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

Every surgical procedure taxes the hemostatic defenses of the patient. If his hemostatic mechanism is sound, he is unlikely to have a bleeding problem during or after an operation, unless, of course, a suture or clip slips off. Two classes of patients do present bleeding problems to the surgeon. One group has a pre-existing bleeding tendency, the other acquires it during or after the operation. The recognition of patients with severe hemostatic disabilities, such as hemophilia, presents no problem since the patient is aware of the disease. The mild bleeder is less likely to be detected by screening tests than by adroit questioning. The major hemostatic defect that may develop during an operation, or shortly thereafter, is disseminated intravascular coagulation. This syndrome, always secondary, may accompany shock, mismatched blood transfusion, septicemia, or extensive malignancy. Its prevention or early recongnition is much easier than treatment after circulating platelets and some coagulation factors have been consumed and fibrinolysis is destroying fibrin and fibrinogen.
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PMID:Surgical hemostasis. 37 88

Tissue factor is an ubiquitous phospholipid-protein complex, which triggers blood coagulation through the so-called extrinsic pathway. Reactions initiated by tissue factor bypass many of the early stages of coagulation (contact phase) and involve factors VII, X, V, II and fibrinogen but also factor IX (and VIII) as it was recently demonstrated. So, it appears that tissue factor has a key-role in the haemostasic process as it has been suggested by the mildness or the absence of haemorrhagic syndrome in contact factors deficiencies. Tissue factor activity has been found in many types of cells, especially in white bloods cells. Experimental studies have demonstrated the presence of tissue factor activity in polymorphonuclears, lymphocytes, monocytes (or macrophages). This activity is enhanced by gram-negative endotoxin stimulation, inflammation, cell mediated immunologic phenomena or malignancy. These data are in good agreement with a wild range of features observed in human pathology: fibrin deposits in inflammatory lesions, disseminated intravascular coagulation (DIC) during the course of gram-negative septicemias or acute promyelocytic leukemias, local thrombi at the early phase of graft rejection. The protective effect of a phospholipase C against DIC induced in rats by tissue factor infusion suggests in the future, a specific therapy would be possible in man that, in the frequent clinical conditions involving clotting activation through tissue factor pathway.
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PMID:[Initiation in vivo of blood coagulation. The role of white blood cells and tissue factor (author's transl)]. 39 57

Peripheral blood lymphocytes from 32 patients with malignant melanoma were tested for cell-mediated cytotoxicity (CMC) against cultured autologous melanoma cells. Effector cells were prepared from venous blood by defibrination, gel sedimentation, nylon column filtration, and lysis of remaining erythrocytes with NH4Cl. Melanoma cells prelabelled with [3H])proline were used as target cells in a 40-h assay and CMC was evaluated against standards obtained with blood lymphocytes from the least reactive normal donor. Reproducible autologous CMC was detected in 18 of 32 patients in a series of 367 total tests. CMC correlated with tumor volume (5-500 cm3) but not with tumor stage or DNCB reactivity. Preliminary results indicated that autologous CMC was not affected by treatment with DTIC, dexamethasone, intralesional BCG, radiation therapy, or partial surgical excision. Lack of consistent CMC in 14 patients could not be attributed to a measurable decrease in general immune capacity or to increased resistance of the patients' melanoma cells to CMC in general. Fibroblasts were more resistant to CMC than melanoma cells, and therefore of questionable value for defining specificity in direct tests.
Int J Cancer 1979 Jul 15
PMID:Cell-mediated cytotoxicity for cultured autologous melanoma cells. 47 90

In a study of 1729 consecutive autopsies, the histopathologic diagnosis of disseminated intravascular coagulation (DIC) confirmed by the presence of microthrombi in more than two organs was made in 51 cases. Among them, 38 cases (74.5%) were clinically not suspected of having DIC. Microthrombi were most frequent in the kidneys, followed by the lungs, spleen, adrenals, heart, brain, and liver, in descending order of frequency. Furthermore, a wide variety of visceral lesions was another important histologic feature of DIC. Kidney lesions assumed a position of prime importance, and special attention was given to the high frequency of acute renal failure due to so-called acute tubular necrosis and bilateral renal cortical necrosis. Infections, often associated with shock, and malignancies were the most common underlying causes of DIC. DIC is a frequent, often fatal pathophysiologic condition complicating many disorders. The true incidence of DIC at autopsy may be higher. It should be noted that demonstration of microthrombi and visceral alterations related to intravascular clotting is important for the evaluation of cases suspected of having DIC.
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PMID:Disseminated intravascular coagulation in autopsy cases. Its incidence and clinicopathologic significance. 53 Aug 89

The hematologic manifestations of neuroblastoma are numerous and varied. Bone marrow invasion by tumor cells may cause leukoerythroblastic changes or depression of one or more of the cell lines in the peripheral blood; occasionally bone marrow involvement may be so extensive that tumor cells may be released into the peripheral blood and lead to an erroneous diagnosis of leukemia. Anemia in neuroblastoma patients may result not only from bone marrow involvement, but also from bleeding into a tumor mass or from the hemolysis accompanying a consumption coagulopathy. A specific morphologic abnormality, the cogwheel erythrocyte, has been reported in patients with neuroblastoma. Neuroblastoma may also be associated with elevation of the platelet count or a hypercoagulable state. Recognition of these protean hematologic manifestations may facilitate diagnosis in children with atypical presentations of this highly malignant tumor.
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PMID:The multiple hematologic manifestations of neuroblastoma. 54 14

A technique using computerized data handling for following the fate of 125I-fibrinogen through various physiological compartments is presented. Its use in detecting fibrin build up in patients with metastatic tumors and cancer-caused DIC is explained. An increase in j3u (fractional catabolic rate as seen in the urine data) throughout the course of a study was found to be an important indicator of extravascular fibrin build up.
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PMID:Use of 125I-fibrinogen kinetic data to detect disseminated intravascular coagulation and deposition of fibrin in patients with metastatic cancer. 57 29

The medical records of 118 cases who met laboratory criteria of DIC were studied. The most frequent etiologies were: Generalized infection (39.8%), trauma (16.9%), malignancy (6.8%) and surgical cases (6.8%). The main clinical manifestations which appeared to be related solely to DIC were (in a decreasing order of frequency): Bleeding (64.4%), renal dysfunction (24.6%), liver dysfunction (18.6%), respiratory dysfunction (16.1%), shock (14.4%), thromboembolic phenonmena (6.8%) and central nervous system involvement (1.7%). In 26 patients none of these manifestations were observed. In patients with infection, liver and renal dysfunction were frequent and respiratory dysfunction rare, whereas in trauma cases, liver and renal dysfunctions were rare and respiratory dysfunction frequent. This variability indicates that the clinical manifestations are affected not only by the process of intravascular coagulation but also by the underlying clinical disorders. The most impaired coagulation tests were prothrombin time, partial thromboplastin time, platelet count and thrombin time. The degree of abnormality of these coagulation tests was found to be related to the extensiveness of organ involvement. The mortality (overall 54.7%) increased independently with age, with the number of clinical manifestations and with the degree of abnormality of the above-mentioned four most impaired coagulation tests. In addition, older patients were more likely to have an increased number of clinical manifestations and more impaired coagulation tests. Mortality was similar in the various etiologies except for trauma patients in whom it was lower (30%).
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PMID:Clinical and laboratory aspects of disseminated intravascular coagulation (DIC): a study of 118 cases. 58 Apr 88

Experiments were made to evaluate the potential role played by thrombogenic factors on the hematogenous arrest of circulating tumor cells in mice with demonstrable coagulopathies associated with the presence of a primary tumor, by administration of "therapeutic" doses of anticoagulants. The effects of warfarin, aspirin and heparin administration on the early arrest patterns of 125IdUrd-labelled TA3 carcinoma and Gardner lymphosarcoma cells injected intravenously into tumor-bearing mice were examined. Several hematologic parameters of carcinoma- and lymphosarcoma-bearing animals were measured prior to anticoagulation experiments and the results indicated that mice had coagulopathies similar to those found in cancer patients with disseminated intravascular coagulation syndrome, i.e., thrombocytopenia and elevated fibrinogen levels. Despite the presence of coagulation abnormalities and effective anticoagulation in recipient animals, all three agents were without effect on localization patterns of both tumor types. It was concluded that the proposed involvement of thrombogenesis in metastasis was probably not due to any role played by those clotting factors inhibited by aspirin, warfarin and heparin in early intravascular tumor cell arrest.
Int J Cancer 1978 Jun 15
PMID:Initial tumor cell arrest in animals of defined coagulative status. 58 Sep 32

Five days following implantation of a Yoshida sarcoma, female rats developed an increase in plasma fibrinogen concentration and a decrease in the number of platelets. The endotoxin induced fibrinisation of the microcirculation, as measured in percent involvement of glomerula, was found to be five to ten times higher than in control animals. A single injection of endotoxin without infusion was sufficient in tumor bearing animals to induce glomerular capillary thrombosis. The Yoshida sarcoma induced pathophysiological changes with a "preparative" effect on the endotoxin-induced disseminated intravascular coagulation.
Cancer 1978 Apr
PMID:Preparation for disseminated intravascular coagulation by Yoshida sarcoma in rats. 63 18

Plasma fibronectin (cold-insoluble globulin) is known to be cross-linked to fibrin during the final stage of blood coagulation and is probably the major nonspecific opsonin of blood. We measured the concentration of plasma fibronectin in 36 hospitalized patients (11 with malignancy, 12 with infection, 13 with other underlying diseases) with evidence of fibrin depostion and lysis. Plasma fibronectin concentration was greater than 2 S.D. below the mean of normals in 17 of the patients (p less than 0.001). Depression of fibronectin was not related to severity of disseminated intravascular coagulation, as assessed by fibrinogen concentration and the quantity of FDP in serum. Depressed plasma fibronectin concentration and the quantity of FDP in serum. Depressed plasma fibronectin concentration was an unfavorable prognostic finding, inasmuch as 12 of the 17 patients with depressed fibronectin concentrations died during hospitalization as compared to five of the 19 patients with normal fibronectin concentrations (p less than 0.02). We speculate that specific depletion of plasma fibronectin, because of codeposition with fibrin or due to increased utilization as a nonspecific opsonin, may contribute to the organ failure seen in severely ill patients.
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PMID:Fibronectin concentration is decreased in plasma of severely ill patients with disseminated intravascular coagulation. 64 97


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