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

We measured plasma heparin cofactor II (HC II) activity in patients with disseminated intravascular coagulation (DIC) due to various underlying diseases together with the levels of antithrombin III (AT III), pseudocholinesterase (a marker of hepatic synthesis), and various haemostatic molecular markers. Both HC II and AT III were decreased in DIC secondary to all the underlying diseases studied, except acute promyelocytic leukemia (APL), when compared with healthy subjects. The lowest HC II and AT III levels was observed in coagulopathy secondary to liver disease, the HC II level in sepsis was the second lowest. In DIC due to APL, the decrease in HC II was not accompanied by a decrease in AT III. Thus, we divided all 124 samples tested into APL and non-APL groups. The HC II level correlated positively with fibrinogen and plasminogen in both the APL and non-APL groups. In the APL group, the HC II level had a significant negative correlation with the thrombin-AT III complex (TAT), fibrinogen/fibrin degradation products, and D-dimer levels as well as the prothrombin time, while AT III showed no correlations with any of the haemostatic parameters. These results suggest that HC II may be consumed preferentially by thrombin in APL patients with DIC, and thus may spare the consumption of AT III. Accordingly, HC II seems to be a superior indicator of DIC than AT III in APL patients. Moreover, replacement therapy with HC II instead of AT III may be useful to treat DIC associated with APL. In the non-APL group, the HC II levels were positively correlated with the levels of AT III and pseudocholinesterase activity. This indicates that plasma HC II levels are closely related not only to consumption coagulopathy but also to hepatic synthetic activity, as is the case for plasma AT III.
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PMID:Preferential consumption of heparin cofactor II in disseminated intravascular coagulation associated with acute promyelocytic leukemia. 141 8

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

Protein C was measured by means of enzyme-linked immunosorbent assay (ELISA) in plasmas from 58 normal subjects, 39 patients with disseminated intravascular coagulation (DIC) and 5 patients with thrombotic thrombocytopenic purpura (TTP). Protein C levels ranged from 69.7 to 163.6% (95% confidence limits) in normal subjects. In patients with DIC, protein C concentrations were significantly decreased, with a geometric mean value of 42.1%. Protein C concentration was positively correlated with plasma prothrombin, antithrombin III and serum pseudocholinesterase, and was negatively correlated with von Willebrand factor antigen (vWF:Ag) and vWF:Ag/factor VIII ratio. These findings suggest that low protein C concentrations in DIC mean a consumption of protein C probably due to its activation by thrombin and/or impaired liver synthetic function. In patients with TTP, protein C levels were normal with a geometric mean value of 116.7%, indicating that the pathophysiology of TTP is quite different from that of DIC.
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PMID:Protein C levels in disseminated intravascular coagulation and thrombotic thrombocytopenic purpura: its correlation with other coagulation parameters. 384 Dec 32

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

We investigated whether depressed plasma antithrombin and protein C activity, considered as a specific finding of disseminated intravascular coagulation (DIC), is due to consumption coagulopathy in septic patients with DIC. An analysis of hemostatic parameters was performed in 139 septic patients (68 with DIC and 71 without DIC). Plasma activity of antithrombin and protein C tended to be significantly decreased in septic patients with DIC but not in those without DIC (p < 0.001). However, when the septic patients were classified into three groups according to the albumin (or choline esterase) level, no significant differences in antithrombin activity or protein C activity were observed between the patients with and without DIC in any of the subgroups. Notably, neither the plasma activity of antithrombin nor protein C was decreased even in septic patients with DIC who had normal plasma levels of albumin (or choline esterase). No significant correlation was observed between plasma levels of thrombin-antithrombin complex (TAT) and antithrombin activity, or between plasma levels of TAT and protein C activity either in septic patients with DIC or without DIC. It is reasonable to conclude that the markedly reduced plasma activity of antithrombin and protein C is not due to consumption coagulopathy in septic patients with DIC.
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PMID:Decreased plasma activity of antithrombin or protein C is not due to consumption coagulopathy in septic patients with disseminated intravascular coagulation. 1173 50

The present study analyzed the incidence and clinical features of disseminated intravascular coagulation (DIC) developed in association with non-Hodgkin lymphoma (NHL). Two hundred thirty-six patients with newly diagnosed NHL were admitted to our institute since Jul. 2008 to Dec. 2014. Coagulation markers were evaluated in 161 of 236 patients at the time of diagnosis. DIC was diagnosed in 18 patients (11.2 %) based on the criteria established by Ministry of Health, Labor, and Welfare of Japan. All of the 18 patients had Ann-Arbor Stage IV advanced disease, and 17 patients were in poor performance status. Liver function panels, such as bilirubin, aminotransferases, serum choline esterase, and albumin levels, were worse in patients with DIC than those without DIC, indicating impaired production of coagulation factors. Importantly, DIC exerts significantly negative impact on prognosis of NHL; median survival of both groups was 176 versus 2430 days. The difference remains significant after statistically adjusting for age, performance status, Ann-Arbor stage, international prognostic index, and liver function panels. Nine of 18 patients with DIC received anti-coagulants, which failed to improve clinical outcome. Nevertheless, early recognition and intervention to DIC state may contribute to improve prognosis of NHL.
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PMID:Disseminated intravascular coagulation in non-Hodgkin lymphoma. 2627 5