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)

Platelets contain heparin neutralizing activity, which is released into plasma following aggregation. This material is probably identical to platelet factor 4. We describe a technic to measure heparin neutralizing activity in platelet-poor plasma based on the serial heparin dilution technic of Harada and Zucker. Heparin neutralizing activity was depressed in thrombocytopenia due to immune thrombocytopenia and bone marrow depression, and elevated in thrombocytopenia due to disseminated intravascular coagulation. Secondary thrombocytosis is characterized by markedly elevated heparin neutralizing activity, while thrombocytosis associated with myeloproliferative disorders has normal heparin neutralizing activity.
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PMID:Plasma heparin neutralizing activity. Its use in the evaluation of thrombocytopenia and thrombocytosis. 94 87

A rapid technique suitable for routine laboratory use for determining the percentage of large platelets in the peripheral blood is described. In 50 haematologically normal subjects, megathrombocytes (platelets with a volume of 16-33 fl) constituted 3.0-16.6% (mean +/- 2 SD) of the platelet count. Of the 10 patients examined with immune thrombocytopenic purpura, an increased percentage of megathrombocytes (mean 26.6%) was found in all with severe thrombocytopenia, and in 6 of 8 (mean 19.8%) with moderate thrombocytopenia; the percentages were not influenced by prior splenectomy. Six of 12 patients with severe hypomegakaryocytic thrombocytopenia had an increased percentage of large platelets (mean 15.9%), as did one of 21 patients (mean 9.9%) with moderate thrombocytopenia of simimlar aetiology. When patients with nearly identical platelet counts were compared, the mean percentage of megathrombocytes was greater in immune than in hypomegakaryocytic thrombocytopenia for both severe (t=3.17, P less than 0.01) and moderate (t=4.5, P less than 0.001) thrombocytopenia. An increased percentage of large platelets (mean 21.9%) was found in 6 to 8 patients with disseminated intravascular coagulation, in 7 of 20 (mean 15.8%) with chronic myeloproliferative disorders and in one of 15 (mean 8.8%) with reactive thrombocytosis. Determination of the percentage of megathrombocytes by this technique assists in differentiating immune thrombocytopenia from hypomegakaryocytic thrombocytopenia, in diagnosing mild disseminated intravascular coagulation, and in determining whether thrombocytosis is reactive or a consequence of a myeloproliferative disorders.
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PMID:A rapid method for assessing megathrombocytes: its application to thrombocytotic and acquired thrombocytopenic states. 98 70

This study was designed to assess whether factors other than high haemoglobin, thrombocytosis and abnormal platelet function predispose to thrombosis in polycythaemia rubra vera (PRV). Components of the fibrinolytic system and concentrations of the naturally occurring anticoagulants were measured in patients and controls in the resting state; the fibrinolytic capacity was reassessed after venous occlusion. The results were related to presence or absence of a history of thromboembolism. Under resting conditions, patients with PRV had reduced plasminogen activator inhibitor antigen levels and higher fibrin plate lysis area and tissue plasminogen activator activity. Protein C, protein S and factor V levels were reduced. Those patients with a history of thromboembolism had decreased tissue plasminogen activator activity after venous occlusion compared to those who had not experienced a thrombosis. We conclude that reduced fibrinolytic capacity may predispose to thrombosis in PRV. Despite treatment to normalize haemoglobin levels, the patients have persistent activation of their fibrinolytic systems. This, and reduced levels of proteins C and S, may be secondary to a chronic, clinically occult, disseminated intravascular coagulation.
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PMID:The fibrinolytic system and proteins C and S in treated polycythaemia rubra vera. 148 3

Platelet counts were evaluated in 714 patients with advanced non-small cell lung cancer (N-SCLC), small cell carcinoma of the lung (SCCL), and colon cancer entered to a clinical trial. Patients had not received prior chemotherapy. Platelet counts were not different in patients who had received radiation therapy prior to entry to the study. In comparison to the other tumor types, patients with N-SCLC demonstrated an increased prevalence of thrombocytosis (counts greater than 400,000/mm3), higher platelet counts at the time of entry to the study, higher over all mean platelet counts, relative preservation of high platelet levels during disease progression, and no relationship between platelet numbers and the amount of chemotherapy given. By contrast, platelet counts in patients with SCCL were negatively correlated with the absolute amount of cyclophosphamide and adriamycin given, and declined most dramatically with disease progression and death. Platelet numbers did not correlate with fibrinopeptide A or fibrin split product levels suggesting that disseminated intravascular coagulation or fibrinolysis may have had less influence on platelet numbers than certain other factors. By contrast, significant correlations were found for all three tumor types between platelet numbers and other indicators of bone marrow function including anemia, total leukocyte count, and absolute neutrophil count; and the fibrinogen level. Based upon these findings, we postulate that the host response to malignancy, possibly in the form of production of bone marrow-stimulating cytokines, may play a prominent role in regulation of platelet counts in these (and perhaps other) neoplasms, and that a particularly prominent and persistent degree of marrow stimulation exists in patients with N-SCLC.
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PMID:The platelet count in carcinoma of the lung and colon. 196 50

The paraneoplastic syndrome (PNS) is an association of symptoms and signs not directly related to the site or local manifestations of a malignant tumor or its metastases. Hematologic abnormalities as PNS include erythrocytosis, anemia, neutrophilia, neutropenia, eosinophilia, thrombocytosis, thrombocytopenia, venous thromboembolism and disseminated intravascular coagulation (DIC). These abnormalities are, by and large, due to the production of biologically active growth factors, hormones or as yet unidentified "humors" by the tumor. As our understanding of growth factors controlling hematopoiesis has increased in recent years, the biologic basis of hematologic PNS are better understood. For instance, tumor-associated neutrophilia is now known to be caused by the production of G-CSF by the tumor. The mechanism by which tumor causes thromboembolism have also been extensively investigated. Cancer cells induce platelet aggregation both in vitro and in vivo. Platelet aggregating material has been isolated and partially characterized from tumor cells. The involvement of platelet glycoprotein II b/IIIa in the tumor-platelet interaction has also been shown. Malignant cells contain a unique procoagulant, cancer procoagulant A, that directly activates factor X. Together with tissue factor, this procoagulant appears to have been contribute to a high incidence of thromboembolism in cancer patients. Better understanding of hematologic PNS is important for clinical care of the patients with cancer.
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PMID:[Paraneoplastic syndrome hematologic abnormalities]. 200 36

Platelet abnormalities associated with hepatobiliary diseases include increased (thrombocytosis) and decreased (thrombocytopenia) numbers of platelets as well as abnormalities in function (thrombocytopathy or thrombasthenia). Hepatic diseases that are accompanied by platelet abnormalities include hepatitis, cirrhosis, portal hypertension, and neoplastic disorders both benign and malignant. The objective of this work is to examine the platelet abnormalities that occur with a variety of hepatobiliary disorders. Thrombocytosis is seen as a reactive entity following splenectomy. Thrombocytopenia is associated with hypersplenism, dysproteinemias and liver disease related disseminated intravascular coagulation (DIC). Qualitative platelet abnormalities are found in hepatic failure, liver diseases associated with high or low levels of lipid, and with medications given for a variety of hepatocellular diseases. Clinically common and significant platelet abnormalities associated with liver disease are thrombocytopenia secondary to portal hypertension and the thrombasthenias following metabolic changes and/or therapeutic interventions of liver disease.
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PMID:Platelet abnormalities in hepatobiliary diseases. 218 3

In 2% of the newborn children, hemorrhagic or nonhemorrhagic events may appear. The wider range of paraclinical investigations used nowadays permitted a better knowledge of physiopathological bases of these diseases. The paper reports on all the forms of hemorrhage: vascular hemorrhages, disturbances of the thrombocytic function (congenital and acquired), thrombocytopenias (following a low medullary function, or an increased destruction and the mixed ones), thrombocytosis. Coagulopathies generated by congenital diseases, with lack of different factors of homeostasis, hemorrhages due to the liver diseases and DIC (disseminated intravascular clotting) are also dealt with. All the chapters review etiology, diagnosis, prognosis, treatment, prophylaxis. Tables with etiologic forms, investigation schemes for differential diagnosis and treatment complete each chapter.
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PMID:[Hemorrhagic diseases in newborn infants]. 251 80

Hematologic dysfunction occurs commonly in patients with malignancy. Over half are anemic, often because of acute or chronic blood loss, marrow involvement by the malignancy, marrow suppressive effects of chemotherapy or radiation therapy, or because of the anemia of chronic disease. Less frequently, anemia may result from red cell aplasia, folate or B12 deficiency, hemolytic processes, or hypersplenism. Occasional patients may become polycythemic because of erythropoietin-producing tumors such as renal adenocarcinomas or cerebellar hemangiomas. Elevation of the white cell count is commonly seen, especially in patients with lung cancer. Monocytosis and thrombocytosis, which may be early signs of an underlying malignancy, are also very common and occur in up to half of patients. Thrombocytopenia is commonly a result of therapy or marrow replacement; a few patients may have a syndrome resembling immune thrombocytopenic purpura. Abnormalities of coagulation are present in many patients, and may lead to superficial or deep venous thromboses, pulmonary emboli, nonbacterial thrombotic endocarditis with arterial emboli, bleeding, or acute disseminated intravascular coagulation. A sound understanding of the potential hematologic complications that can result from the malignant process is essential to the clinician caring for cancer patients.
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PMID:Hematologic manifestations of malignancy. 268 Mar 58

After observing a child with systemic onset juvenile rheumatoid arthritis (S-JRA) who developed purpura fulminans in association with disseminated intravascular coagulation, with subsequent gangrene and autoamputation, we undertook a prospective study of coagulation parameters in children with JRA. Ten consecutive children with S-JRA, 10 children with rheumatoid factor-negative, polyarticular juvenile rheumatoid arthritis (P-JRA), and 10 age- and sex-matched controls were studied. Routine coagulation screening tests were performed, as were tests for plasma fibrinopeptide A (a sensitive measure of intravascular thrombin generation), factor VIII-related antigen (an endothelial cell protein), and platelet factor 4 (a platelet-secreted protein). Our studies suggest that activation of intravascular coagulation is common in systemic onset JRA, but not in rheumatoid factor-negative, polyarticular disease. The coagulopathy may cause severe morbidity. In addition, marked elevations of plasma factor VIII-related antigen suggest perturbation of endothelial cells and vascular involvement in S-JRA, but not in P-JRA. Normal ranges of platelet factor 4 indicate that intravascular platelet consumption does not occur in either type of JRA, despite the thrombocytosis common in both.
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PMID:Evidence for intravascular coagulation in systemic onset, but not polyarticular, juvenile rheumatoid arthritis. 397 74

In 284 children with sepsis coagulation analyses were carried out. In sepsis in the postnatal period number of thrombocytes, plasminogen, antithrombin III, alpha 2-macroglobulin and factor V were initially decreased on an average, but fibrinogen, alpha 2-antiplasmin, the factors II and X as well as the trypsin inhibitor capacity were increased. The initially on an average reduced parameters often still considerably decreased, in order to increase after this to the norm of age within one to two weeks. The thrombocytopenia longest persists, often to the third week. The components initially found increased on an average in most cases rapidly increase and beyond the norm of age. They behave as acute phase proteins. In sepsis beyond the neonatal period the quality of the acute phase protein is in numerous components still more distinct than in the postnatal period. Several parameters also showed a completely other dynamics: the thrombocytopenia is of lesser size and shorter duration and is very often changed by a thrombocytosis. Here alpha 2-macroglobulin also has the quality of an acute phase protein. From the dynamics observed is concluded that disseminated intravascular coagulation processes frequently accompany the initial phase of the sepsis. They cause an eminent over-production of coagulation components which is limited by their production capacity and partly compensates the defects. The diversity of the constellation is explained by different sizes of consumption and compensation. The parameters in their dynamics have diagnostic valency. As far as the difference from fibrinogen level and number of thrombocytes is concerned it could already proved by simple means.
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PMID:[Effect on hemostasis and thrombogenesis by septic processes especially in childhood]. 646 15


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