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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical relevance of determination of plasma antithrombin III(ATIII) and alpha 2-plasmin inhibitor (alpha 2 PI) activities in patients with disseminated intravascular coagulation (DIC) was analyzed. Although the plasma ATIII activity was decreased in patients with DIC, no significant correlation was observed between plasma level of ATIII and that of thrombin-antithrombin III complex or prothrombin fragment 1+2. The extent of the decrease of ATIII in DIC was the most marked in cases associated with septicemia. The plasma level of ATIII in septicemia without DIC was significantly lower than that in DIC cases without septicemia, suggesting that the decrease of ATIII level could not be related to the pathophysiology of DIC, but to that of septicemia. The plasma half-life of ATIII in septicemia without DIC was significantly shortened in the absence of the increase of TAT level, suggesting that the extravasation of ATIII might be induced probably due to the endothelial damage in septicemia. The alpha 2-Plasmin inhibitor level was decreased in DIC patients. The decrease was the most marked (lower than 60% of normal) in patients with excessive fibrinolysis in which fibrinogen degradation was induced. The plasma level of alpha 2PI was significantly higher in the DIC cases with septicemia than in those without septicemia. The ATIII/alpha 2PI ratio was significantly lower in DIC cases with septicemia than in those with solid tumor or acute leukemia. Moreover, the ATIII/alpha 2PI ratio was significantly lower in MOF cases than in non-MOF cases in septicemia. The mortality of the MOF cases did not correlate with the ATIII/alpha 2PI ratio, but with the plasma level of PAI-1, suggesting that the decrease of ATIII/alpha 2PI ratio might not reflect the irreversible endothelial cell damage. Based on these observations, the calculation of ATIII/alpha 2PI in DIC patients would provide the following information; (1) a low ATIII/alpha 2PI ratio (less than 0.6) was frequently observed in septicemia, which could be related to the occurrence of organ dysfunction; (2) a high ATIII/alpha 2PI ratio (higher than 1.0) with the marked decrease of alpha 2PI level (lower than 60% of normal) suggests the occurrence of excessive fibrinolysis in which anti-fibrinolytic therapy should be considered when clinical bleeding was present; (3) The ATIII/alpha 2PI ratio near 1.0 was observed in DIC associated with the pathological conditions other than described above, such as solid tumors, in which the coagulation and fibrinolysis was almost equally activated.
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PMID:[Clinical relevance of determination of plasma ATIII and alpha 2 PI activities in patients with DIC--application of the molecular markers for the analysis of pathophysiology of DIC]. 810 83

A patient with acute leukemia is presented in whom the leukemic cells, as seen by light microscopy were typical promyelocytes. The cells had normal or slightly invaginated nuclei with typical cytoplasmic granules and the diagnosis was confirmed by cytochemistry. The clinical course was rapid and the patient died of disseminated intravascular coagulation and urosepsis within a few days of diagnosis. However, electron microscopic examination showed cells with extremely convoluted and lobulated nuclei with nuclear pockets and cytoplasmic bridges as well as the complete absence of cytoplasmic granules in the majority of the cells. Furthermore, the urine lysozyme (muramidase) was elevated. These findings suggest that the leukemia in this patient may be classified as a hypogranular variant of acute promyelocytic leukemia (APL), with monocytoid ultrastructural appearances.
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PMID:Ultrastructural observations on a variant of acute promyelocytic leukemia. 834 79

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

The main cause of DIC (disseminated intravascular syndrome) is contact of tissue factor with circulating blood. The main symptoms of DIC are bleeding diathesis caused by consumption coagulopathy and organ dysfunction related to circulatory disturbances due to multiple thrombi. However, the symptoms of DIC differ according to degree of fibrinolysis which is characterized by causal disease of DIC. Usually, enhanced fibrinolysis does not cause organ failure but hemorrhagic diathesis, while impaired fibrinolysis does not cause severe bleeding but organ dysfunction. In almost all cases of acute leukemia and in some cases of solid cancer with DIC, hyperfibrinolysis is common. In cases of severe infection with DIC, impaired fibrinolysis due to abnormal elevation of plasminogen activator inhibitor-1 is frequently seen.
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PMID:[Disseminated intravascular coagulation--pathophysiology]. 843 9

Unusual patterns of presentation of acute leukemia are discussed, with an emphasis on the diagnostic and therapeutic challenges that they pose. Clinical syndromes reviewed include the leukostasis syndrome, disseminated intravascular coagulation, granulocytic sarcoma, central nervous system leukemia, leukemia cutis, Sweet's syndrome, pyoderma gangrenosum, and acute leukemia diagnosed during pregnancy. Each of these uncommon presentations of acute leukemia has a unique impact on patient management.
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PMID:Management of unusual presentations of acute leukemia. 844 62

Assessment of peripheral blood counts and blood film analysis are frequently performed as diagnostic procedures in emergency medicine. Far fewer situations exist, however, in which these analyses are the main clue in establishing an emergency diagnosis. Artifacts can lead to wrong diagnosis, e.g. pseudo-thrombocytopenia, which is defined as a low platelet count resulting from a laboratory artifact. Severe neutropenia (agranulocytosis) and extreme hyperleukocytosis, as well as suspicion of acute leukemia, require a rapid diagnostic work-up. A newly detected anemia should not necessarily be treated by packed red cell transfusions. The decision whether an anemic patient ought to receive transfusions should be based on the speed with which the anemia has developed, as well as on clinical judgement. As a rule a chronic anemia patient with hemoglobin above 70 g/l does not need transfusions. An uncritical transfusion policy can even cause emergencies, e.g. in patients with megaloblastic anemia or in anemic multiple myeloma patients with a hyperviscosity syndrome. An elevated hematocrit requires prompt further investigations. This is of utmost importance if one considers the diagnosis of polycythemia vera rubra, a disease in which patients are particularly prone to thrombotic complications. Fragmented red cells (schistocytes) on peripheral blood smears constitute a cardinal diagnostic clue for the detection of microangiopathic hemolytic anemias (MAHA), in particular for the diagnosis of the life-threatening thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS). Malaria is another example for a chief role of blood smears examination in achieving a rapid diagnosis. If one encounters an unexpected severe thrombocytopenia, a marrow examination reveals whether it is due to rapid peripheral destruction, or due to a marrow failure. Furthermore, in any patients with an unanticipated thrombocytopenia, a disseminated intravascular coagulation and a MAHA should be ruled out. Heparin-induced thrombocytopenia is a rare, but possibly fatal complication of therapy with heparins.
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PMID:[Emergency blood picture]. 848 74

Two cases of unexpected post-partum death of women with acute leukemia are described. In the first case (1st pregnancy) the diagnosis (acute promyelocytic leukemia: M3) was performed one week before delivery and death occurred 3 days later, because of hemorrhagic and renal DIC complication. Since one month before hospitalization, laboratory exams indicated a serious hematological pathology and no further exams were carried out by the physicians, elements of professional fault were recognized in them, considering that because of the diagnostic omission it was impossible to make an early diagnosis and thus perform to specific therapy, adopted only in the terminal phase. This specific therapy is able to determine remission from most cases of acute promyelocytic leukemia. In the second case (2nd pregnancy) the diagnosis (acute myelomonocytic leukemia: M4) was performed only postmortem because, during the whole pregnancy, no signs of disease were evident. After a few hours from the spontaneous delivery, death occurred as a result of an intractable + hemorrhagic syndrome caused by primary hyperfibrinolysis and repeated episodes of cardiac arrest, without possibility of recognizing it. The medical procedures for this case, both throughout pregnancy and terminal phases, appeared free of censure.
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PMID:[2 fatal cases of acute myeloid leukemia (M3, M4) during pregnancy]. 853 3

We examined plasma antigen levels of tissue factor (TF) in 95 cases of disseminated intravascular coagulation (DIC), to investigate the role of TF in DIC. A significant elevation of plasma antigen levels of TF was observed in cases of DIC associated with cancer. However, no such significant elevation was observed in cases of DIC associated with acute promyelocytic leukemia (APL), acute leukemia except APL, blastic crisis of chronic myelogenous leukemia, non-Hodgkin lymphoma (NHL), sepsis or fulminant hepatitis. No significant elevation of TF was observed in patients without DIC, except 4 cases of cancer who developed DIC thereafter. Plasma antigen levels of TF were higher in both cases of DIC with renal failure and chronic renal failure without DIC than its levels in those without renal failure. Therefore, plasma antigen levels of TF in DIC patients with renal failure were considered to be carefully estimated. The levels of TF were decreased with the clinical improvement in some cases of DIC but were further increased or remained at high levels in patients who showed no improvement of DIC. Thus, plasma antigen levels of TF is an important marker to predict the development and/or prognosis of DIC, especially in patients with cancer.
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PMID:Role of tissue factor in disseminated intravascular coagulation. 857 48

The early stage of the state in which coagulation or fibrinolytic pathway is activated has been difficult to estimate. It has become possible to detect disseminated intravascular coagulation (DIC) at an early stage due to the development of highly sensitive methods which quantitate so called "molecular markers". Herein, to evaluate the clinical usefulness of plasmin-alpha 2-plasmin inhibitor complex (PIC) and tissue factor activity in plasma were examined. The first time, monitoring the plasma levels of PIC might be useful for the diagnosis of a pre-DIC condition and for effective control of therapy. We believed that combination assay for both PIC and D dimer will be adequate to differentiate whether the hemostatic abnormalities are induced mainly by DIC or hepatic insufficiency. Recently, new clinical usefulness of PIC has been reported. The PIC/thrombin-antithrombin III complex ratio was lower in patients with poor prognosis than in those with good prognosis, and it was also lower in those with organ failure than in those without it. The tissue factor is a major activator of the coagulation cascade and may play a role in initiating thrombosis. A simple chromogenic substrate assay for the quantitation of tissue factor activity in plasma samples was developed. Abnormally high levels were found in 80% of the patients with DIC, predominantly in patients with non-hematological solid tumors and acute leukemia. Serial determinations of plasma tissue factor demonstrated that plasma tissue factor changes immediately with the course of DIC. Plasma tissue factor did not correlate with hemostatic markers of DIC such as thrombin-antithrombin III complex, PIC, FDP D-dimer. Tissue factor activity correlated well with membrane anchoring region of tissue factor protein levels. Tissue factor activity correlate with tumor necrosis factor alpha levels in patients with non-hematological solid tumors without hepatocellular carcinoma. These findings suggest that the plasma tissue factor is potentially valuable for monitoring the progress of DIC in a limited population of patients.
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PMID:[Clinical usefulness of the measurements of plasmin-alpha 2-plasmin inhibitor complex and plasma tissue factor activity in patients with disseminated intravascular coagulation]. 881 61

After clinical assessment, pertinent history, and family history, the clinician often has a good idea concerning the cause of a patient's bleeding. The most appropriate laboratory tests can then be ordered. Routine screening tests include a complete blood cell count, platelet count, and evaluation of a peripheral blood sample, a prothrombin time, and an activated partial thromboplastin time. Thrombocytopenia may result from idiopathic thrombocytopenic purpura, disseminated intravascular coagulation, or, less commonly, acute leukemia, aplastic anemia, thrombotic thrombocytopenic purpura, or a particular drug that a patient is taking. Again, the patient's history, physical findings, and evaluation of a well-prepared peripheral blood smear will be helpful in determining the cause of the patient's thrombocytopenia. An isolated prolongation of the activated partial thromboplastin time may result from low levels of factors VIII, IX, or XI. A slightly prolonged activated partial thromboplastin time and a moderate decrease in factor VIII may reflect von Willebrand disease or the "carrier" state for hemophilia A. In women a greatly prolonged activated partial thromboplastin time and very low levels of factor VIII (< 3%) most often result from an acquired factor VIII inhibitor (autoantibody against factor VIII) or from severe (type III) von Willebrand disease. If von Willebrand disease is suspected (because of menorrhagia with or without other mucous membrane bleeding, a positive family history, and a prolonged activated partial thromboplastin time), more specific laboratory tests for this disease should be done. These include assays of factor VIII, von Willebrand factor antigen, von Willebrand factor activity (measured by the ristocetin cofactor assay), and template bleeding time. In von Willebrand disease the defect is in von Willebrand factor. The affected individual may have subnormal levels of structurally and functionally normal von Willebrand factor (this is called "classic" or type I von Willebrand disease) or may produce von Willebrand factor that is structurally and functionally abnormal (von Willebrand disease type 2). Individuals who inherit a gene for von Willebrand disease from both parents have severe (type 3) von Willebrand disease and will have extremely low levels (< 3%) of von Willebrand factor and factor VIII and will have a very prolonged bleeding time. In most populations type I disease is the most common form, whereas type 3 is the least commonly encountered form. It should be noted that levels of von Willebrand factor can be influenced by the patient's blood type (persons who have blood type AB have 60% to 70% higher levels than do persons who have blood type O) and can be elevated during pregnancy, stress, and hyperthyroidism. The two major functions of von Willebrand factor are to serve as a "bridge" between platelets and injury sites in blood vessel walls and to protect circulating factor VIII from rapid proteolytic degradation. Thus, if a patient has either too little or functionally abnormal von Willebrand factor, the bleeding time will be prolonged and factor VIII will be decreased (because it is not being protected by von Willebrand factor). It should be determined which type of von Willebrand disease a particular patient has because treatment depends on type. Multimeric analysis of von Willebrand factor can be done with use of sodium dodecyl sulfate gels, radiolabeled antibody to von Willebrand's factor, and autoradiography. This will allow visualization of the multimeric structure of von Willebrand factor. In type I disease all bands are present, whereas in the type 2 variants 2A and 2B no high-molecular-weight multimers are seen. Desmopressin acetate (which is available in parenteral form for intravenous use and in a highly concentrated intranasal spray formulation) is the treatment of choice for classic type I disease. The drug effects a rapid release of von Willebrand factor from endothelial cell stor
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PMID:Screening and diagnosis of coagulation disorders. 882 61


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