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)

Dysgonic fermenter 2 (DF-2) is a slow-growing gram-negative bacillus causing a zoonotic infection that is acquired through dog bites or other contact with dogs. Splenectomized patients and those with alcoholic liver disease are most susceptible to DF-2 infection. The clinical picture can be one of fulminant septicemia and disseminated intravascular coagulation in the splenectomized patient; the presentation is milder in the alcoholic patient. The overall mortality from DF-2 septicemia among the 41 cases reported in the literature is 27%. The organism is sensitive to penicillin, resistant to aminoglycosides, and not easily grown on common media. It appears to be serum-sensitive in tests with normal human serum. Penicillin prophylaxis of dog bite wounds is especially important in high-risk patients. DF-2 infection should be considered when any splenectomized patient develops fulminant septicemia, disseminated intravascular coagulation, and peripheral gangrene. Examination of a gram stain of the peripheral blood or buffy coat is of value in such cases.
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PMID:Dysgonic fermenter 2 septicemia. 331 33

Reports in the literature on the difficulty of differential diagnosis between Disseminated Intravascular Coagulation (DIC) Pseudo-DIC and Primary Fibrinolysis (PF) in patients with liver disease, stimulated a study of various coagulation parameters (PT, PTT, Platelets, Fibrinogen, FDP) in 28 cirrhotic patients. The study confirmed reports in the literature on the high incidence of circulating FDP among liver disease patients. The vital role these play in maintaining alterations in haemostasis means that cirrhosis cases must be approached with extreme caution, avoiding any therapeutic or instrumental procedure liable to worsen the already disturbed coagulation pattern in such patients.
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PMID:[Evaluation of several parameters of coagulation in liver cirrhosis: disseminated intravascular coagulation or pseudo-disseminated intravascular coagulation?]. 336

A new practicable and precise functional protein C evaluation test is based on the activation of protein C by a snake venom activator and determination of PC activity by its property to prolong the aPTT in a clotting assay (VK = 1.9% and 4% for intra- and interassay variance respectively). In 40 healthy controls there was a good correlation (r = 0.74) between the functional and immunological (ELISA) evaluation. In 123 patients with both evaluation methods but more pronounced with the measurement of the protein C activity a significant protein C deficiency was found in the patient groups with disseminated solid tumors, inflammatory diseases and myocardial infarction. Besides detection of hereditary PC deficiency Type II (generation of functionally abnormal PC) the functional assay profits by recording PC inhibitor complexes and otherwise dysfunctional PC in DIC. Thus, in patients with hematological neoplasias, only protein C activity was significantly decreases. Decrease of PC activity was more pronounced compared to PC Ag in liver disease indicating synthesis of functionally deficient PC, and in oral anticoagulant treatment due to detection of PIVKA-PC.
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PMID:[Immunologic and functional protein C determination in various internal diseases]. 343 Oct 26

Protein C is, after activation by thrombin, a potent inhibitor of blood coagulation. An isolated deficiency of protein C increases the risk of thrombosis. The two forms of protein C deficiency, the heterozygous and the homozygous deficiency state, have different clinical features. Patients with heterozygous protein C deficiency are at a high risk to develop venous thrombosis and pulmonary embolism. In newborns with homozygous protein C deficiency with very low protein C levels (1%) a purpura fulminans like syndrome was observed. Heparin and coumarin derivatives are effective drugs in heterozygous protein C deficiency, homozygous patients may be treated either by replacement of protein C or coumarin derivatives. Decreased protein C levels were observed in various other diseases: Chronic and acute liver disease, disseminated intravascular coagulation, malignancy, postoperatively and during treatment with asparaginase. The role of protein C in these diseases to trigger thrombosis is not yet established.
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PMID:Clinical relevance of protein C. 352 11

Serious hepatotoxicity is uncommon with the proper therapeutic use of non-narcotic analgesics but experience with new non-steroidal anti-inflammatory drugs (NSAIDs) is limited. Drugs such as ibufenac, fenclofenac and benoxaprofen were withdrawn from the market because of hepatotoxicity, and liver damage has been reported on occasion with virtually all non-narcotic analgesics. However, a clear pattern of toxicity with characteristic clinical, biochemical and histopathological abnormalities has emerged with relatively few. With the exception of acute hepatic necrosis following overdosage of paracetamol, little is known of the mechanisms of liver injury induced by non-narcotic analgesics. Involvement of the liver in a generalised drug reaction does not imply specific hepatotoxicity. About 50% of patients given aspirin regularly in anti-inflammatory doses develop mild, dose-dependent reversible liver damage as shown by elevation of the plasma aminotransferase activity. Liver damage is more severe in a small minority and it may rarely be complicated by disseminated intravascular coagulation and encephalopathy with a fatal outcome. There have also been isolated reports of chronic active hepatitis associated with the use of salicylates. Salicylate hepatitis has been reported most often in young females with connective tissue diseases. Many patients with Reye's syndrome have been given aspirin during the prodromal phase, and this serious condition closely resembles subacute salicylate intoxication in children. Salicylate probably has a causal or contributory role in Reye's syndrome, but many refuse to accept this and the issue is the subject of heated debate. Paracetamol in overdosage causes acute hepatic necrosis, and liver damage has been attributed to its therapeutic use. However, most reports have involved chronic alcoholics who took excessive doses and in these patients the clinical, biochemical and pathological findings were typical of paracetamol overdosage. Many authors have failed to make the distinction between therapeutic use and a therapeutic dose. In other cases liver damage could have been caused by exposure to other agents, viral infection or naturally occurring liver disease. If these cases are excluded, there are very few reports of liver damage associated with the proper therapeutic use of paracetamol. In some cases, the picture resembled chronic active hepatitis but no causal relationship has been established between this condition and paracetamol use. Paracetamol does not cause deterioration in liver function in patients with chronic liver disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of non-narcotic analgesics on the liver. 355 80

Antithrombin III (AT III) determinations were done in healthy and sick horses using the chromogenic substrate Chromozym TH. Reference values for adult horses at 25 degrees C were 18-25 IU AT III per ml plasma and 84-118% AT III activity of normal horse plasma, respectively. Precision and accuracy were good (intra assay coefficient of variation less than 2%, accuracy 10%). Surgical operations on healthy horses led to a biphasic decrease in AT III activity touching the lower border of the reference values on the second postoperative day. Other reasons for acquired AT III deficiencies included disseminated intravascular coagulation (DIC), liver disease and glomerulonephritis. Using follow-up studies, differences in the dynamics of acquired AT III deficiency and coagulation promoting factors were demonstrated. 12 of 35 horses with decreased AT III values suffered from phlebothrombosis of the jugular veins. It was presumed that acquired AT III deficiencies promote development and progression of phlebothrombosis/thrombophlebitis in horses.
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PMID:[Antithrombin III determination in horses. Reference values and acquired antithrombin III deficiency]. 359 Jan 68

Heparin cofactor II (HC II) levels were measured by electro-immunoassay in healthy volunteers, and patients with liver disease, DIC, proteinuria or a history of venous thrombosis. Analysis of the data in 107 healthy volunteers revealed that plasma HC II increases with age (at least between 20 and 50 years). HC II was found to be decreased in most patients with liver disease (mean value: 43%) and only in some patients with DIC. Elevated levels were found in patients with proteinuria (mean value 145%). In 277 patients with a history of unexplained venous thrombosis three patients were identified with a HC II below the lower limit of the normal range (60%). Family studies demonstrated hereditary HC II deficiency in two cases. Among the 9 heterozygotes for HC II deficiency only one patient had a well documented history of unexplained thrombosis. Therefore the question was raised whether heterozygotes for HC II deficiency can also be found among healthy volunteers. When defining a group of individuals suspected of HC II deficiency as those who have a 90% probability that their plasma HC II is below the 95% tolerance limits of the normal distribution in the relevant age group, 2 suspected HC II deficiencies were identified among the healthy volunteers. In one case the hereditary nature of the defect could be established. It is concluded that hereditary HC II deficiency is as prevalent among healthy volunteers as in patients with thrombotic disease. Further it is unlikely that heterozygosity for HC II deficiency in itself is a risk factor for the development of venous thrombosis.
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PMID:Hereditary heparin cofactor II deficiency and the risk of development of thrombosis. 360 11

An enzyme-linked immunosorbent assay (ELISA) for measuring human protein C by using two monoclonal antibodies directed toward the heavy chain of protein C is reported. This assay enabled the determination of protein C in concentrations of 10 to 400 ng/ml in less than 3 hours with a single antigen-antibody reaction. Within-run and between-run coefficients of variation were less than 8%. The mean concentrations of protein C in plasma of 42 normal subjects, 24 patients with liver disease, 27 with DIC, 48 with warfarin therapy and 15 with congenital protein C deficiency, were 4.2, 3.0, 2.3, 2.1 and 1.9 micrograms/ml, respectively. The results obtained with the present ELISA correlated well with those of radioimmunoassay (r = 0.935, n = 81) as well as those of Laurell's Rocket method (r = 0.910, n = 81) by using rabbit anti-human protein C serum. The present method was sensitive and specific for measurement of protein C and also PIVKA-protein C in plasma.
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PMID:Enzyme immunoassay of human protein C by using monoclonal antibodies. 389 62

An outline has been given of the major abnormalities of coagulation which can occur secondary to diseases in previously normal individuals. First, the disorders due to deficiency of the vitamin K-dependent clotting factors are described. Vitamin K deficiency can occur in the newborn, or at later stages in life when there is intestinal malabsorption. The malabsorption disorders, such as coeliac disease, together with major abdominal surgery or prolonged use of broad-spectrum antibiotics can give rise to vitamin K deficiency. Additionally, in obstructive jaundice the lack of secretion of bile salts into the upper intestine causes vitamin K malabsorption. The use of oral anticoagulants is associated with haemorrhage in a small proportion of patients. These patients usually have an excessively prolonged prothrombin time, due to overdosage with anticoagulants, but occasionally haemorrhage can occur from a localized bleeding site, such as a duodenal ulcer, in patients under good anticoagulant control. The large number of drugs which can interact with anticoagulants are listed, from which it can be seen that careful monitoring of all patients on oral anticoagulants must be carried out. The haemostatic defects associated with liver disease are then tabulated. In this situation abnormalities may be due to deficient synthesis of coagulation factors in hepatocellular failure, by failure of vitamin K absorption, and also by disseminated intravascular coagulation (DIC). DIC occurs in hepatocellular failure, because the liver cells are normally responsible for clearing activated products of the coagulation and fibrinolytic enzyme systems. The presence of clinical haemorrhage and haemostatic breakdown in hepatic disease usually indicates a serious prognosis, but appropriate replacement therapy is indicated in this situation. Disseminated intravascular coagulation embraces a large number of clinical haemorrhagic syndromes, where intravascular activation of the coagulation system takes place accompanied by compensatory fibrinolytic activity. DIC can be initiated by intravascular release of procoagulant substances, such as tissue thromboplastin, or by damage to vascular endothelium and platelets. The main clinical conditions associated with DIC comprise the severe infections and septicaemias, obstetric accidents, shock and trauma, neoplasia and snake-bite envenoming. In all instances, the pathophysiological disorder of haemostasis is managed by treating the underlying disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acquired coagulation disorders. 389 41

The authors assessed the diagnostic value of the plasma anti-thrombin III (AT III) assay in 112 adult hospitalized patients with abnormal hemostatic parameters, using the Protopath procedure. In 100 patients tested only once, low AT III was observed in 25 of 29 cases of acute disseminated intravascular coagulation (DIC); 7 of 10 with infections; 8 of 11 with acute liver disease; 19 of 20 with chronic liver disease; and 16 of 30 with other illnesses. The authors conclude that the assay cannot distinguish among disease categories, although it is a sensitive index of DIC. AT III was also repeatedly measured at various time intervals in 12 additional patients. The results suggest enhancement of the diagnostic and prognostic value of the assay with serial testing.
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PMID:Fluorometric assay of antithrombin III. Diagnostic value in 112 patients with abnormal hemostasis. 402 21


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