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)

Part I: Immunological assays of clotting factors in the diagnosis of liver diseases. The immunological determination of Antithrombin III is a good measure of the capacity of the liver to synthesize plasma proteins. Antithrombin III concentration in serum correlated significantly with the prothrombin time and the activity of cholinesterase. The immunological determination of factor VIII related antigen seems to be important for the early recognition of the transition of an acute hepatitis into a chronic course. While following uncomplicated acute hepatitis the level of factor VIII related antigen is normal after 40 weeks, it remains high in cases which become chronic. Immunological assay of factor XIII seems to be not very useful in the diagnosis of liver diseases. Part II: Management of coagulation disturbances in liver diseases. Except cases of hepatic coma the hemostatic abnormalities in chronic liver diseases are rarely severe enough that correction is necessary. Prothrombin concentrates are considered by most of the discussants as unnecessary and potentially dangerous. Transfusion of platelets is only neccessary when the platelet count is below 40.000 and surgery is planned. It is uncertain whether patients with chronical liver disease and laboratory signs of DIC benefit from heparin therapy. Although laboratory tests may be improved, prognosis, especially in cases of acute oesophageal bleeding, seems to be not changed by this treatment.
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PMID:[Summary of work session 1: Blood coagulation in gastroenterology]. 78 39

Systematic clotting studies were performed in 157 patients with de novo acute nonlymphoblastic leukemia (ANLL) prior to treatment. Sixteen patients had disseminated intravascular coagulation (DIC). Three of the patients with DIC (two with M3, one with M5 leukemia) had a marked isolated factor-X deficiency (factor X:C 21%, 33%, and 41%, respectively). Another four patients had a mild isolated factor-X deficiency (factor X:C 55%-68%). In these seven patients the remaining liver-synthesized clotting factors (factors II, VII, IX, V) as well as serum albumin and cholinesterase were within the normal range. Liver disease or vitamin-K deficiency could therefore be excluded. In none of the 141 patients without DIC was a marked isolated factor X deficiency observed; two patients had moderately reduced factor X:C levels but normal liver-synthesized proteins. Induction treatment led to the control of DIC with an almost parallel increase of fibrinogen and factor X up to normal in all patients with factor-X deficiency who achieved complete remission. In one patient, recurrence of leukemia was associated with reoccurrence of DIC and marked factor-X deficiency. We conclude that there is a coincidence of isolated factor-X deficiency and DIC in some patients with ANLL. In some patients, this factor-X deficiency may be severe enough to contribute to the bleeding tendency.
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PMID:Coincidence of acquired factor-X deficiency and disseminated intravascular coagulation in patients with acute nonlymphoblastic leukemia. 204 64

To examine the pathogenesis of thrombocytopenia associated with liver cirrhosis, the platelet count, spleen size and serum cholinesterase levels were measured together with plasma concentration of beta-thromboglobulin, fibrinopeptide A and serum albumin in 38 patients with histologically proven, severe but stable liver cirrhosis. The spleen size contributed most significantly to thrombocytopenia in this disorder and the serum cholinesterase level also correlated with the platelet count, both in decompensated and compensated liver cirrhosis. Plasma beta-thromboglobulin, serum fibrinopeptide A levels and serum albumin did not correlate with the platelet count. These findings indicate that disseminated intravascular coagulation is not likely to be the cause of thrombocytopenia in liver cirrhosis. Splenomegaly as well as the diminished protein synthetic activity of the liver participates in the pathogenesis of the thrombocytopenia in this disease.
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PMID:Thrombocytopenia in liver cirrhosis. 261 53

When compared to values recorded in the 32 healthy control subjects, plasma protein C activity was found to be significantly decreased in the 29 patients with acute leukemia and especially in those considered to be in a critical condition. On the other hand, plasma antithrombin III activity did not significantly differ from the values noted in control subjects. The concomitantly occurring high plasma fibrinogen levels and low serum cholinesterase activity were highly suggestive for a switch of hepatic protein synthesis towards the production of acute phase proteins. It is therefore considered that in the absence of a consumption coagulopathy, changes affecting plasma protein C and antithrombin III should be related to a modified pattern of hepatic protein synthesis.
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PMID:Plasma protein C and antithrombin III in patients with acute leukemia. 786 37

When compared to 32 healthy normal weight normolipidemic control subjects, plasma protein C antigen and serum cholinesterase activity were significantly decreased in 17 patients with decompensated cirrhosis of the liver and in 29 critically-ill surgical patients displaying the acute phase reaction, most of them without evidence of consumption coagulopathy. The low levels of these variables are considered to be subsequent to impaired and dysregulated hepatic protein synthesis. On the contrary, plasma protein C and serum cholinesterase were increased in 20 nephrotic patients and in 20 overweight hypertriglyceridemic subjects, a finding highly suggestive of enhanced hepatic synthesis probably related to an accelerated turnover of triglycerides. A discrepancy between low serum cholinesterase activity and normal or even high plasma protein C antigen was noted in 15 patients with cholestasis. This was particularly evident in 7 subjects with extrahepatic cholestasis and an abnormal pattern of hepatic protein synthesis or impaired clearance of plasma protein C would appear to develop in such pathological conditions.
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PMID:Clinical studies on plasma protein C. Correlation with serum cholinesterase. 829 22