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

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.
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PMID:Initial tumor cell arrest in animals of defined coagulative status. 58 Sep 32

Two cases of microangiopathic hemolytic anemia in disseminated carcinoma are reported. Both showed the classical features of this illness, namely acute generalized hemorrhagic diathesis, severe hemolytic anemia, thrombocytopenia, fragmentation of erythrocytes in the peripheral blood smear, increased erythropoiesis and megakaryopoiesis or tumor cell invasion in the bone marrow, tumor cell emboli in venules and disseminated intravascular coagulation. In both cases the microangiopathic hemolytic anemia was the first sign of the disseminated carcinoma. Differential diagnosis, pathogenesis and therapy are discussed.
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PMID:[Microangiopathic hemolytic anemia in malignant tumors. 2 cases]. 62 35

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.
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PMID:Preparation for disseminated intravascular coagulation by Yoshida sarcoma in rats. 63 18

6275 autopsies performed at the Institute of Pathology of the University of Zurich in the period 1973--1976 included 47 microscopically verified cases of thrombotic endocarditis. Thirty of these patients harboured a neoplasm, most often of the gastro-intestinal tract. Twelve died from arterial emboli, particularly to the central nervous system, although valvular disease of the heart was not manifest clinically. The association of thrombotic endocarditis and histologic evidence of disseminated intravascular coagulation was seen in a different group of 30 cases. Patients with carcinomas and thrombotic endocarditis exhibited microthrombi to a significantly higher degree than a comparable control group with carcinomas but without thrombotic endocarditis. There results confirm that hypercoagulability may well be the denominator common to both thrombotic endocarditis and disseminated intravascular coagulation.
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PMID:[Trombotic endocarditis and its correlation to disseminated intravascular coagulation]. 65 32

The incidence and type of hemorrhage were studied in 718 patients with solid tumors. All patients were receiving myelosuppressive chemotherapeutic agents. Seventy-five patients (10.4%) experienced one or more episodes of hemorrhage. Bleeding was due to tumor invasion in 25 patients (33.3%), was due to disseminated intravascular coagulation in seven patients (9.3%), and was unrelated to malignant neoplasms or drug treatment in six patients (8%). Thirty-seven patients (49.3%) had hemorrhages associated with drug-induced thrombocytopenia. There was a quantitative relationship between the incidence of hemorrhage and the platelet count for both the thrombocytopenic group and the total group of patients with hemorrhages from all causes. The incidence of hemorrhage was low until the platelet count decreased below 10,000/cu mm.
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PMID:Incidence of hemorrhagic complications in patients with cancer. 66 Jul 90

This study assess the effects of oral BCG, as a single agent, on tumor progression and on cell-mediated immune function in patients with metastatic malignant melanoma. Thirty patients were studied including 22 with measurable metastatic lesions and 8 with no detectable disease, following treatment of metastases by surgery, radiotherapy, or 5-(3, 3-dimethyl-1 -triazeno)-imidazole-4-carboxamide (DTIC; DIC). Oral BCG was given in doses of 120--240 mg, 1--3 times per week for periods ranging from 9 to 80 weeks and to total doses of from 1.2 to 20.1 gm. Patients were assessed by direct measurements of tumor mass, PPD skin test and in vitro blastogenic responses to PPD PHA. Of the 22 patient with measureable disease, 19 showed tumor progression and none showed regression of any lesion. Of the 8 without apparent disease, 5 remained stable and 3 had tumor recurrence. Of the total group of 30 patients, 8 showed some increased sensitivity to skin testing with PPD. Of 19 tested, 3 showed an increased PPD response in vitro, while 3 showed a decreased response. Six of 20 tested showed an increased PHA response in vitro. Oral BCG alone was not effective as an antitumor agent in patients with metastatic malignant melanoma.
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PMID:The use of oral BCG in the treatment or metastatic malignant melanoma. 78 99

The two cases reported here were clinically misleading because of the negative history. A 49-year-old woman was treated for thrombosis migrans of the vena cava and a consumption coagulopathy; a 15-year-old boy for gastro-intestinal hemorrhages and hematemesis with fibrinolysis syndrome. Since the coagulation disturbances did not subside in spite of the treatment, an exploratory laparotomy was performed which revealed a solid carcinoma of the stomach in both cases. The hemorrhagic tendency can be traced back to the coagulation accelerator factors which escape from the tumor and metastases into the blood.
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PMID:[Defibrination syndrome in gastric tumors (author's transl)]. 80 32

Other investigators have demonstrated fibrin deposition in tumors. Experiments were therefore designed to test whether systemic defibrination would alter tumor growth or tumor response to chemotherapy with cyclophosphamide. Defibrination with Ancrod, a venom extract of Agkistrodon rhodostoma, did not significantly affect tumor sensitivity to chemotherapy. Similarly, defibrination plus fibrinolytic therapy with streptokinase did not affect responsiveness to cyclophosphamide. Long-term defibrination did not affect tumor growth. These results suggest three possible interpretations: (a) the coagulation system may not be important in tumor growth and response to chemotherapy; (b) adequate clearing of fibrin from the tumor was not accomplished in our experiments; or (c) other factors such as platelet deposition may be involved and platelet function was not inhibited by the therapies used in our experiments.
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PMID:Effect of defibrination on tumor growth and response to chemotherapy. 95 85

Sixty-five cases of nonbacterial thrombotic endocarditis (NBTE) were discovered at autopsy during a 10 year period--an incidence of 1.6 per cent in the adult autopsy population. In 51 cases, one or more malignant neoplasms were associated; adenocarcinoma represented the most frequent histologic type of related neoplasm. Coagulation abnormalities suggestive of disseminated intravascular coagulation (DIC) were present in 18.5 per cent of the cases. It is possible that both the valvular and peripheral intravascular thromboses in at least some cases of NBTE represent the abnormal coagulation of DIC. Arterial thrombosis with infarction occurred in many peripheral organs. Splenic and renal were most frequent, but cerebral and cardiac consequences were the most significant.
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PMID:Non-bacterial thrombotic endocarditis: clinicopathologic correlations. 99 78

A newborn infant with a large hepatic hemangioma developed congestive heart failure, consumption coagulopathy, microangiopathic hemolytic anemia, and obstructive jaundice. The patient was mildly heparinized (250 units per kg and day) and underwent successful resection of the tumor without lobectomy at the age of 3 days. Blood volume increased from 93.9 ml/kg at the age of 5 h to 124.2 ml/kg prior to surgery. Red-cell mass simultaneously decreased from 53.8 to 39.4 ml/kg. The increase of blood volume is explained by congestive heart failure, the decrease of red-cell mass by intravascular coagulation within the tumor resulting in formation of thrombi and microangiopathic hemolytic anemia. A review of the literature on infants with symptoms caused by an intrahepatic hemangioma during the first month of life confirms that surgical intervention is the treatment of choice for infants with giant solitary hemangioma of the liver.
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PMID:Solitary hepatic hemangioma in a newborn infant complicated by cardiac failure, consumption coagulopathy, microangiopathic hemolytic anemia, and obstructive jaundice. Case report and review of the literature. 100 25


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