Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Measurement of Protein S in human plasma is clinically important because of deficiency of this protein, which functions as a cofactor of the naturally occurring anticoagulant activated Protein C, is a risk factor for venous thromboembolism. We describe a two-site, enzyme-linked immunosorbent assay (ELISA) for measuring Protein S in which a monoclonal IgG directed against the calcium-independent conformation of Protein S is the capture antibody. The range of detection for the assay was 10 to 160 ng of Protein S per milliliter. The coefficients of variation were 4.6%-7.3% within-assay and 7.7%-10.1% between-assay. We compared this assay with an ELISA involving a polyclonal anti-Protein S rabbit IgG as capture antibody (I) and with Laurell's electroimmunoassay (II) to measure Protein S in plasma from 32 normal subjects and 121 patients or individuals expected to have low concentrations of total Protein S (full-term newborns, pregnant women after the 18th week of gestation, patients with disseminated intravascular coagulation or liver cirrhosis, patients receiving therapy with warfarin, and patients with congenital Protein S deficiency). In general, the results obtained with the monoclonal antibody-based ELISA correlated well with those from I (r = 0.94), less well with those from II (r = 0.86).
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PMID:A monoclonal antibody to human protein S used as the capture antibody for measuring total protein S by enzyme immunoassay. 213 55

A new screening procedure, an easy and specific assay for determining functional Protein S activity, has been developed, with use of Protein C activated by venom activator (Protac). Purified Protein C (100% amidolytic activity) was activated by venom activator (6 units/mL). To a mixture of 100 microL of Protein S-deficient plasma, 20 microL of sample plasma, 100 microL of cephalin (Actin), and 20 microL of activated Protein C we added 100 microL of 25 mmol/L CaCl2 solution and measured the clotting time with a KC 10 coagulometer. The functional Protein S activity correlated well with the concentrations of Protein S antigen measured by enzyme immunoassay and the Laurell rocket technique (r = 0.810 and 0.850, respectively) in normal subjects, patients with myocardial infarction undergoing warfarin therapy, and patients with liver cirrhosis.
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PMID:Functional activity of protein S determined with use of protein C activated by venom activator. 252 95

The activation of coagulation and fibrinolysis as well as coagulation inhibitors in the blood of patients with compensated (n = 25) and decompensated (n = 25) liver cirrhosis were studied. Protein C (PC) was decreased in a more pronounced manner than antithrombin III (AT III) in liver cirrhosis. Thereby, PC proved to be a highly sensible indicator of liver cell dysfunction. Decreased levels of PC activity (PC ratio activity/antigen 0.82) in decompensated liver cirrhosis suggest production of dysfunctional, undercarboxylated PC. We observed increased blood concentrations of fibrinopeptide A (FPA) (p less than 0.05) in both groups of patients compared to healthy volunteers (n = 25), while D-Dimer was increased only in patients with decompensated liver cirrhosis (p less than 0.01). Comparing both groups of patients. D-Dimer was significantly different with higher levels in decompensated liver cirrhosis (p less than 0.01). The ratio D-Dimer/FPA was significantly increased in decompensated liver cirrhosis compared to both other groups. These observations indicate that efflux from the extravascular space, e.g. ascitic fluid, contributes to the high contents of fibrin degradation products (D-Dimer) in patients with decompensated liver cirrhosis. In summary we conclude that patients with liver cirrhosis have enhanced activation of both coagulation and fibrinolysis but that the balance is not significantly displaced.
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PMID:[The effect of liver cirrhosis on activation of the coagulation and fibrinolysis system and on coagulation inhibitors]. 259 77

Protein C, one of the vitamin K-dependent plasma proteins synthesized in the liver, was measured immunologically in normal subjects (n = 20), patients with hepatocellular carcinoma (n = 60), liver cirrhosis (n = 60), acute hepatitis (n = 16), chronic hepatitis (n = 19), malignant neoplasms other than hepatocellular carcinoma (n = 35) and patients on warfarin treatment (n = 20). We also assayed gamma-carboxyglutamic acid-complete (carboxylated) protein C in these population by using a monoclonal antibody directed against human protein C, JTC-1, which recognizes the gamma-carboxyglutamic acid domain-related conformational change induced by metal ions. We demonstrated that the plasma of patients with hepatocellular carcinoma contains considerable amounts of gamma-carboxyglutamic acid-incomplete protein C, evidenced by the significantly reduced protein C:gamma-carboxyglutamic acid/protein C:antigen ratios in hepatocellular carcinoma as compared to those seen in normal controls, other liver diseases and other malignant neoplasms (p less than 0.01). In two patients with hepatocellular carcinoma with the reduced protein C:gamma-carboxyglutamic acid/protein C:antigen ratios, successful treatment (transcatheter hepatic arterial embolization or lipiodolization of antitumor agent) led to the very rapid normalization of the ratios. Intravenous administration of vitamin K, however, induced no such effects in three other patients with hepatocellular carcinoma with the abnormality. We conclude that the impaired vitamin K-dependent gamma-carboxylation observed in patients with hepatocellular carcinoma involves not only prothrombin, but also protein C, and that the impairment is not due to vitamin K deficiency.
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PMID:The acquired vitamin K-dependent gamma-carboxylation deficiency in hepatocellular carcinoma involves not only prothrombin, but also protein C. 283 89

Two assay methods for Protein C (PC) are described. Both tests are based on the activation of PC by a fraction of the venom of the Copperhead snake. Activated PC can be measured either by cleaving of a chromogenic substrate or by an APTT test. Both tests were compared with ELISA tests for PC. In 27 healthy persons the results were around 100% by all test systems when compared with normal pooled plasma. In 13 patients under stable anticoagulant therapy the average results were 54% for the ELISA and 52% for the chromogenic substrate test whilst the corresponding figures were 22% for the APTT test and 25% for the Quick test. In 4 cases of liver cirrhosis PC was diminished and there was no difference between the three tests. In two patients with congenital PC deficiency all results were close to 50% and in three patients the ELISA and the substrate tests were normal but the APTT test showed results of 44, 28 and 54% respectively. These results give rise to the conclusion that the snake venom activator is also capable of activation of decarboxylated PC molecules which can thereby split a chromogenic substrate but remain inactive in an APTT test.
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PMID:Protein C: comparison of different assays in normal and abnormal plasma samples. 359 Jan 7

Protein C, a naturally occurring inhibitor of blood coagulation, was measured immunologically in 160 patients with acute and chronic liver and biliary disease. In 31 patients with acute viral hepatitis serially studied from admission to discharge from hospital, protein C antigen (PC:Ag) was low on admission in a high proportion of cases (61%) but became normal in 90% of them after two weeks at a time when the prothrombin time was still prolonged in 46% of the cases. PC:Ag was also low in 25 cirrhotic patients and in 20 patients with chronic active hepatitis. In chronic hepatitis and cirrhosis, PC:Ag levels significantly correlated with indexes of liver synthetic function. In primary biliary cirrhosis (n:40), PC:Ag was low in patients with advanced disease (stages III-IV) but high in the early phases, when cholestasis was not yet accompanied by impaired protein synthesis. PC:Ag was also very high in 20 patients with large bile duct obstruction and highly correlated with indexes of cholestasis. The authors' findings indicate that PC:Ag is reduced in liver disease proportionally to the impairment of the liver synthetic function and that its normalization after acute hepatitis might represent an early marker of recovery of this function.
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PMID:The significance of protein C antigen in acute and chronic liver biliary disease. 403 76

A new solid phase enzyme-linked immunosorbent assay (ELISA) was developed for the quantitation of human protein C antigen. Anti-protein C F(ab')2 fragments were adsorbed to polystyrene plates. The binding of serial dilutions of control or test plasma, containing protein C, was detected by incubation with peroxidase-labeled anti-protein. C-IgG followed by the addition of hydrogen peroxyde and 0-phenylenediamine. This ELISA is specific, sensitive (detection limit: 0.02%) and accurate (variation coefficient: 3 to 10%). When results are compared to those obtained by the Laurell technique (electroimmunodiffusion, EID), the correlation coefficient is 0.95 in all tested plasmas. Protein C antigen was measured by ELISA and EID in plasma from 40 controls, 14 patients with congenital protein C deficiency, 15 patients with liver cirrhosis and 40 dicoumarol-treated cases. In normal plasma, protein C ranged from 70 to 126%. In congenital deficiency, protein C was between 35 and 58% in 13 cases and 9% in one of them. In patients with liver cirrhosis and dicoumarol-treated cases, levels of protein C antigen were compared to those of other vitamin K dependent factors, i.e. Factors II and IX measured by EID and Factor X assayed by EID and ELISA. In liver cirrhosis, the amount of protein C was significantly lower than that of Factors II, IX and X. In short-term and long-term dicoumarol-treated patients, the highest correlation (r = 0.72) was observed between protein C and Factor X levels. In the plasma of patients undergoing oral anticoagulant therapy, protein C decreased more rapidly than Factors X or II and migrated in presence of calcium as a double peak, one with a normal mobility and one more anodal corresponding to the non carboxylated form of protein C.
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PMID:A new method for the estimation of protein C by ELISA. 608 75

Protein C activity was determined in 70 patients with liver disease, 30 with acute viral hepatitis and 40 with liver cirrhosis. Statistical comparison of the values for patients with those for healthy Ivorians showed a significant decrease in protein C activity, positively correlated with a prolongation of the prothrombin time.
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PMID:Functional activity of protein C in liver cirrhosis and acute viral hepatitis on the Ivory Coast. 797 Dec 57

Portal vein thrombosis (PVT) is a rare disorder that is associated with a variety of underlying condition of which liver cirrhosis, malignancy and myeloproliferative disorders are the most common. It is of two types, acute and chronic portal vein thrombosis. Anticoagulation therapy is recommended for all patients with acute portal vein thrombosis. Chronic portal vein thrombosis is characterised by the development o f portal hypertension. Bleeding from ruptured varices is the main complication. In the absence of bleeding, continuous anticoagulation therapy should be considered for chronic portal vein thrombosis in whom an underlying prothrombotic factor is to be identified. Here in this report a 13-year-old girl presented with haematemesis. The spleen was hugely enlarged. Her Hb was 8.38 g/dl. Grade III oesophageal varices were found in oesophagogastroduodenostomy. CT abdomen showed portal cavernoma formation with increased splenic collateral. Protein C activity was 45% and protein S activity was 40%. She was treated with beta-blocker, endoscopic variceal ligation followed by low molecular weight heparin and warfarin.
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PMID:Chronic portal vein thrombosis due to combined deficiency of protein C and protein S. 2248 25

Vitamin K is frequently administered in cirrhotic patients to correct their coagulopathy, but evidence for such practice is lacking. We aimed to assess whether vitamin K administration increases the levels of the vitamin K-dependent factor VII (FVII), protein C, and protein S in patients with different stages of liver dysfunction. Eighty-nine patients were recruited into four groups: group 1 [hepatitis B virus (HBV) inactive carriers, n = 23]; group 2 [chronic HBV and hepatitis C virus (HCV) hepatitis, n = 21]; group 3 (cirrhosis, n = 24); group 4 (hepatocellular carcinoma, n = 21); and a healthy control group (n = 39). A single dose of 10 mg of vitamin K1 was administered subcutaneously to all patients. Prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), fibrinogen, FVII, protein C, total and free protein S, and proteins induced by vitamin K absence (PIVKA)-II (des-gamma-carboxy prothrombin) were measured at baseline and 72 h after vitamin K administration. There was progressive increment in baseline PIVKA-II, and decrements in fibrinogen, FVII, protein C, and protein S across study groups (P < 0.0001). Compared to baseline, vitamin K administration did not affect the measured parameters, whereas TT showed no reduction in any of the groups. Protein C levels declined in group 2, whereas FVII, total and free protein S did not increase in any group, for all parameters. Vitamin K therapy does not cause significant improvements in the majority of coagulation parameters and hence does not seem to be routinely indicated in patients with liver disease.
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PMID:The coagulopathy of liver disease: does vitamin K help? 2308 Mar 65


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