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)

We describe the simple and rapid enzyme immunoassay of protein C in human plasma with use of a Cobas Fara centrifugal analyzer. The antibody, labeled with horseradish peroxidase, is reacted with antigen (protein C) for 15 min. The peroxidase activity of the resulting antigen-antibody conjugate is measured at 500 nm for 5 min in the presence of excess H2O2, phenol, and 4-aminoantipyrine, as compared with that of free conjugates. Results are calculated from a stored standard curve and expressed as a percentage of the value determined for a pooled specimen of normal adult plasma. The standard curve is linear from 0% to 200%. The CV is generally less than 4% for different concentrations of protein C. In liver cirrhosis, hepatocellular carcinoma, therapy with warfarin, thrombosis, and disseminated intravascular coagulation, protein C concentrations are about 40-70% of normal. Results obtained with the present homogeneous enzyme immunoassay correlated well with those by enzyme-labeled immunosorbent assay (r = 0.97).
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PMID:Protein C in human plasma determined by homogeneous enzyme immunoassay with use of a centrifugal analyzer. 304 78

This rapid, simple amidolytic assay of protein C activity in whole plasma involves activation by protein C activator from the venom of Agkistrodon contortrix contortrix (Protac) and use of a Cobas Fara spectrophotometer programmed for kinetic assay. Plasma is incubated with activator venom in the presence or absence of antibody to human protein C in the instrument, chromogenic substrate (S-2366) is added, and the absorbance is measured at 405 nm. The difference between the absorbance of the sample plasma with and without antibody to human protein C correlated well with protein C antigen as assayed by enzyme-linked immunosorbent assay (ELISA) and the Laurell rocket technique in normal subjects, patients being treated with warfarin, and patients with liver cirrhosis or disseminated intravascular coagulation. Our mean value for protein C in normal subjects is 115.9 (SD 16.7)% for amidolytic activity, 103.0 (SD 17.4)% for ELISA, and 97.2 (SD 18.1)% for the rocket technique. The high value for normal subjects presumably includes some nonspecific amidolytic activity activated by the activator venom, as indicated by measurable activity in immuno-depleted protein C-deficient plasma. Within-run and between-run CVs were less than 5% at low, normal, and high concentrations of protein C amidolytic activity.
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PMID:Amidolytic kinetic assay of protein C by selective spectrophotometry in a centrifugal analyzer. 318 Apr 21

Using a new rapid coagulant method, protein C activity (PC act) was determined in liver cirrhosis and malignancies and compared with PC antigen and AT III values. PC was decreased in a more pronounced manner than AT III in liver cirrhosis, mainly due to impaired synthesis. This is of special clinical interest because PC proved to be a high sensible indicator of liver cell dysfunction. Decreased levels of PC act (PC ratio act/ag less than 1) in decompensated liver cirrhosis may be caused by the synthesis of dysfunctional PC and/or vitamin K deficiency with production of undercarboxylated PC most sensitively registered by this coagulant assay. An increased clearance of in vivo activated PC induced by DIC may play an insignificant role. In patients with liver metastases, PC act (but not AT III and immunological parameters) was significantly reduced, supporting the conclusion that in these patients liver dysfunction concomitant with synthesis of dysfunctional PC must be discussed as the main cause of this alteration.
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PMID:Immunological and functional determination of the protease inhibitors, protein C and antithrombin III, in liver cirrhosis and in neoplasia. 320 4

Protein C and protein S serve as natural anticoagulants. Deficiencies of these proteins are often associated with recurrent deep vein thrombosis and coumarin induced skin necrosis. These two proteins function by selectively inactivating factors Va and VIIIa, two of the "cofactors" of blood coagulation. Hence, inhibition of coagulation by this pathway complements the better known inhibition mediated by the antithrombin III-heparin system. These observations suggest that protein C and/or activated protein C may prove useful in controlling thrombosis and/or DIC. We have developed a Ca2+ dependent monoclonal antibody which allows the rapid isolation of human protein C. This rapid isolation has allowed us to demonstrate that activated protein C can protect baboons from the lethal effects of E. coli/endotoxin and that protein C supplementation can minimize fibrinogen consumption following tissue factor infusion into dogs.
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PMID:Protein C, isolation and potential use in prevention of thrombosis. 330 68

In eighteen patients with fulminant hepatic failure (FHF), in grade III or IV coma, both protein C antigen and activity were significantly decreased (0.35 +/- 0.03 u/ml and 0.35 +/- 0.03 u/ml respectively). There was a significant correlation between protein C antigen and activity (r = 0.61, p less than 0.01). Protein C antigen levels were inversely correlated with prothrombin time (r = -0.57, p less than 0.05) as were protein C activity levels (r = -0.57, p less than 0.05). There was also significant correlations between fibrinogen and protein C antigen (r = 0.69, p less than 0.01) and protein C activity (r = 0.61, p less than 0.01). These results demonstrate that the naturally occurring inhibitor of coagulation, protein C, is present at low levels in FHF and this is probably due to the lack of synthesis of the protein in the damaged liver. The low levels of protein C may make these patients more susceptible to the disseminated intravascular coagulation which is known to occur in FHF and this in turn will lead to a further reduction in protein C levels.
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PMID:The effect of fulminant hepatic failure on protein C antigen and activity. 338

Hemostatic abnormalities are common in patients with metastatic malignancy and are attributed, in part, to materials secreted by tumor cells. Tumor stimulation might therefore cause further perturbation of hemostasis. This article reports observations on the effects of androgen stimulation on multiple hemostatic parameters in patients with metastatic prostate cancer. Testosterone was given before chemotherapy in an experimental protocol designed to increase tumor sensitivity to cytotoxic agents. The following parameters were measured on day 0 (before) and days 2 and 4 of fluoxymesterone administration: PT, APTT, platelet count, plasma betathromboglobulin (BTG), platelet factor 4 (PF4), fibrinogen, fibrin(ogen) split products (FSP), factor VIII coagulant activity (VIII C), von Willebrand factor antigen (vWF Ag), fibrinopeptide A (FPA), antithrombin III (AT III), and protein C antigen (PC). Ten patients were studied during 17 cycles of hormonal stimulation. Baseline levels of BTG, PF4, fibrinogen, FSP, factor VIII C, vWF Ag, and FPA were significantly elevated compared with normal control. Although androgen stimulation resulted in elevation of BTG, FPA, and FSP levels by day 4 in many patients, the changes for the entire group were not statistically significant. Other parameters remained unchanged or were only slightly elevated. Two patients developed laboratory evidence of disseminated intravascular coagulation (DIC) but were clinically unaffected. Our data suggest that most patients with metastatic prostate cancer show evidence of ongoing activation of platelets, coagulation, and fibrinolysis. In a few individual patients, androgen stimulation of this hormonally dependent tumor may cause further activation of platelets, coagulation, and fibrinolysis.
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PMID:Hemostatic effects of hormonal stimulation in patients with metastatic prostate cancer. 340 35

Both anticoagulant and amidolytic activities of protein C (PC) were measured using a snake venom activator in 4 patients with hereditary PC deficiency, 37 with disseminated intravascular coagulation (DIC), and 30 under stabilized warfarin therapy. The results were compared with those obtained by an immunological assay (ELISA). PC levels measured by different functional and immunological assays were very close in patients with hereditary PC deficiency and DIC. In patients under stable oral anticoagulant therapy, there was no detectable difference between amidolytic activity and antigen levels of PC in each patient plasma, whereas a decrease in anticoagulant activity was much more pronounced. These results indicate that the present activity assays measure PC specifically, and that the snake venom activator is capable of activating both carboxylated and hypocarboxylated forms of PC, but only anticoagulant assay can evaluate the physiological PC function in vitamin K-deficient states.
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PMID:Fast functional assay of protein C in whole plasma using a snake venom activator: evaluation in patients with congenital and acquired protein C deficiencies. 341 83

Defiency of protein C has been reported to be associated with recurrent thrombosis and pulmonary embolism, disseminated intravascular coagulation, and coumarin-induced skin necrosis and peripheral gangrene. That all of these serious and eventually lethal complications of protein C deficiency, including embolic myocardial infarction, may occur in the same person is the subject of this case report and description of pathological findings.
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PMID:Recurrent thromboembolism, disseminated intravascular coagulation, and coumarin-induced skin necrosis associated with protein C deficiency. 342 32

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 a natural vitamin K-dependent plasma anticoagulant, deficiencies of which have been found in patients with recurrent thrombosis and warfarin-induced skin necrosis. To appreciate more fully the role of protein C in disease states and during oral anticoagulation, a new functional assay for protein C involving adsorption of plasma protein C on a Ca+2-dependent monoclonal antibody, elution, quantitative activation, and assessment of plasma anticoagulant activity, has been developed. When oral anticoagulation is initiated, the anticoagulant activity of protein C decreases to a greater extent than either the amidolytic or immunologic levels. During stabilized warfarin treatment, there is no correlation between either amidolytic or antigenic levels and the functional protein C activity, suggesting that measurement of protein C anticoagulant activity may be necessary to reflect adequately the anticoagulant protection afforded by this protein. In contrast, there was a strong correlation between anticoagulant and amidolytic and immunologic levels in liver failure and disseminated intravascular coagulation. Two patients with thromboembolic disease have been identified who exhibit a marked decrease in anticoagulant activity, but who have normal immunologic and amidolytic levels. Thus, this assay permits assessment of protein C in individuals who have received anticoagulant treatment and identification of a new class of protein C-deficient individuals.
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PMID:Relationship between protein C antigen and anticoagulant activity during oral anticoagulation and in selected disease states. 351 Oct 97


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