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)

In 29 patients with dengue hemorrhagic fever (DHF), 12 with grade 2 and 17 with grades 3 and 4, fibrinogen metabolism was studied by using 125I-fibrinogen; 11 of these patients were studied during shock. Hemostatic studies were also performed to search for evidence of disseminated intravascular coagulation (DIC). Increased intravascular coagulation, as judged by rapid T1/2 of 125I-fibrinogen, as well as evidence of DIC by hemostatic patients with DHF grade 2 had rapid T1/2 and only 17% had DIC. Of the 11 patients studied during shock, 91% had both rapid T1/2 and evidence of DIC, whereas 63% of the 18 patients without shock had rapid T1/2 and only 11% of this latter group had DIC. A correlation between the increased fibrinogen consumption as judged by rapid T1/2 of 125I-fibrinogen, DIC, clinical severity, and shock was demonstrated. The role of DIC in the pathogenesis of DHF is discussed, and heparin is suggested for patients with prolonged shock and severe acidosis when DIC becomes clinically apparent.
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PMID:Fibrinogen metabolism and disseminated intravascular coagulation in dengue hemorrhagic fever. 86 4

Nephropathia epidemica (NE) in Scandinavia is a zoonosis caused by Puumala virus. The main animal reservoir is the bank vole. NE predominantly affects men. Its annual incidence varies in a cyclic fashion, with peaks occurring every third to fourth year. The clinical picture of NE in Scandinavia is similar to that of hemorrhagic fever with renal syndrome in other parts of the world, although NE generally has a milder course. The case-fatality rate is approximately 0.2%. The most common clinical findings in NE are an acute onset of symptoms, fever (greater than or equal to 38 degrees C), oliguria, headache, back pain, and polyuria. Hemorrhagic manifestations are seen in about one-third of cases, and up to 5% of patients have gastrointestinal bleeding or disseminated intravascular coagulation. Thrombocytopenia occurs in a majority of patients. In the acute phase, the glomerular filtration rate is markedly decreased and tubular dysfunction is evident. Most patients with NE recover within 6 months.
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PMID:Nephropathia epidemica (hemorrhagic fever with renal syndrome) in Scandinavia. 168 81

This study refers to the clinical features of 11 cases of hemorrhagic fever with renal syndrome (HFRS) which was prevalent in Nagoya City University Medical School. The clinical course was divided into two parts: the febrile stage and the polyuria stage. Symptoms such as lumbago, muscular pain, general malaise and anorexia disappeared along with a fall of fever. The incubation period of this disease was estimated to be about three weeks. Polyuria, proteinuria, gastric complication and impairment of liver function seemed to be some of clinical features of this disease. There was no HFRS patient with severe renal failure in our cases. The presence of disseminated intravascular coagulation (DIC) was confirmed in 3 of these 11 cases. Therefore, it was suggested that hemorrhagic tendency of this disease might be attributed to DIC. From our experiences, the most important factor for the treatment of the severe case was the earliest detection whether they were complicated by DIC or not. If they were suspected of DIC, it could be necessary to start treatment for DIC as soon as possible. Prophylactic measures for HFRS in our animal facility could contribute to the prevention of this disease.
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PMID:Clinical studies on hemorrhagic fever with renal syndrome found in Nagoya City University Medical School. 168 5

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

The analysis of 88 lethal outcomes of hemorrhagic fever with renal syndrome (HERS) showed the occurrence of adenohypophyseal hemorrhage and necrotic foci in 75.5% of cases as well as combined involvement of adenohypophysis and adrenals in 18.4%. Pathogenetically, adenohypophyseal affection is related to anatomical-physiological features of the vessels, microcirculatory disorders, acute venous congestion. Contributing factors may be acute DIC syndrome, relapsing and prolonged collapses, hyperhydration leading to brain edema and hemostasis. Uncontrollable vomiting recorded in all the deceased patients seemed to promote destruction of adenohypophysis. Clinically, this gross pathomorphology ++ was equivalent to severe form of the disease--hypopituitary coma. Proper prophylaxis of the above complications is one of the conditions entailing reduction of mortality in HFRS.
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PMID:[Analysis of fatal outcome in hemorrhagic fever with renal syndrome]. 198 56

Hemorrhage is a prominent feature of hemorrhagic fever with renal syndrome (HFRS) in China. It occurs in all phases of the disease and is an important cause of death. Petechiae involving skin and oropharyngeal mucosa are the commonest manifestation of hemorrhage, occurring in more than 90% of patients. Gastrointestinal hemorrhage is the next commonest manifestation, occurring in approximately 50% of patients. Suggested mechanisms of hemorrhage include vascular injury, thrombocytopenia and platelet dysfunction, disseminated intravascular coagulation, circulating heparin-like activity, and uremia. Controlled trials of treatment regimens for hemostatic impairment in HFRS have not been performed. Support of blood pressure can lessen hemorrhage by limiting the adverse consequences of hypotension and shock. Dialysis is of benefit in patients with hemorrhage and significant renal failure.
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PMID:Hemorrhage in hemorrhagic fever with renal syndrome in China. 256 78

The pathophysiology of bleeding manifestations in hemorrhagic fever with renal syndrome (HFRS) was elucidated by serially evaluating coagulation and fibrinolytic profiles and complement alterations in patients with HFRS. In the early stage of the disease, platelet counts, platelet survival time, and platelet aggregation in vitro decreased. Prolongation of bleeding time, prothrombin time, and activated partial thromboplastin time was noted, with decreases in coagulation factors II, V, VIII, IX, and X. Levels of fibrinogen were decreased, and those of fibrinogen-fibrin degradation products in serum and urine were increased. Concentrations of plasminogen, alpha 2-plasmin inhibitor, and antithrombin III in plasma were depressed. Procoagulant activity was present in plasma. Circulating immune complexes were found, whereas serum levels of C3 were decreased. In the early stage of HFRS, thrombocytopenia, defects in platelet function, and disseminated intravascular coagulation may play central roles in the pathogenesis of bleeding manifestations. Vasculopathy and immunologic aberrations also may play a role.
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PMID:Coagulopathy in hemorrhagic fever with renal syndrome (Korean hemorrhagic fever). 256 77

The clinical and laboratory characteristics of a severe form of hemorrhagic fever with renal syndrome (HFRS) in Greece are presented. Twenty-seven patients with serologically confirmed HFRS were studied; 10 required renal dialysis, six had hemorrhagic manifestations, and four died. In patients with hemorrhagic manifestations, the platelet counts were generally less than 100,000 cells/microL. In three patients findings were compatible with disseminated intravascular coagulation. Laboratory investigation showed a consistent rise in levels of serum urea nitrogen and creatinine beginning on the fifth or sixth day of illness and reaching a maximum level between the ninth and 12th days of illness. The disease in Greece more closely resembles the Asian form of HFRS (Korean hemorrhagic fever) than the Scandinavian form of the disease (nephropathia epidemica) because of the high mortality rate, the occurrence of hemorrhagic manifestations, and the severity of the clinical disease.
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PMID:Hemorrhagic fever with renal syndrome in Greece: clinical and laboratory characteristics. 256 79

Lipid peroxidation as shown by plasma levels of malonic dialdehyde and acyl hydroperoxides was studied in 92 patients with hemorrhagic fever with renal syndrome (HFRS). It was found that intensity of lipid peroxidation rose and reached maximum values in severe course of the disease. This phenomenon and causes underlying it are under discussion. Disturbances in lipid peroxidation in HFRS patients may play a role in the genesis of pathophysiological processes observed in the above patients including DIC syndrome. In addition, the authors consider prognostic relevance of the recorded shifts.
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PMID:[Significance of lipid peroxidation in the pathogenesis of hemorrhagic fever with nephrotic syndrome]. 257 91

The great majority of viral infections are not associated with significant alterations in hemostasis. Occasionally, common viral pathogens lead to illnesses in which hemostatic impairment is an important feature. In these instances, two clinical syndromes usually are present: thrombocytopenic purpura and disseminated intravascular coagulation. Immune mechanisms are implicated in the first, while the second is associated with severe disease. Hepatitis viruses produce hemorrhage by a third mechanism. In cases of fulminant hepatitis, hepatocellular injury leads to decreased production of multiple coagulation factors and impairment of other hepatic functions that modulate hemostasis. A small number of viruses stand apart by virtue of the frequency with which they cause hemorrhage. These are the hemorrhagic fever viruses. Much more needs to be learned about how these viruses cause disease and induce hemorrhage. The first line of therapy in viral infections complicated by hemorrhage is early treatment with an antiviral agent. Unfortunately, effective antiviral therapy is usually not available. There is little useful information and no controlled studies on the efficacy of therapy aimed directly at correcting hemostatic impairment.
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PMID:Viruses and hemostasis. 266 6


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