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)

To gain further insight into the interdependent pathogenic processes in Ebola hemorrhagic fever (EHF), we have examined the dynamics of host responses in individual rhesus macaques infected with Zaire ebolavirus over the entire disease course. Examination of coagulation parameters revealed that decreased coagulation inhibitor activity triggered severe coagulopathy as indicated by prolonged coagulation times and decreased fibrinogen levels. This has been proposed as one of the significant mechanisms underlying disseminated intravascular coagulation in EHF patients. Furthermore, monitoring of expression levels for cytokines/chemokines suggested a mixed anti-inflammatory response syndrome (MARS), which indicates that a catastrophic uncontrolled immunological status contributes to the development of fatal hemorrhagic fever. These results highlight the pathological analogies between EHF and severe sepsis and not only contribute to our understanding of the pathogenic process, but will also help to establish novel postexposure treatment modalities.
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PMID:Host response dynamics following lethal infection of rhesus macaques with Zaire ebolavirus. 2198 81

Dengue hemorrhagic fever is a more serious form of disease characterised by plasma leakage syndrome, thrombocytopenia and disseminated intravascular coagulation. We present a 51 year old male who presented with fever, petechiae and acute onset of breathlessness. Emergency chest rhoentogram showed a massive right sided pleural effusion. On insertion of intercostal drain, there was a sudden gush of blood tinged fluid suggestive of hemothorax. There was no history of trauma or bleeding tendencies. Laboratory investigations revealed a raised hematocrit and severe thrombocytopenia. Dengue IgM was surprisingly positive. After aggressive supportive management the patient gradually improved and was discharged. While bilateral pleural effusion is a known occurrence in dengue hemorrhagic fever, massive hemothorax is unheard of. We report the first case in literature of dengue hemorrhagic fever presenting as unilateral massive hemothorax. A suspicion of dengue must also be borne in mind in cases of non-traumatic hemothorax especially in endemic areas.
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PMID:Unilateral massive hemothorax in Dengue hemorrhagic fever: a unique presentation. 2280 31

Four families of enveloped RNA viruses, filoviruses, flaviviruses, arenaviruses, and bunyaviruses, cause hemorrhagic fevers. These viruses are maintained in specific natural cycles involving nonhuman primates, bats, rodents, domestic ruminants, humans, mosquitoes, and ticks. Vascular instability varies from mild to fatal shock, and hemorrhage ranges from none to life threatening. The pathogenic mechanisms are extremely diverse and include deficiency of hepatic synthesis of coagulation factors owing to hepatocellular necrosis, cytokine storm, increased permeability by vascular endothelial growth factor, complement activation, and disseminated intravascular coagulation in one or more hemorrhagic fevers. The severity of disease caused by these agents varies tremendously; there are extremely high fatality rates in Ebola and Marburg hemorrhagic fevers, and asymptomatic infection predominates in yellow fever and dengue viral infections. Although ineffective immunity and high viral loads are characteristic of several viral hemorrhagic fevers, severe plasma leakage occurs at the time of viral clearance and defervescence in dengue hemorrhagic fever.
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PMID:Pathogenesis of the viral hemorrhagic fevers. 2312 Oct 52

The hantaviruses classified in Hantavirus genus of Bunyaviridae family, may cause two different types of clinical conditions, namely hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). Mortality may reach up to 40% in these infections. Hantavirus subtypes (Sin Nombre, Hantaan, Seoul, Puumala, Dobrava, etc) with different virulences represent one of the most significant factors affecting the mortality. Additionally, many other factors including age, gender, humoral immune response, genetic factors, patient's clinical and laboratory findings, transfusion, mechanical ventilation requirement, antiviral treatment and immunotherapy administered to the patient are prognostically important. Increasing age had an unfavorable effect on mortality. While the disease is commonly observed in the male gender, mortality rate is higher in the female gender. The higher the emergent neutralizing antibody response, the virus spread, the number of the infected cells and the cytotoxic T lymphocyte-mediated injury will be lower. The requirement for dialysis is reported to be higher with a poorer prognosis in individuals with HLA-B8, -DR3, -DQ2 alleles, and those with HLA-B27 allele usually experience a milder clinical course. Clinically, the risk of mortality increases in patients with multiple, central nervous system hemorrhage, sepsis, disseminated intravascular coagulation (DIC) and secondary infection. The presence of adult respiratory distress syndrome (ARDS), the requirement for mechanical ventilation, the presence of dyspnea and hemoconcentration in HPS are reported to be the most important prognostic factors associated with death. The correlation of severity and the transfusion requirement with mortality was demonstrated. High serum levels of white blood cells, blood urea nitrogen (BUN), creatinine phophokinase (CPK), C-reactive protein (CRP), prothrombin time (PT), activated partial thromboplastin time (aPTT), D-dimer and INR (International normalized ratio) are prognostic factors that increase the mortality risk. Hemodialysis support is particularly important in cases infected with Hantaan and Dobrava viruses. Respiratory support and mechanical ventilation can be life-saving in HPS cases. Extracorporeal membrane oxygenation support has been demonstrated to have a favorable contribution to the patient survival in HPS. While there are some human and animal trials showing that ribavirin reduces the severity of HFRS, hemodialysis requirement and mortality, its efficacy for HPS has not yet been demonstrated. As a result, a proper evaluation of the prognostic factors will provide physicians a perspective with respect to the disease course and the necessary treatment approach.
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PMID:[Prognostic factors in hantavirus infections]. 2450 30

Existing mouse models of lethal Ebola virus infection do not reproduce hallmark symptoms of Ebola hemorrhagic fever, neither delayed blood coagulation and disseminated intravascular coagulation nor death from shock, thus restricting pathogenesis studies to nonhuman primates. Here we show that mice from the Collaborative Cross panel of recombinant inbred mice exhibit distinct disease phenotypes after mouse-adapted Ebola virus infection. Phenotypes range from complete resistance to lethal disease to severe hemorrhagic fever characterized by prolonged coagulation times and 100% mortality. Inflammatory signaling was associated with vascular permeability and endothelial activation, and resistance to lethal infection arose by induction of lymphocyte differentiation and cellular adhesion, probably mediated by the susceptibility allele Tek. These data indicate that genetic background determines susceptibility to Ebola hemorrhagic fever.
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PMID:Host genetic diversity enables Ebola hemorrhagic fever pathogenesis and resistance. 2535 52

Severe fever with thrombocytopenia syndrome (SFTS) caused by SFTS virus (SFTSV), a novel phlebovirus, was reported to be endemic to central and northeastern PR China and was also to be endemic to South Korea and western Japan. SFTS is an emerging viral infection, which should be categorized as a viral hemorrhagic fever disease as Crimean-Congo hemorrhagic fever (CCHF) is caused by CCHF virus. SFTS is a tick-borne viral infection. SFTSV is maintained between several species of ticks and wild and domestic animals in nature. Patients with SFTS show symptoms of fever, general fatigue, and gastrointestinal symptoms such as bloody diarrhea. The severely ill SFTS patients usually show gastrointestinal hemorrhage and deteriorated consciousness. The case fatality rate of SFTS ranges from 5 to 40%. Pathological studies on SFTS have revealed that the mechanisms behind the high case fatality rate are virus infection-related hemophagocytic syndrome associated with cytokine storm, coagulopathy due to disseminated intravascular coagulation causing bleeding tendency, and multi-organ failure. Favipiravir was reported to show efficacy in the prevention and treatment of SFTSV infections in an animal model. A clinical study to evaluate the efficacy of favipiravir in the treatment of SFTS patients has been initiated in Japan. SFTSV is circulating in nature in PR China, Korea, and Japan, indicating that we cannot escape from the risk being infected with SFTSV. The development of specific therapy and preventive measures is a pressing issue requiring resolution to reduce the morbidity and mortality of SFTS patients.
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PMID:Pathophysiology of severe fever with thrombocytopenia syndrome and development of specific antiviral therapy. 3009 14

Inbred strain 13/N guinea pigs are used as small animal models for the study of hemorrhagic fever viruses. Coagulation abnormalities, including prolonged clotting times and bleeding, are characteristic of hemorrhagic fever in humans; patients often meet criteria for disseminated intravascular coagulation (DIC). Comprehensively evaluating coagulation function is critical in model development and studies of viral pathogenesis and therapeutic efficacy. Here, using the VetScan VSpro veterinary point-of-care platform, we developed reference intervals in both juvenile and adult strain 13/N guinea pigs for three coagulation parameters: prothrombin time (PT), activated partial thromboplastin time (aPTT), and fibrinogen. In addition, for situations or species with limited availability of blood for clinical analysis, we investigated the validity of a modified collection approach for low-volume (0.1 mL) blood sample analysis of PT and aPTT.
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PMID:Prothrombin Time, Activated Partial Thromboplastin Time, and Fibrinogen Reference Intervals for Inbred Strain 13/N Guinea Pigs (Cavia porcellus) and Validation of Low Volume Sample Analysis. 3272 69


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