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

Ebola virus (EBOV) infection causes a severe and often fatal hemorrhagic disease in humans and nonhuman primates. Whether infection of endothelial cells is central to the pathogenesis of EBOV hemorrhagic fever (HF) remains unknown. To clarify the role of endothelial cells in EBOV HF, we examined tissues of 21 EBOV-infected cynomolgus monkeys throughout time, and also evaluated EBOV infection of primary human umbilical vein endothelial cells and primary human lung-derived microvascular endothelial cells in vitro. Results showed that endothelial cells were not early cellular targets of EBOV in vivo, as viral replication was not consistently observed until day 5 after infection, a full day after the onset of disseminated intravascular coagulation. Moreover, the endothelium remained relatively intact even at terminal stages of disease. Although human umbilical vein endothelial cells and human lung-derived microvascular endothelial cells were highly permissive to EBOV replication, significant cytopathic effects were not observed. Analysis of host cell gene response at 24 to 144 hours after infection showed some evidence of endothelial cell activation, but changes were unremarkable considering the extent of viral replication. Together, these data suggest that coagulation abnormalities associated with EBOV HF are not the direct result of EBOV-induced cytolysis of endothelial cells, and are likely triggered by immune-mediated mechanisms.
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PMID:Pathogenesis of Ebola hemorrhagic fever in primate models: evidence that hemorrhage is not a direct effect of virus-induced cytolysis of endothelial cells. 1463 9

Disseminated intravascular coagulation is a prominent manifestation of Ebola virus (EBOV) infection. Here, we report that tissue factor (TF) plays an important role in triggering the hemorrhagic complications that characterize EBOV infections. Analysis of samples obtained from 25 macaques showed increased levels of TF associated with lymphoid macrophages, whereas analysis of peripheral blood-cell RNA showed increased levels of TF transcripts by day 3. Plasma from macaques contained increased numbers of TF-expressing membrane microparticles. Dysregulation of the fibrinolytic system developed during the course of infection, including a rapid decrease in plasma levels of protein C. Infection of primary human monocytes/macrophages (PHMs) was used to further evaluate the role of TF in EBOV infections. Analysis of PHM RNA at 1-48 h showed increased TF transcripts, whereas levels of TF protein were dramatically increased by day 2. Thus, chemotherapeutic strategies aimed at controlling overexpression of TF may ameliorate the effects of EBOV hemorrhagic fever.
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PMID:Mechanisms underlying coagulation abnormalities in ebola hemorrhagic fever: overexpression of tissue factor in primate monocytes/macrophages is a key event. 1463 30

To demonstrate the differences of clinical features and hematologic abnormalities between dengue fever (DF) and dengue hemorrhagic fever (DHF), 359 pediatric patients admitted St. Luke's Medical Center in Quezon City, between 1999 and 2001 in Metro Manila, and adjoining provinces the Philippines, with a laboratory-confirmed dengue virus infection were evaluated. One third of the patients had DHF, and most of these patients were without shock. Restlessness, epistaxis, and abdominal pain were more associated with DHF. The platelet count was significantly lower in the DHF group than in the DF group before and after defervescence. In the DHF patients, the hematocrit was significantly increased before defervescence, and decreased the day after due to administration of intravenous fluid. Coagulation abnormalities associated with most DHF patients were thrombocytopenia and an increased fibrinolysis, but not disseminated intravascular coagulation. We present recent data on readily obtained clinical and laboratory data that can be used for early diagnosis and consequently earlier appropriate treatment of dengue virus infections.
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PMID:Comparison of clinical features and hematologic abnormalities between dengue fever and dengue hemorrhagic fever among children in the Philippines. 1610 17

Dengue is an arthropod-borne viral disease whose frequency has increased steadily in the Americas over the past 25 years. The type of dengue that carries the highest mortality is the clinical variant known as dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS). Even though no vaccine or drug against the disease is available, successful management consists of preventing serious illness through patient follow-up and monitoring danger signals so as to be able to initiate aggressive intravenous rehydration and prevent shock or treat it early and successfully. These measures are also useful in preventing other complications, such as massive hemorrhage, disseminated intravascular coagulation, multiple organ failure, and respiratory failure due to non-cardiogenic pulmonary edema. Primary health care (PHC) settings and the community are ideal spaces for this type of preventive management based on health education and active case detection. It involves training all medical and nursing staff, students, and community health workers, as well as reorganizing health care in PHC units and hospitals and redistributing available resources during a dengue epidemic.
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PMID:[Preventing deaths from dengue: a space and challenge for primary health care]. 1701 26

This is the first report of the largest epidemic of dengue hemorrhagic fever (DHF) virus infection (2006) with IgM-confirmed cases from Karachi, Pakistan. Medical records of 172 IgM-positive patients were reviewed retrospectively for demographic, clinical and laboratory data. Patients were categorized into dengue fever (DF) and DHF according to the WHO severity grading scale. The mean+/-SD age of the patients was 25.9+/-12.8 years, 55.8% were males and the hemoconcentration was recorded in a small number of patients [10 (7.0%)]. Male gender [odds ratio (OR)=14.7, P=0.003), positive history of vomiting (OR=4.3, P=0.047), thrombocytopenia at presentation (OR=225.2, P<0.001) and monocytosis (OR=5.8, P=0.030) were independently associated with DHF, but not with DF. Five cases (2.9%) had a fatal outcome, with a male-to-female ratio of 1:4. Three were from a pediatric group (<15 years). Pulmonary hemorrhages, disseminated intravascular coagulation and cerebral edema preceded death in these patients. The results have highlighted significant findings, such as adult susceptibility to DHF, pronounced abdominal symptoms and lack of hemoconcentration at time of presentation in the study population. These findings may play an important role in the case definitions of future studies from this part of the world.
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PMID:Dengue outbreak in Karachi, Pakistan, 2006: experience at a tertiary care center. 1770 59

A 46 year old woman who presented with severe multiorgans involvement including liver brain, cardio-pulmonary failure, gastrointestinal bleeding, progressive cytopenia, DIC and hemophagocytic syndrome during the convalescent phase of Dengue type II has been successfully treated primarily with pulse methyl prednisolone and high dose intravenous immunoglobulin G. The authors believe that HPCS are not infrequently seen with high mortality and recommended early diagnosis and treatment with the regimen. This is the first complete report of hemophagocytic syndrome in adult dengue hemorrhagic fever in Thailand. The literature of HPCS in DHF was reviewed and discussed.
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PMID:Hemophagocytic syndrome in Dengue hemorrhagic fever with severe multiorgan complications. 1838 53

Management of patients with dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS) requires especial care. It is based on physiological replacement therapy and fluid control. The use of blood products has its own criteria, especially during the disseminated intravascular coagulation (DIC) in the hemorrhagic phase. Monitoring bleeding manifestations and laboratory tests are needed. It has been shown that preventive transfusion does not have advantages in the treatment of this disease; on the contrary it increases the length of hospitalization and the development of pulmonary edema, among other transfusion-related risks.
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PMID:[Indication for haemoderivatives in dengue]. 1884 69

Severe infection and inflammation almost invariably lead to hemostatic abnormalities, ranging from insignificant laboratory changes to severe disseminated intravascular coagulation. Systemic inflammation as a result of severe infection leads to activation of coagulation, due to tissue factor-mediated thrombin generation, downregulation of physiological anticoagulant mechanisms, and inhibition of fibrinolysis. Proinflammatory 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 results of the treatment of severe systemic infection with modulators of coagulation and inflammation.
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PMID:Disseminated intravascular coagulation in infectious disease. 2061 89

Hemophagocytic Syndrome (HS) is a clinico-pathologic entity characterized by activation of T lymphocytes and macrophages. It may be diagnosed in association with malignant, genetic, or autoimmune diseases, but is most linked with Epstein-Barr virus. There are few reports of association between HS and Dengue in pediatrics. Dengue fever, caused by a flavivirus, is an important mosquito-transmitted disease. It can cause increased vascular permeability that leads to a bleeding diathesis or disseminated intravascular coagulation known as dengue hemorrhagic fever (DHF). We present the case of a 10 month-old-female who developed DHF and dengue shock syndrome, requiring admission to intensive care unit. She developed hemophagocytosis diagnosed by bone marrow aspiration and atypical skin changes that have not been previously described in association with dengue fever. This is an unusual case of dengue related hemophagocytic syndrome that adds to the limited pediatric cases reported in literature.
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PMID:Dengue virus associated hemophagocytic syndrome in children: a case report. 2085 75

Ebolavirus and Marburgvirus are members of the filovirus family and induce a fatal hemorrhagic disease in humans and nonhuman primates with 90% case fatality. To develop a small nonhuman primate model for filovirus disease, common marmosets (Callithrix jacchus) were intramuscularly inoculated with wild type Marburgvirus Musoke or Ebolavirus Zaire. The infection resulted in a systemic fatal disease with clinical and morphological features closely resembling human infection. Animals experienced weight loss, fever, high virus titers in tissue, thrombocytopenia, neutrophilia, high liver transaminases and phosphatases and disseminated intravascular coagulation. Evidence of a severe disseminated viral infection characterized principally by multifocal to coalescing hepatic necrosis was seen in EBOV animals. MARV-infected animals displayed only moderate fibrin deposition in the spleen. Lymphoid necrosis and lymphocytic depletion observed in spleen. These findings provide support for the use of the common marmoset as a small nonhuman primate model for filovirus induced hemorrhagic fever.
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PMID:A small nonhuman primate model for filovirus-induced disease. 2195 17


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