fragments, with a calculated true platelet count of 4 x 10(9)/1. The presence of cell fragments masquerading as platelets should be suspected in leukaemia patients with bleeding symptoms and normal or near normal platelet counts.
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PMID:Spurious platelet counts in acute leukaemia with DIC due to cell fragmentation. 145 3

We investigated the imbalance between thrombin and plasmin activity in vivo with various grades of severity of disseminated intravascular coagulation (DIC) in relation to the underlying diseases. Plasma thrombin-antithrombin-III complex (TAT) and plasmin-alpha 2-antiplasmin complex (PAP) levels were measured in 133 blood samples obtained from patients with DIC. The TAT/PAP ratio was higher in patients with sepsis or solid cancer than in those with hematologic malignancies. In acute promyelocytic leukemia (APL), the TAT levels were the highest, but the PAP levels were even higher and the TAT/PAP ratio was the lowest. As for the severity of DIC, in mild DIC, both thrombin and plasmin activities were increased. In moderate DIC, the TAT/PAP ratio increased, and thrombin activity was much more predominant. However, in severe DIC, the ratio decreased, and plasmin activity became excessive. In 3 patients with acute myeloblastic leukemia, APL and pancreatic cancer, respectively, the PAP level remained high during heparin therapy although the TAT level was decreased. When tranexamic acid was given, the PAP level was selectively reduced, and the TAT/PAP ratio was markedly decreased along with clinical improvement. These results indicate that monitoring of the TAT/PAP ratio may contribute to decisions regarding the institution and performance of combination therapy for DIC using anticoagulants and antifibrinolytic agents.
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PMID:Imbalance between thrombin and plasmin activity in disseminated intravascular coagulation. Assessment by the thrombin-antithrombin-III complex/plasmin-alpha-2-antiplasmin complex ratio. 146 20

The case history of a 15 year old boy in whom thrombosis of the internal carotid artery was associated with severe disseminated intravascular thrombosis (DIC) is described. Both peripheral blood smear and bone marrow aspirate revealed acute myelogenous leukemia FAB M-2 type as the cause of the disease. Consumption coagulopathy is common sign of hemostasis disturbances in leukemia. It is frequently observed in acute promyelocytic leukemia, but rarely it may be seen in the other forms of hemoblastosis, too.
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PMID:[Incidence of internal carotid artery thrombosis and disseminated intravascular coagulopathy in the early stages of acute myeloid leukemia]. 154 13

Case of hematological disorders associated with acute myocardial infarction had been found in five of forty five autopsy cases which had hematological disorders during the past seven years. The five cases of hematological disorders consisted of two cases of myelodysplastic syndrome, a case of aplastic anemia, a case of primary myelofibrosis in blast transformation, and a case of acute myelogenous leukemia. All the patients were over 60 years old. Four patients had coronary artery stenosis and extensive myocardial infarction. Fibrinogen degradation products were elevated in four patients. DIC was recognized in two and suspected in two others. In all cases, platelet counts markedly decreased to less than 2.5 x 10(10)/L. Since no chest pain was noted by any patient, it was difficult to diagnose acute myocardial infarction without autopsy, except in one case. It is important to recognize the possibility of severe cardiac dysfunction due to myocardial infarction in thrombocytopenia, especially in the aged with DIC.
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PMID:[Five cases of hematological disorders associated with acute myocardial infarction in thrombocytopenia]. 160 11

A 57-year-old male who had suffered from polycythemia vera (PV) and had been treated with pipobroman, carbazilquinon and busulfan for ten years presented with fever. CBC revealed anemia and thrombocytopenia without an increase of leukemic blasts (WBC, 7,700/microliters, RBC 294 x 10(4)/microliters, Hb 9.1 g/dl, Plt 1.5 x 10(4)/microliters). Bone marrow aspiration resulted in dry tap. Bone marrow biopsy showed hyperplastic marrow with fibrosis and no increase in leukemic blasts. Eleven days later the patient became leukemic and he died of DIC. Blast cells showed a high nucleo-cytoplasmic ratio, basophilic cytoplasm and cytoplasmic blebs. Cytochemical and immunophenotype analysis of the blast cells showed the following results; myeloperoxidase (-), chloroacetate esterase (-), Sudan black (-), acid phosphatase (+), acetate esterase (+), PAS (+), HLA-DR (+) and GPIIb/IIIa (+). Platelet peroxidase reaction on electron microscopy was positive in perinuclear spaces and endoplasmic reticulum. A diagnosis of megakaryoblastic transformation of PV was made. Although acute myelogenous leukemia has been shown to develop occasionally in the course of PV, acute megakaryoblastic leukemia with DIC following PV is a very rare condition.
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PMID:[Megakaryoblastic transformation associated with disseminated intravascular coagulation in the course of polycythemia vera: a case report]. 160 15

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

Eight pts with acute myeloid leukemia were studied to assess coagulation and fibrinolysis disturbances as a cause of hemorrhages associated to thrombopenia. Fibrinogen, products of fibrinogen to fibrin degradation, D-dimer, antithrombin III, protein C, plasminogen and alpha-2 antiplasmin determinations were performed at admission, during and after chemotherapy. All pts were on heparin during induction chemotherapy. Coagulation activation, which increased with the onset of chemotherapy (increases in D-dimer) and a decreasing trend at the end of the antileukemic therapy (normalization of fibrinogen levels) was observed. During the whole observation period alpha-2 antiplasmin levels remained very low. No significant changes were observed in antithrombin III or protein C levels. In conclusion, disseminated intravascular coagulation with associated thrombopenia is an important event in acute leukemia and an increased fibrinolytic activity due to low alpha-2 antiplasmin levels may take part in the genesis of hemorrhage. These data suggest that both heparin administration and the use of antifibrinolytic drugs may have a therapeutic effect.
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PMID:[Intravascular coagulation in acute promyelocytic leukemia: analysis of coagulation and fibrinolysis parameters]. 184 6

The pharmacokinetics of retinol palmitate were studied, and a therapeutic trial was performed in patients with ANLL. In the pharmacokinetics study, retinol was the only metabolite that was detected in plasma, and the peak concentration was 332 micrograms/dl (about 1.2 x 10(-5) M) 2.1 h after administration of retinol palmitate. Five patients with ANLL (4 with ANLL-M3 and one with ANLL-M2) were treated with retinol palmitate. In all patients with ANLL-M3, bone marrow suspension culture studies revealed that retinol induced both morphological and functional differentiation of immature leukemic cells. During the course of the treatment with retinol palmitate, morphological differentiation of bone marrow immature leukemic cells was observed in all patients with ANLL-M3 within 3-4 days after initiation of the therapy. In three of the four patients who underwent conventional chemotherapy, the sequential treatment with retinol palmitate resulted in a complete remission: controlling residual bone marrow leukemic cells. None of the patients showed any signs of aggravation of DIC in the coagulation parameters. These findings suggest the possibility that retinol palmitate functions as salvage therapy by inducing maturation and slowing proliferation, there by clearing out the residual leukemic cells following conventional chemotherapy.
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PMID:Pharmacological studies of retinol palmitate and its clinical effect in patients with acute non-lymphocytic leukemia. 186 32


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