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

A patient with laboratory-acquired Rocky Mountain spotted fever (RMSF) and concomitant influenza virus infection was studied from the third day of clinical illness. The course of his illness was marked by petechial rash, thrombocytopenia, and elevation of fibrin split products. No evidence of complement activation was observed. Plasma proteins were elevated in a pattern characteristic of the "acute phase reaction." The patient recovered completely, and vascular collapse or clinically important disseminated intravascular coagulation had developed. In febrile patients who had influenza or a clinically similar noninfluenzal respiratory syndrome, no changes in coagulation, complement, or plasma proteins developed. We conclude that aberrations in the patient's laboratory values reflected RMSF, and that complement played no critical role in his illness.
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PMID:Coagulation and complement studies in Rocky Mountain spotted fever. 64 36

The clinical and laboratory findings in four cases of acute renal failure following the onset of influenza A viral infection (Port Chalmers/1/73) are presented. Although the pathophysiologic mechanisms affecting the kidney in these cases varied, the ensuing renal failure in each patient was severe. Findings suggestive of acute myoglobinuria developed in one patient, and disseminated intravascular coagulation (DIC) occurred in another. The role of viruses in the pathogenesis of renal disease is reviewed. Despite inconclusive evidence that the influenza virus can cause human renal disease, the secondary pathways that can be triggered by viral infections may be even more significant in producing various degrees of renal dysfunction. The occurrence of renal failure during an episode of influenza represents a serious complication which may influence significantly the morbidity and mortality of patients with this viral infection.
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PMID:Influenza A viral infection associated with acute renal failure. 98 71

The pathogenesis of arenavirus infection is considered separately for the haemorrhagic fever (HF) syndrome and for lymphocytic choriomeningitis (LCM) virus infection of rodents. Experimental models of HF have received only limited study, mainly because of the virulence of the causal agents. Two useful models (Junin virus in guinea-pigs and Machupo virus in rhesus monkeys) are now available and an attempt is made to delineate crucial questions for future studies, including the physiology of shock, disseminated intravascular coagulation, immune mediation of disease, efficacy of antibody in treatment, and relative utility of attenuated and inactivated vaccines. Immunobiologic problems currently under investigation in LCM virus infection include the mechanism of immune destruction of infected tissues, the H-2 restriction of in vitro T-cell-mediated lysis of infected target cells, the transient immunodepression that accompanies acute primary LCM virus infection, and the mechanism of T-cell-mediated clearance of virus from infected tissues following adoptive immunization of persistently infected carrier mice.
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PMID:Directions for future research on the pathogenesis of arenaviral infections. 108 29

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

Seven rabbits experimentally infected with rabbit haemorrhagic disease virus were examined haematologically and histologically. Haematologically, activated partial thromboplastin time and prothrombin time were markedly prolonged in the terminal phase of the disease, just prior to death (all the animals died between 27 and 40 hr after inoculation with rabbit haemorrhagic disease virus). There was an increase in the titre of fibrin degradation products and a decrease in antithrombin III activity during the same interval. Acute necrotic hepatitis and disseminated intravascular coagulation (DIC) in many organs, including the lung, kidney, spleen and heart were the characteristic histopathological changes. Thus, the haematological and histological changes suggested that DIC was induced by rabbit haemorrhagic disease virus infection. Severe liver necrosis was considered to be a factor causing DIC by inducing a hypercoagulable condition in the systemic blood circulation.
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PMID:Disseminated intravascular coagulation (DIC) in rabbit haemorrhagic disease. 133 94

Hemorrhagic fever with renal syndrome (HFRS) is an acute viral disease that occurs over wide areas of Europe and Asia. Hantaviruses are the cause of this syndrome. The hallmark of HFRS is the triad of fever, hemorrhage, and renal failure. In its severe form it is associated with significant mortality. The syndrome evolves through five phases: febrile, hypotensive, oliguric, diuretic, and convalescent. The central physiologic derangement in HFRS is vascular dysfunction, manifested by impaired vascular tone and increased vascular permeability. The systemic effects of this dysfunction account for the occurrence of hypotension and shock, while local effects are probably important in the development of renal failure. Shock in HFRS has distributive and oligemic features, while renal failure has features of acute tubular necrosis. Hemorrhage is a consequence of vascular injury and a deficit of functional platelets. Vascular and platelet dysfunction are both compounded by uremia. Disseminated intravascular coagulation contributes to hemorrhage in some patients. Although hantaviruses are infectious for endothelial cells and may cause direct injury, a large body of evidence suggests that immune mechanisms play an important role in the pathogenesis of HFRS.
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PMID:Mechanisms of disease in Hantavirus infection: pathophysiology of hemorrhagic fever with renal syndrome. 167 61

Rhesus monkeys inoculated intravenously with Rift Valley fever (RVF) virus presented clinical disease syndromes similar to human cases of RVF. All 17 infected monkeys had high-titered viremias but disease ranged from clinically inapparent to death. Three (18%) RVF virus-infected monkeys developed signs of hemorrhagic fever characterized by epistaxis, petechial to purpuric cutaneous lesions, anorexia, and vomiting prior to death. The 14 remaining monkeys survived RVF viral infection but, 7 showed clinical signs of illness characterized by diminished food intake, cutaneous petechiae, and occasional vomiting. The other 7 monkeys showed no evidence of clinical disease. All monkeys had detectable serum interferon 24-30 h after infection, but 4 of 7 monkeys that did not develop clinical illness had serum interferon titers within 12 h after infection. In lethally infected macaques, indices of hepatic function and blood coagulation were abnormal within 2 days, implicating early pathogenetic events as critical determinants of survival. Serum transferase values were elevated in proportion to severity of clinical disease and outcome of infection. Both myocardial damage and laboratory evidence consistent with disseminated intravascular coagulation were present in fatal infections. All surviving monkeys developed neutralizing antibodies to RVF virus 4-7 days after infection, and this coincided with termination of viremia. Two fatally infected monkeys were viremic until death on days 6 and 8, and the third cleared viremia on day 5 and developed antibody on day 6 but died on day 15. There was a significant correlation between a delayed interferon response and mortality, suggesting that the early appearance of interferon was influential in limiting the severity of disease.
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PMID:Pathogenesis of Rift Valley fever in rhesus monkeys: role of interferon response. 169 May 34

White-tailed deer (Odocoileus virginianus) were inoculated with bluetongue virus serotype 17 and sequentially euthanatized during infection. Ultrastructural changes in the microvasculature of tongue, buccal mucosa, heart, and pulmonary artery, platelets, and bone marrow were evaluated. Bluetongue virus was found in endothelial cells of the microvasculature by postinoculation day 4. Viral replication was associated with the development of viral matrices, viral-associated macrotubules, and aggregates of mature viral particles in the cytoplasm of infected cells. Viral infection of pericytes and vascular smooth muscle cells developed subsequent to endothelial cell infection. Viral infection was associated with striking changes in the endothelial lining of the microvasculature by postinoculation day 4. Endothelial cell degeneration and necrosis, which resulted in denudation of the endothelial lining, and endothelial cell hypertrophy frequently were observed. Thrombosis, hemorrhage, and vessel rupture developed subsequent to endothelial damage. Bluetongue virus neither infected nor directly damaged platelets or bone marrow cells. It was concluded that viral-induced endothelial damage is the primary triggering mechanism for disseminated intravascular coagulation in bluetongue virus infection. Vascular damage coupled with the development of disseminated intravascular coagulation is responsible for the hemorrhagic diathesis, which is characteristic of bluetongue virus infection in white-tailed deer.
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PMID:Experimentally induced bluetongue virus infection in white-tailed deer: ultrastructural findings. 285 10

Five of 610 adults developed chickenpox between 35 days and 9.2 years after renal transplantation, and only one patient survived. All patients received prednisolone and azathioprine during the incubation period. Corticosteroid therapy was continued, but azathioprine was stopped after diagnosis. Four patients were treated with acyclovir, but three were given suboptimal doses. The patient who survived had been taking the lowest dose of azathioprine and was given the recommended dose of acyclovir. All patients who died developed disseminated intravascular coagulation, and at postmortem examination were found to have had cerebral haemorrhage. None of the patients treated with acyclovir had evidence of active varicella-zoster virus infection at post-mortem examination, but two had disseminated bacterial and fungal infections. Chickenpox follows a severe and often fatal course in adults with renal transplants. Prompt acyclovir therapy can be effective, provided an adequate dose is given. Attention should be directed towards prevention by the identification and immunisation of at risk patients prior to transplantation.
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PMID:Chickenpox in adult renal transplant recipients. 311 Jun 82

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


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