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

Although many viral infections have on occasion been associated with hemorrhagic complications, infection with any of several RNA viruses regularly results in vascular involvement and the syndrome called viral hemorrhagic fever (VHF). In spite of clinically useful similarities among various VHFs, there are significant differences in their pathogenesis and clinical evolution; these are often related to characteristics of their viral taxon. Infection with Rift Valley fever (RVF) virus, a phlebovirus, appears to be regulated by interferon and terminated by neutralizing antibody. In contrast, Lassa fever (LF) virus, an arenavirus, is resistant to interferon, and LF is terminated by cellular immune effector mechanisms. The lytic virus-cell interaction typical of RVF virus suggests its major effects occur by direct, virus-induced cellular necrosis, particularly in the liver. In the primate RVF model, disseminated intravascular coagulation (DIC) may be important. LF virus--characteristically noncytopathic--may exert its effects through induction of mediator secretion from infected macrophages. DIC does not appear to be a central pathogenetic mechanism in LF. Pichinde virus, which is not pathogenic for humans, provides an alternate model for study of LF. Infected guinea pigs do not show histologic lesions that could explain their body wasting, cardiovascular deterioration, and pulmonary edema. In the heart, for example, loss of tissue mass, protein, and contractile function proceed without direct viral involvement or myocarditis. Sulfidopeptide leukotrienes have been implicated as one relevant soluble mediator participating in the disease state.
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PMID:Pathogenesis of viral hemorrhagic fevers: Rift Valley fever and Lassa fever contrasted. 266 11

Hemorrhagic fever with renal syndrome in Korea (Korean hemorrhagic fever) is an acute viral disease characterized by fever, hemorrhage and renal failure. In Korean patients, the disease manifests more distinctive bleeding tendencies than those of hemorrhagic fever with renal syndrome found in western countries. To investigate the nature and role of the coagulation, fibrinolysis, kinin and immune system in the pathogenesis of such a hemorrhagic manifestation, alterations of these systems were assessed from the early phase of the disease. Decreased platelet count and shortened platelet survival were observed with giant platelets in the peripheral blood. The marked prolongations of bleeding time, prothrombin time and partial thromboplastin time were noticed with the decreased plasma activities of coagulation factors II, V, VIII, IX and X. Shortened half life of fibrinogen, increased fibrinogen-fibrin degradation product, with decreased plasma levels and activities of plasminogen, alpha 2-plasmin inhibitor and antithrombin III were found. On thrombelastogram, the existence of procoagulant activity was confirmed, and prolonged reaction time and clot formation time with decreased maximum amplitude were observed. The appearance of circulating immune complexes was found along with decreased C3 and normal C4 in the serum. Significant decrease of serum C3 was evident in the patients with disseminated intravascular coagulation. These findings of coagulopathy were normalized within ten days of the illness in most cases. Therefore, it can be concluded that disseminated intravascular coagulation and thrombocytopenia in the early phase, and azotemia developing later might play an important role in the pathogenesis of bleeding tendency in Korean hemorrhagic fever.
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PMID:Coagulopathy in patients with hemorrhagic fever with renal syndrome. 315 65

Rift Valley fever (RVF) is a major cause of human morbidity and mortality in endemic areas of sub-Saharan Africa and has the potential to cause epidemic disease in receptive areas world-wide. In this study, a RVF viral isolate from the 1977 Egyptian epidemic (ZH-501) inoculated intravenously into rhesus macaques caused a benign viremic infection in most, but resulted in the hemorrhagic fever syndrome in 20 per cent (3 of 15). Serious disease of this type has not previously been observed in nonhuman primates inoculated with RVF virus and may be a consequence of the viral strain used or the route of inoculation. Severe disease was accompanied by extensive liver necrosis, disseminated intravascular coagulation, and microangiopathic hemolytic anemia. We also attempted to prevent RVF by passive transfer of serum from vaccinated rhesus monkeys (plaque-reduction neutralization test titer 1:2,560). As little as 0.025 ml/kg prevented the development of viremia in naive rhesus monkeys after subcutaneous inoculation of virus. The monkey model should be helpful in understanding the pathogenesis and prevention of human RVF.
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PMID:Experimental Rift Valley fever in rhesus macaques. 335 74

To investigate the nature and role of coagulation and complement alterations in the pathogenesis of Korean hemorrhagic fever (KHF), the profiles from the early stages in 27 male patients were serially evaluated. Evidence of disseminated intravascular coagulation (DIC) was observed in 14 of the 27 patients (51.8%) sometime during the course of the disease. The earlier the coagulation tests were performed, the more frequently the evidence of DIC was found. The mean serum C3 concentration was significantly decreased during the early stages, while serum C4 concentrations revealed no significant variation. A significant decrease of the serum C3 concentration, however, was found only in the group with DIC. Korean hemorrhagic fever (KHF) is an acute, systemic disease characterized by fever, hemorrhagic manifestations, and renal failure. This disease has been known to occur from the Pacific Ocean to the Baltic Sea under various synonyms and toponyms including epidemic hemorrhagic fever, hemorrhagic nephrosonephritis and hemorrhagic fever with renal syndrome. Recent investigations demonstrated the identity of these conditions described from Korea, the Soviet Union, Japan, and China. Nephropathia epidemica of Scandinavia was also revealed to have a close serological relation to this disease, but with antigenic differences. The etiologic agent was identified in 1978 by Lee et al., who isolated a viral antigen from a field mouse, Apodemus agrarius coreae, which is the natural reservoir of this disease in Korea. The KHF or Hantaan virus has been propagated in cell cultures and observed electronmicroscopically. In thin sections, the virus was detected within the cytoplasmic granular matrices (viroplasms) of the infected cells. Virus particles were spherical and had an extremely electron-dense core. Negative-contrast staining showed that the virus had an icosahedral structure and annular surface capsomeres. The morphology and morphogenesis of the virus were similar to those of the orbiviruses. The characteristic pathologic findings observed in fatal cases of KHF are congestion and hemorrhage of the renal medulla, hemorrhage in the right atrial wall of the heart, and hemorrhage and necrosis in the anterior lobe of the pituitary gland. The microscopic characteristics of these lesions consist of hemorrhage, coagulation necrosis, and mononuclear cell infiltration. The clinical course of typical KHF may be divided into five phases, each designated for a characteristic physiologic aberration; febrile, hypotensive, oliguric, diuretic, and convalescent.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Disseminated intravascular coagulation in Korean hemorrhagic fever. 614 86

Collaborative studies on hemostasis in dengue hemorrhagic fever (DHF) patients by Indonesian and Japanese teams revealed that all DHF patients had manifestations of the acute type of disseminated intravascular coagulation (DIC). Prolongations of activated partial thromboplastin time and prothrombin time and decreases of platelet counts, fibrinogen, prothrombin, factor VIII, plasminogen and antithrombin III activities were observed transiently during the acute stage of DHF. It was also found that alpha 2 antiplasmin was decreased in the acute stage to 32% of the normal level on the average. This may characterize the hemorrhagic diathesis of the DHF patients.
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PMID:Features of DIC in dengue hemorrhagic fever. 666 46

Coagulation is explored in 129 children infected by dengue virus and presenting either banal symptoms, or an hemorrhagic fever. Results are given, and commented according to the disease's clinical staging. A disseminated intravascular coagulation symdrome is brought out in all the cases, but with less or more intensity, though it belongs to dengue virus infection. Etio-pathogenic mechanism is then discussed.
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PMID:[Hemorrhagic dengue fever: evidence of consumption coagulopathy (author's transl)]. 738 88

Abstract. Abnormal hemostasis in dengue hemorrhagic fever includes:- 1. Vasculopathy which occurs during the early febrile to pre-shock and shock phase. The evidences support are: 1.1 Increased anaphylatoxin, released by complement activation causing leakage of intravascular fluid in to serous space. 1.2 Positive tourniquet test, some of which occur preceeding thrombocytopenia in the acute phase of DHF. 1.3 Excessive increased in PGI2 which is the most potent vasodilator and platelet aggregation inhibitor. 2. Platelets: 2.1 Thrombocytopenia due to 2.1.1 The bone marrow hypocellularity with increased in all forms of megakaryocytes but the vacuolated and disintegrated ones. 2.1.2 Destruction by the liver and spleen. 2.1.3 Immune-mediated injury as demonstration of dengue antibody complexes on the platelet surface. 2.1.4 The in vitro spontaneous aggregation to vascular endothelial cell pre-infected by dengue virus inducing platelet aggregation, causing lysis and platelet destruction. 2.2 Dysfunction shown by 2.2.1 Increased release of betathromboglobulin (BTG), PF4 and PGI2. 2.2.2 In vitro hypoaggregation stimulated by ADP and defect in ADP-releasing ability. 3. Coagulopathy including: 3.1 Prothrombin complex deficiency due to liver damage. 3.2 Consumptive coagulopathy due to the activation by mononuclear phagocytes, PF3 released from platelet aggregation. DIC is seen in prolonged shock cases of DSS.
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PMID:Abnormal hemostasis in dengue hemorrhagic fever. 788 14

Four serologically confirmed fatal cases of nephropathia epidemica (NE), the mild form of hemorrhagic fever with renal syndrome (HFRS) are described. All the patients had disseminated intravascular coagulation. Autopsies revealed hemorrhage and necrotic areas of their pituitary glands, myocarditis, venous congestion and hemorrhage of the kidneys as well as pulmonary edema and hemorrhage of the lungs in all patients. This report provides new evidence that NE can be a fatal disease.
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PMID:Four fatal cases of nephropathia epidemica. 858 46

On September 10, 2000, the Ministry of Health (MOH), Kingdom of Saudi Arabia, and subsequently the Ministry of Health of Yemen received reports of unexplained hemorrhagic fever in humans and associated animal deaths from the southwestern border of Saudi Arabia and Yemen. Signs and symptoms of ill persons included low grade fever, abdominal pain, vomiting, diarrhea, jaundice with liver and renal dysfunction often progressing to disseminated intravascular coagulation, hepatorenal syndrome, and death. On September 15, using ELISA (antigen detection and IgM), polymerase chain reaction, virus isolation, and immunohistochemistry, CDC confirmed the diagnosis of Rift Valley fever (RVF) in all four serum samples submitted from Saudi Arabia. This report summarizes the preliminary results of the collaborative epidemiologic investigation performed by the Saudi Arabian MOH, CDC, and the National Institute of Virology, South Africa, of the first confirmed occurrence of RVF outside Africa.
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PMID:Outbreak of Rift Valley fever--Saudi Arabia, August-October, 2000. 1104 43

Severe infection and inflammation almost invariably lead to hemostatic abnormalities, ranging from insignificant laboratory changes to severe disseminated intravascular coagulation (DIC). Systemic inflammation results in activation of coagulation, due to tissue factor-mediated thrombin generation, downregulation of physiological anticoagulant mechanisms, and inhibition of fibrinolysis. Pro-inflammatory cytokines play a central role in the differential effects on the coagulation and fibrinolysis pathways. Vice-versa, activation of the coagulation system may importantly affect inflammatory responses by direct and indirect mechanisms. Apart from the general coagulation response to inflammation associated with severe infection, specific infections may cause distinct features, such as hemorrhagic fever or thrombotic microangiopathy. The relevance of the cross-talk between inflammation and coagulation is underlined by the promising results in the treatment of severe systemic infection with modulators of coagulation and inflammation.
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PMID:Infection and inflammation and the coagulation system. 1452 4


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