Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

An outbreak of chronic liver disease was investigated in a kennel of dogs. Anorexia, depression, polyuria, polydipsia, icterus and a terminal hemorrhagic diathesis were noted in clinically affected dogs. Thrombocytopenia, hypofibrinogenemia, elevated fibrinogen degradation products and prolonged activated partial thrombosplastin times (PTT) and one-stage prothrombin times (PT) were associated with the hemorrhagic crisis. Aflatoxicosis was confirmed by the presence of significant levels of aflatoxicosis was confirmed by the presence of significant levels of aflatoxin B in the commercial dog food being fed. A subacute hepatitis was found on necropsy. Disseminated intravascular coagulation was suspected as the cause of the hemorrhage in these cases and treatment was instituted.
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PMID:Disseminated intravascular coagulation complicating aflatoxicosis in dogs. 55 87

Coagulation factor XIII and plasma fibrinogen chromatographic assays have been performed serially in patients suffering from acute myocardial and cerebral infarction, and in others with disseminated intravascular coagulation. The findings were compared with 2 groups of "controls"; normal clinically-well subjects and hospitalized patients with cerebral infarction who exhibited minimal, stable, or improving neurological deficits. Substantial depression of factor XIII concentrations developed in the 3 patient groups, together with concomitant significant increases in the proportion and concentration of plasma high molecular weight fibrin(ogen) complexes (HMWFC). An inverse correlation (p less than 0.05) between coagulation factor XIII concentration and percentage of HMWFC was demonstrated in the early stages of the illness. These findings suggest that depression of coagulation factor XIII concentration in these states, is secondary to extravascular or intravascular coagulation and may reflect its degree.
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PMID:Reduction of coagulation factor XIII concentration in patients with myocardial infarction, cerebral infarction, and other thromboembolic disorders. 57 91

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

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

Blood coagulation screening profiles were performed in 512 patients who underwent open-heart surgery with extracorporeal circulation. Severe coagulation disorders were found in 29 (5.6 per cent) patients. The most common abnormalities were low one-stage prothrombin time (PT) activities and impaired whole blood clot retractions. In the majority of patients the discrepancy between low PT's and normal or only slightly depressed factor II, V, VII, and X activities was explained by the presence of an inhibitor of the extrinsic system. Eight patients demonstrated the heparin rebound phenomenon but only 1 bled excessively. The pattern of severe hepatic dysfunction was found in 4 and severe depression of vitamin K-dependent factors due to oral anticoagulants in 2. Two had disseminated intravascular coagulation. Seventeen patients with normal coagulation screening profiles bled excessively postoperatively. Of these, 2 had moderate thrombocytopenia associated with a marked platelet functional abnormality. Revision of the wound in 13 revealed a surgical hemostatic defect and in 2 the cause of bleeding could not be determined.
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PMID:The hemostatic mechanism after open-heart surgery. I. Studies on plasma coagulation factors and fibrinolysis in 512 patients after extracorporeal circulation. 115 4

The objective of this study was to characterize the hemostatic defect in dogs with infectious canine hepatitis (ICH), a naturally occurring viral disease of dogs. Five littermate dogs were inoculated with 10(3) TCID50 of ICH virus intravenously. Two littermates were controls. The clinicopathologic manifestations of ICH were fever, depression, anorexia, hematemesis, melena, widespread mucocutaneous petechiae, prolonged bleeding from venipunctures, faceial edema, leukopenia, and proteinuria. The hemostatic defect of ICH was characterized by thrombocytopenia, abnormal platelet function, prolonged one-stage prothrombin time and activated partial thromboplastin time, normal thrombin times, depressed factor VIII activity, and increased fibrin-fibrinogen degradation products. These findings suggested that the central pathologic mechanism of the abnormal hemostasis in ICH was disseminated intravascular coagulation (DIC). ICH is an example of DIC induced by viral infection. This disease is a suitable model for investigation of the detection, pathogenesis, and therapy of DIC.
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PMID:Infectious canine hepatitis: animal model for viral-induced disseminated intravascular coagulation. 124 23

Hemostasis studies of 152 patients with inflammatory dystrophic and circulatory diseases of the retina and the uveal tract have shown that the major hemostasis disorders consisted in the presence of soluble fibrin monomer complexes in the blood of 62-90.5% of patients and in retarded lysis of the blood euglobulin fraction. Patients with the above hemostasis disorders and central serous chorioretinopathies and abiotrophies develop delayed formation of the fibrin clot and its poor retraction, that is characteristic of latent imbalance of the coagulation and fibrinolysis processes and liability to DIC. Patients with retinal vein thrombosis develop, besides delayed fibrin polymerization in the clot and reduction of platelet contractility, a drastic depression of the blood and lacrimal fibrinolytic activity. Central choroiditis and uveitis was associated with a marked increase of lacrimal fibrinolysis and reduced blood plasma fibrinolysis, along with enhanced paracoagulation and prolonged lysis of the blood euglobulin fraction, this resulting in hypoproteolytic hypercoagulation. Local and systemic fibrinolysis test may help choose the drugs for local and general pathogenetic therapy.
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PMID:[Hemostasis in patients with diseases of the retina and uveal tract]. 152 88

The cardiovascular and haematological effects of purified prothrombin activator derived from the venom of the Australian Common Brown Snake (Pseudonaja textilis) were studied in anaesthetised, mechanically ventilated dogs. Severe depression of systemic blood pressure and cardiac output and a rise in central venous pressure were observed. Thrombocytopenia, prolongation of both prothrombin time and activated partial thromboplastin time and a reduction in serum fibrinogen were also observed. All of these observed effects were prevented by the prior administration of heparin--a naturally occurring anticoagulant. We conclude that the prothrombin activator in Pseudonaja textilis venom may cause cardiovascular depression due to myocardial dysfunction secondary to disseminated intravascular coagulation.
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PMID:The cardiovascular and haematological effects of purified prothrombin activator from the common brown snake (Pseudonaja textilis) and their antagonism with heparin. 160 37

A study was made of changes in functional status of complementary system in 42 patients with chronic renal failure on programmed hemodialysis. Early stages of hemodialysis were accompanied by short-term and reversible activation of complementary system. 100 sessions were followed by complement depression. Complement system was found to be involved in two pathogenetic mechanisms of respiratory insufficiency: block of pulmonary microcirculation by leukocytic aggregates and DIC syndrome associated with microthrombosis of the lesser circulation vessels. To manage the above complications, plasmapheresis is advocated.
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PMID:[The role of the complement system in the origin of respiratory insufficiency in patients on hemodialysis]. 180 18


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