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)

A prospective analysis of the morbidity and mortality after peritoneovenous shunting was carried out in 25 patients who had a total of 27 shunts for refractory ascites. Major complications were limited to the patients in whom ascites was secondary to hepatic rather than peritoneal disease. Immediate postoperative complications followed 17 out of the 23 shunts carried out in patients with liver disease and included septicaemia (two), profound hypotension (two), pulmonary oedema (one), and clinically evident disseminated intravascular coagulation (14). Long term morbidity was again limited to the patients with liver disease and included chronic shunt infection (two) and major venous thrombosis (two). Shunt associated mortality was only seen in the patients with liver disease. Despite late shunt blockage in five long term survivors with alcoholic liver disease fluid retention was easily controlled by simple medical means probably because of improved liver function associated with abstinence from alcohol. It is concluded that: (1) patients with hepatic and malignant ascites respond differently to the insertion of a peritoneovenous shunt; (2) Shunt patency should be monitored regularly in patients with liver disease and, because of the potential for septic and thrombotic complications, if blocked the shunt should be removed and; (3) because of the morbidity and mortality of peritoneovenous shunt surgery in patients with liver disease and refractory ascites, an alternative mode of therapy, such as repeated ultrafiltration and reinfusion of ascitic fluid, may be a more effective initial therapeutic approach especially in patients in whom there is a reversible element to their underlying liver disease.
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PMID:Morbidity and mortality after peritoneovenous shunt surgery for refractory ascites. 405 6

The development of a purpura-fulminans-like disorder which is a human equivalent of a local Shwartzman reaction in a woman with active chronic hepatitis is described. The cyclical appearance of blue-black, well circumscribed, haemorrhagic, acutely painful lesions in the buttocks, over the lateral aspects of the thighs, and on the arms suggested the diagnosis. Evidence of increased intravascular coagulation was obtained although interpretation of clotting factor deficiencies in the presence of parenchymal liver disease was difficult. Treatment with heparin arrested the disorder on three separate occasions. The reasons for the development of the syndrome are not clear and even more surprising was the occurrence of such a disorder in the presence of increased fibrinolysis. While disseminated intravascular coagulation has been described in association with liver disease, the development of features of purpura fulminans in such patients does not appear to have been noted.
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PMID:Local 'Schwartzman equivalent' reaction in active chronic hepatitis. 506 Jun 68

The concentration of antithrombin III (AT) was determined with a chromogenic method in plasma samples from 1,302 patients referred for evaluation of the haemostatic system. A clearly subnormal AT level (below 60%) was found in 129 patients. In ten cases, this was explained by known (8 cases) or suspected (2 newborns) hereditary deficiency. Only in 5% of the 600 cases referred with definite or suspected thrombosis, AT was below 60%. These cases had a lethality of about 20%. In about 30% of the cases with liver disease, AT was below 60%. In a group of 72 patients with either severe infection, cardiac insufficiency, malignancy or suspected DIC for other reasons, AT was below 60%. Also in this group lethality was about 50% despite lack of a clear DIC blood profile in 67 of the 72 patients. The results indicate that an AT value below 60% of normal, unexplained by hereditary deficiency, carries a grave prognosis.
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PMID:On the clinical significance of acquired antithrombin deficiency. 608 56

To identifiy causative factors responsible for the disseminated intravascular coagulation complicating peritoneovenous (LeVeen) shunts, the ascitic fluid from 12 patients with alcoholic liver disease or peritoneal malignancy was examined for its effects on human platelets. In all patients, concentrated ascitic fluid caused irreversible platelet aggregation. Properties of the aggregating factor suggested that it is collagen, and subsequently, the presence of collagen in ascitic fluid was confirmed. This finding, together with the known effects of collagen on platelets and contact clotting factors, would be sufficient to explain the development of disseminated intravascular coagulation following this procedure. Aspirin by inhibiting collagen-induced aggregation may have a therapeutic role in the management of this problem.
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PMID:The aggregation of human platelets by ascitic fluid: a possible mechanism for disseminated intravascular coagulation complicating LeVeen shunts. 627 73

Current management of hemorrhage in cirrhotic patients is disappointing, probably because it deals only with the portal hypertension, while the coagulation disorders are neglected. Some new suggestions can be made : 1) Hemorrhage originates in coagulation disorders. The mechanical lesion of the mucosa is only the opportunity for these disorders to become apparent. The lesion may be : infrequently, a ruptured esophageal varix or a gastroduodenal peptic ulcer ; a lesion of the cardia (hiatal hernia, reflux, esophagitis, minimal traumatic tears) ; a gastric anomaly (hemorrhagic gastritis, superficial ulcerations, petechiae) ; in some cases no mucosal lesion is apparent. 2) Any widespread liver disease results in lasting hypercoagulability which is responsible for : permanent lysis, consumption, DIC. The spleen is responsible for the functional alteration of the platelets. Splenectomy is followed by permanent recovery. 3) Changes involving the platelets are responsible for most hemorrhages. Thrombopenia and severe anomalies of platelet aggregation are common findings in liver cirrhosis. Further deterioration can be induced by acetylsalicylic acid, especially if it is absorbed after an immoderate ingestion of alcohol. Emergency treatment consists in platelet transfusions. 4) Stasis in the portal system may, however, result in permanent activation of coagulation. 5) Cirrhosis results in chronic hypercoagulability and severe platelet deterioration. Any stress involving coagulation mechanisms may therefore induce hemorrhage : infection, acetyl salicylic acid, respiratory distress, estrogens, massive transfusion. It is always dangerous to "feed" consumption or to restrain lysis. 6) Coagulation tests should be performed rapidly, in order to evaluate hypercoagulability, consumption, lysis, and evidence of DIC ; FDP can probably be responsible for inflammatory changes in the liver and spleen. 8) Coagulation disorders are permanent since the hepatic alterations are irreversible.
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PMID:[Hemorrhage in liver cirrhosis : new suggestions (author's transl)]. 627 81

Antithrombin III (AT III) is a plasma protein which acts as the principal inhibitor of thrombin and is a major modulator of intravascular coagulation. Hereditary deficiency of AT III leads to recurrent episodes of thromboembolism. Acquired deficiency of AT III occurs in persons with a variety of conditions, including severe liver disease and disseminated intravascular coagulation. Replacement of AT III may be important in some deficient persons. To determine if cryoprecipitate is a useful source of AT III, we measured the AT III content of cryoprecipitate prepared from citrate phosphate dextrose blood using coagulation and fluorogenic assays and immunoassays. Using the fluorogenic assay, we also determined the effect of adding heparin to blood on the cryoprecipitation of AT III. Functional and antigenic AT III levels were similar to those of normal plasma in all citrate phosphate dextrose blood units tested, indicating that AT III is not concentrated in cryoprecipitate. Heparin had no effect on the cryoprecipitation of AT III.
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PMID:The antithrombin III content of cryoprecipitate prepared from blood collected with and without heparin. 640 59

A case of fetal demise and maternal recovery after acetaminophen overdose is presented, to our knowledge the first reported. Fetal liver and maternal serum concentrations indicate overdose to be the cause of fetal death. Maternal disseminated intravascular coagulation (DIC) may have been related to maternal acetaminophen-induced liver disease alone or to a combination of liver disease and the presence of a dead fetus.
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PMID:Acetaminophen overdose with fetal demise. 646 90

We measured levels of protein C inhibitor in patients with disseminated intravascular coagulation (DIC) and liver disease using a functional assay. Levels in 24 normal subjects averaged 93% of the amount in normal pooled plasma, giving a normal range of 65 to 121%. Levels were below normal in 8 of 17 patients with DIC, in 4 of 19 patients with liver cirrhosis, and in 3 patients with acute hepatic necrosis. Levels were normal or elevated in 9 of 10 patients with cirrhosis and accelerated fibrinolysis, and in 6 patients receiving warfarin. We conclude that protein C inhibitor may be involved in regulation of protein C activity during pathologic activation of the hemostatic system (DIC). Decreased protein C inhibitor does not appear to contribute to the pathogenesis of accelerated fibrinolysis in liver disease. The liver may be the site of synthesis of protein C inhibitor.
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PMID:Behaviour of protein C inhibitor in intravascular coagulation and liver disease. 654 88

We describe a functional assay for protein C in human plasma samples based on the ability of activated protein C to prolong the kaolin-cephalin activated partial thromboplastin time of normal plasma. Protein C is separated from its inhibitor by elution of a barium citrate precipitate, and activated by incubation with human alpha-thrombin for one hour. Thrombin is then inhibited by antithrombin III and heparin, heparin neutralized by protamine sulfate, and protein C activity measured in the partial thromboplastin time. 24 normal subjects had a mean protein C level of 94 +/- 12% (SD) of the activity in pooled normal plasma. Seven patients with severe liver disease had a mean protein C of 28%. Eleven patients with disseminated intravascular coagulation had a mean protein C of 29%. Eight patients receiving warfarin therapy had a mean protein C of 17%. The assay is relatively simple and should be suitable for general laboratory use.
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PMID:A functional assay for protein C in human plasma. 668 83

Coagulation studies were performed on 16 children with gram-negative septicemia without the complications of septic shock, liver disease, malnutrition, or laboratory evidence of classic disseminated intravascular coagulation (DIC). Ten (63%) of the 16 cases were found to have abnormal partial thromboplastin and/or prothrombin times. The coagulopathy was caused by a reduction in the vitamin K-dependent coagulation factors. The mechanism that produced this coagulopathy was not known, but evidence was found that suggested that endotoxin may interfere with the vitamin K-carboxylation reaction. The data indicated that abnormal coagulation screening test results in children with gram-negative septicemia were not specific for DIC and that a significant number of patients had a coagulopathy not related to DIC.
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PMID:Vitamin K-dependent coagulation factors in gram-negative septicemia. 670 67


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