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)

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

Plasma levels of tissue-plasminogen activator.plasminogen activator inhibitor (t-PA.PAI) complex and active PAI were assayed in 58 cases of disseminated intravascular coagulation (DIC). A significant elevation of both parameters was observed in most cases of DIC, especially in patients with non-Hodgkin lymphoma, sepsis, or some patients with acute leukemia, but no such elevation was observed in patients with acute promyelocytic leukemia (APL). The levels of both parameters were higher in cases of DIC with multiple organ failure (MOF) than in those without MOF. Since no elevation of t-PA.PAI complex was observed in most cases of APL, t-PA did not seem to play an important role in the activation of fibrinolytic system in APL. Active PAI, which reflects the inhibitory regulation in fibrinolytic system, was considered to play a role in the progression of MOF. Plasma levels of active PAI were low in the cases of APL, which had no complication of MOF.
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PMID:Changes in plasma levels of tissue-plasminogen activator/inhibitor complex and active plasminogen activator inhibitor in patients with disseminated intravascular coagulation. 130 60

Ten patients with severe hematologic malignancies (four with acute leukemia, three with multiple myeloma, one with prolymphocytic leukemia, one with malignant lymphoma and one with blastic crisis of chronic myelogenous leukemia) developed respiratory failure during the period between April 1986 and May 1990. Clinically, the patients manifested high-fever, dyspnea refractory to oxygen therapy, diffuse pulmonary rales and severe hypoxemia without evidence of cardiogenic pulmonary edema. Chest roentgenograms displayed diffuse alveolar infiltrates. Respiratory failure occurred as early as 48 hours and as late as 66 days after the administration of intensive anti-neoplastic chemotherapy. At that time leukocyte count was between 100/microliters and 54,900/microliters. Marked leukocytosis was observed in two patients with AML and PLL. Respiratory failure was preceded by sepsis in one patient with AML and by pneumonia in nine patients. DIC was diagnosed in four patients. All patients treated with high dose methyl prednisolone (mPSL) within 12 hours after the onset of respiratory failure. Only one patient required assisted ventilation. High dose mPSL had significant effect on seven of ten patients. But three patients died from progressive respiratory failure, sepsis, pneumonia and multi-organ failure.
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PMID:[Clinical investigation on acute respiratory failure in patients with severe hematologic malignancy]. 194 22

In a group of stable, nonthrombocytopenic leukemia patients awaiting bone marrow transplantation, results of paired allogeneic radiolabeled platelet kinetic measurements were correlated with the results of several different platelet and lymphocytotoxic antibody tests to determine which parameters could be used to identify patients who were alloimmunized to platelets. Seven patients with acute leukemia who had been transfused during induction therapy were used as the test group, and, as a control group, five untransfused patients with chronic myelogenous leukemia were also studied. Concurrent fibrinogen survival measurements were performed in all patients to assess whether hemostatic factor consumption (ie, disseminated intravascular coagulation) was present. Allogeneic platelet survival measurements were reduced from normal in all 12 study patients. In 8 of 12 patients, fibrinogen and platelet survival measurements were comparably reduced, suggesting disease-related platelet consumption. In four heavily transfused patients with acute leukemia, allogeneic platelet survivals were markedly reduced to less than or equal to 2.1 days, compared with the 3.5- to 7.4-day platelet survival measurements found in the other eight patients. The disproportionately short platelet survivals compared with fibrinogen survival measurements in these four patients, combined with documented positive antibody tests to their donors' platelets in the three patients with evaluable tests, suggested that these patients had become alloimmunized to platelets because of their prior transfusions. There was substantial concordance between the two radiolabeled allogeneic donor platelet survival measurements performed in each of these patients, suggesting that host rather than donor factors have a major influence on transfusion outcome (r = .93, P less than .001). The platelet cross-match tests, using the radiolabeled protein Staph A assay combined with the IgG enzyme-linked immunosorbent assay test, had the best correlation with the posttransfusion recovery and survival of the donors' platelets.
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PMID:Identification of alloimmunized patients: use of radiolabeled allogeneic platelet kinetic measurements and platelet antibody tests. 203 19

A case was reported in which the patient, whose leukemic cells were not found in the peripheral blood, died several days after the onset of cerebral sinus thrombosis, and after the autopsy acute leukemia was diagnosed. The patient, a 68-year-old female, was admitted with clouding of the consciousness. In the initial examination, she was semicomatose, pendulum-like movement was seen in the eyeballs, and hemorrhagic maculae on the trunk and extremities. Among the laboratory findings, WBC was 8, 100 (B 1, St 6, S 77, L 14, Mon 2), RBC 375 x 10(4), Hb 12.5, Ht 37, PLT 3.5 x 10(4), PT 15.6, PTT 68, Fib 158, FDP 10 and AT-III 75. In contrast enhanced CT, an empty triangular sign was observed. On the third hospital day, the patient died of a cerebral hernia. On autopsy, thrombosis was found in the bilateral sigmoid sinus. In the cerebral tissue, congestion was throughout the brain, and many leukemic cells were seen in the dilated blood vessels, but there was no infiltration into the parenchyma. The bone marrow, hypercellular, showed many intermediate type and blastic myeloid cells. The main neurological complications of leukemia are leukemic infiltration and intracranial hemorrhages. Capillary obstructions associated with the disseminated intravascular coagulation (DIC) syndrome are rarely experienced, but obstructions of thick arteries or thick veins such as venous sinuses are seldom seen in general, and most reports of such cases were those resulting from chemotherapy after making a diagnosis of acute leukemia. In the literature, there have been only two reports in our literature.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case report of acute leukemia following the onset of cerebral sinus thrombosis]. 228 78

The therapeutic effect of highly purified protein C (PC) or activated protein C (APC) on three patients with disseminated intravascular coagulation (DIC) was tested. In two out of three cases, although therapeutic dose of heparin was not effective, PC or APC administration significantly improved the hypercoagulable state. In one case with acute leukemia who developed DIC with the severe gastrointestinal bleeding, APC corrected the hypercoagulable state without aggravating bleeding. These findings suggested that PC and/or APC might be effective in correcting hypercoagulable state without any adverse effect.
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PMID:Treatment of patients with disseminated intravascular coagulation by protein C. 231 13

Vitronectin, also known as serum-spreading factor or S-protein, mediates cell adhesion and inhibits formation of the membrane-lytic complex of complement and the rapid inactivation of thrombin by antithrombin III in the presence of heparin. Vitronectin is normally present in plasma at a concentration of approximately 300 micrograms/mL. The investigators quantified plasma vitronectin with an enzyme-linked immunosorbent assay and visualized reduced and nonreduced vitronectin by immunoblotting after separation of plasma or serum by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The concentration of plasma vitronectin was markedly reduced in some patients with disseminated intravascular coagulation, especially in those with liver failure; it was near normal in patients with metastatic cancer and acute leukemia. Patients with vitronectin levels less than 40% normal invariably had low fibrinogen and antithrombin III and a prolonged prothrombin time. In both normal and patient plasmas there was heterogeneity in the ratio of the 75,000- and 65,000-mol wt polypeptides of reduced vitronectin: 18% had mostly the 75,000-mol wt polypeptide, 59% had roughly equal amounts of the two polypeptides, and 22% had mostly the 65,000-mol wt polypeptide. This polymorphism is inherited and appears to be due to two alleles that are present with approximately equal frequency. The blotting patterns of vitronectin in reduced and nonreduced plasmas were largely unaltered in plasma of patients with defibrination syndrome, fibrinolysis, liver failure, sepsis, metastatic cancer, and acute leukemia. There was no evidence of fragmentation of vitronectin or formation of the disulfide-bonded complex of vitronectin and thrombin-antithrombin III that is found when blood is clotted. Thus these results corroborate in vitro observations that the liver is the major source of plasma vitronectin, suggest that vitronectin may become depleted during disseminated intravascular coagulation, and define a genetic polymorphism of vitronectin.
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PMID:Plasma vitronectin polymorphism in normal subjects and patients with disseminated intravascular coagulation. 245 67

In the present study plasma fibronectin levels were determined in patients with hematopoietic malignancy, particularly leukemias, in an effort to clarify their clinical implications. Among leukemia patients, those with AML, ALL, ATL or CLL had various plasma fibronectin levels that were higher in some cases, while lower in others, as compared to normal control values. An elevation of the fibronectin level was noted often in APL, while lower fibronectin values were observed in many instances of CML. In these types of leukemia, acute exacerbation as well as supervention of infection tended to be associated with lower than normal levels of fibronectin. An especially marked depression of fibronectin occurred, when leukemia was complicated by sepsis or DIC, in which a good parallel was noted between the progress of disease and the fibronectin level. In lymphoproliferative diseases, the fibronectin value varied widely, but low fibronectin levels were frequently associated with intercurrent infection or an extreme deterioration of the general physical conditions.
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PMID:Variation of plasma fibronectin levels in leukemia patients. 248 45

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

We experienced 57 episodes of Pseudomonas aeruginosa bacteremia in 55 patients with hematologic disorders in a 16-year period. Ninety-five percent of the patients had hematologic malignancies such as acute leukemia. All but one patient received cytotoxic or immunosuppressive therapy at or prior to the onset of bacteremia. Seventy-seven percent of the episodes occurred during profound granulocytopenia of below 100/mm3. All the patients acquired their infection in the hospital, and 96% had received antibiotic therapy during the preceding two weeks. Periodontal, anorectal, lower respiratory tract, and urogenital infections were the sources of bacteremia in about three-quarters of the episodes. Periodontal infection tended to progress to cellulitis of the face or the floor of the mouth, often resulting in bacteremia of the unimicrobial type, while anorectal infection predisposed to abscess formation, frequently leading to bacteremia of the polymicrobial type. Cellulitis at onset was seen in 35% of the episodes. Most sites of infection did not become apparent until one to three days after the onset of fever, probably because of depressed inflammatory response associated with severe granulocytopenia. The majority of patients complained of gastrointestinal symptoms such as nausea and vomiting, abdominal pain, diarrhea, and abdominal fullness at the onset of bacteremia. Major complications included bacteremic shock (63%), impaired consciousness (25%), ecthyma gangrenosum or hemorrhagic gangrenous cellulitis (18%), and jaundice (12%). Furthermore, there were one case each of endocarditis and disseminated intravascular coagulation. It was thus suggested that the clinical picture of P. aeruginosa bacteremia complicating hematologic disorders is influenced by the predisposing conditions associated with the underlying diseases and their treatment.
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PMID:[Pseudomonas aeruginosa bacteremia associated with hematologic disorders [I]. Predisposing factors and clinical manifestations]. 250 86


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