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)

A radioimmunoassay (RIA) had been developed for the determination of antithrombin III (AT III) in man. The detection limit was 25 microgram/dl. AT III-RIA level and biological activity (anti-Xa) was significantly correlated (r = 0.737, P less than 0.001). Plasma levels in 36 healthy males (mean +/- SD, 19.9 +/- 2.5 mg/dl) and 21 healthy females (19.1 +/- 2.4 mg/dl) were similar. Serial AT III measurements in normal menstruating females showed lower levels during midcycle and higher concentrations during menstruation. In carcinomas, the AT III levels were lower than normal, particularly in hepatocellular carcinoma. In cirrhosis of liver, the levels were markedly decreased and in some patients were below that found in congenital AT III deficiency. Patients with deep vein thrombosis and patients with heart valve replacement had lower levels than normal, while patients with cerebral vascular occlusion had normal levels. The possible use of AT III as a diagnostic tool of post-operative deep vein thrombosis was demonstrated in one patient after hysterectomy. The increased sensitivity, specificity and precision of this type of assay offer distinct advantages over existing methods of AT III estimation.
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PMID:The determination of antithrombin III by radioimmunoassay and its clinical application. 43 3

New plasma assays for fibrin(ogen) degradation products have become available which are based upon monoclonal antibodies and can be performed in plasma. In this study we have evaluated four of such specific enzyme immuno assays i.e.: for the total of degradation products of fibrin and of fibrinogen (TDP), fibrin degradation products (D-dimer and FbDP) and fibrinogen degradation products (FgDP) in patients suspected of having deep venous thrombosis of the leg (DVT) and patients with cirrhosis of the liver. DVT was assessed by impedance plethysmography (IPG). In each of the (sub) groups of patients, a very good correlation (0.90 less than r less than 0.98) was observed between the actually measured TDP values and the calculated sum of the separately measured FbDP and FgDP levels. Only 2% (5 patients) of the cases showed a discrepancy of more than a factor two between the found TDP values and the calculated sum of the measured FbDP and FgDP levels. About 90% of the fibrin degradation products were crosslinked. FbDP levels correlated well with the FgDP levels (0.72 less than r less than 0.94) and D-dimer levels (0.82 less than r less than 0.91) in both patients with DVT and cirrhotics. In those patients also a good correlation (0.67 less than r less than 0.83) was observed between FgDP and D-dimer levels, but not in patients suspected of having DVT but with a normal IPG test result. Secondary fibrinolysis appeared to be accompanied by fibrinogenolysis.
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PMID:Correlations between plasma levels of fibrin(ogen) derivatives as quantified by different assays based on monoclonal antibodies. 195 61

Sixteen patients with mesenteric venous thrombosis were reviewed retrospectively during a period from 1983 to 1987. Twelve patients had progressive abdominal pain, three had gastrointestinal bleeding, and one had general malaise. Seven of these 16 patients had previous deep-vein thrombosis. After negative routine gastrointestinal and hepatobiliary evaluation, 11 patients underwent an infusion computerized tomographic scan. Of these, 10 had superior mesenteric vein thrombosis; three of these 10 patients had portal vein thrombosis. Selective arteriography was done in two patients because of gastrointestinal bleeding, and a diagnosis of mesenteric vein thrombosis was made on the venous phase of the examination. The remaining four patients developed acute abdominal symptoms requiring surgical exploration, at which time mesenteric venous thrombosis was discovered. An identifiable coagulopathy was detected in nine patients (protein C deficiency in six, protein S deficiency in two, and factor IX deficiency treated with factor IX concentrate in one). No case of congenital antithrombin-III deficiency was identified. Six of these nine patients had a past history of deep venous thrombosis. Of five patients who underwent surgical exploration, all required bowel resection. In follow-up, two patients died of intestinal necrosis and a third died of associated pancreatic cancer. Thirteen patients were discharged from the hospital. Treatment of coagulopathy was by heparin in three patients and sodium warfarin (Coumadin) in four patients. Long-term anticoagulation was not instituted because of gastrointestinal bleeding in three and cirrhosis in three patients. Mesenteric venous thrombosis can occur without gangrenous bowel. Diagnosis should be suspected when acute abdominal symptoms develop in patients with prior thrombotic episodes and a coagulopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mesenteric venous thrombosis. 172 86

A simple assay method of heparin cofactor II (HC II) activity is described. The procedure is based on the following principle: Antithrombin III (AT III) in plasma is inactivated by addition of an IgG fraction of goat serum after immunization of the animals against human AT III. Complete inactivation of AT III could be shown by absence of an anti Xa-effect of heparinized plasma treated with this antibody. Thrombin was only partially inhibited after inactivation of AT III. The characteristics of this inhibition were typical for the action of HC II. This method was applied for an assay of HC II activity. After optimizing of the method practical application in clinical routine screening was carried out. A diminution of HC II was observed in liver cirrhosis and in DIC but not in AT III deficiency. In 15 out of 269 cases of recurrent DVT there were HC II activities below 70% of normal. In 4 out of these patients activities of HC II were repeatedly between 44% and 52%. In arterial obstructive disease there was an HC II activity of less than 60% in 18 out of 583 patients and in 11 of them the HC II levels were repeatedly between 45% and 54%.
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PMID:Heparin cofactor II: a simple assay method and results of its clinical application. 342 87

In Japan, the various hemostatic medicines have been used after operation. On the contrary, in Europe and U.S.A., the anticoagulants are used both before and after operation because of the high incidence of postoperative deep vein thrombosis. We made inquiries about how they have been used to 566 main surgical clinics in Japan. In the half of these surgical facilities, these medicines still have been used routinely. But in 16.9% of surgery, 9.5% of obstetric & gynecological operation and 29.4% of orthopedic surgery, they have never been used at all. In the field of surgery, in 42% of cardiovascular, 32.1% of respiratory and 10.8% of general surgery, they have not been used absolutely. For the patients with liver cirrhosis, obstructive jaundice and the patients who received the massive blood transfusion during operation, more than 80% of facilities have used the hemostatic medicines. After operation, the blood becomes hypercoagulable and tends to form thrombosis, because of increasing coagulability, decreasing AT-III and protein C, hyper-function of platelet, hypofibrinolytic state and high viscosity. Especially cancer patients have the high risk of deep vein thrombosis. Also we investigated the difference of the incidence of the hemorrhagic complications after operation between in the hemostatic drug group and no drug one. No significant difference was observed. It is concluded that the use of hemostatic medicines after operation is not recommended.
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PMID:[Is it necessary to administer hemostatic medicines after surgical operation? The results of questionnaires about the use of hemostatic medicines in Japan]. 380 75

An assay measuring the thrombin inactivating effect of human plasma in the presence of dermatan sulfate (DS) is described. Test plasma, diluted 1/50, is incubated with human thrombin in the presence of DS. Remaining thrombin is determined with chromogenic substrate 2AcOH . H-D-CHG-Ala-Arg-pNA. Three dilutions of reference plasma suffice and the standard curve is linear. Antithrombin III (AT) exerts a small (3-8%) effect in the assay. When test plasma contains heparin above 0.05 U/ml, this unspecific effect of AT increases, but it may be abolished by antibodies against AT. In a normal material (n = 50), the SD of DS cofactor activity was greater (15%) than that of AT (8.7%). DS cofactor was normal in hereditary AT deficiency and in 15 patients with deep venous thrombosis. In liver cirrhosis and in DIC, both inhibitors were markedly depressed, to similar degrees (r = 0.84).
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PMID:Assay of dermatan sulfate cofactor (heparin cofactor II) activity in human plasma. 654 86

In three different disease entities associated with acquired antithrombin III (AT III) deficiency some of the pathogenetic mechanisms were studied. In liver cirrhosis (23 patients) the AT III level was closely correlated to the activity of hepatocellular synthesized clotting factors, indicating decreased AT III synthesis. In glomerular proteinuria (20 patients not on steroid therapy) the plasma level of AT III correlated inversely to the renal AT III clearance. In contrast to liver cirrhosis and proteinuria, in septicaemia (33 patients) the ratio between AT III antigen (radial immunodiffusion) and functional AT III (heparin cofactor assay using a chromogenic substrate) demonstrated an excess of AT III antigen probably due to inactive AT III-enzyme complexes. Therefore consumption of AT III appears to be an important cause of AT III deficiency in septicaemia. There was an inverse correlation between this ratio and the plasma AT III activity. It is well documented that congenital AT III deficiency predisposes to deep venous thrombosis (DVT) and sometimes to disseminated intravascular coagulation. A similar clinical relevance may be assumed for an acquired AT III deficiency, though so far a relationship between AT III deficiency and DVT has been only established in the nephrotic syndrome.
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PMID:[Pathogenetic mechanism and clinical relevance of acquired anti-thrombin III deficiency in internal medicine (author's transl)]. 702 26

The plasma Lp(a) concentrations were evaluated in several groups of patients. Groups with liver cirrhosis (n = 20), type-1 diabetes mellitus (n = 148), type-2 diabetes mellitus (n = 65), hypertension (n = 51), lung cancer (n = 48) and deep venous thrombosis (n = 31) were compared with a group of healthy volunteers (n = 69). Significantly higher median values were found in the hypertension (142 mgl-1 vs. 43 mgl-1, p < 0.001) and lung cancer groups (241 mgl-1 vs. 43 mgl-1; p < 0.0001). Significantly lower values were recorded in the group with liver cirrhosis (11 mgl-1 vs. 43 mgl-1; p = 0.02). But in this last group there were significant differences between patients in the Child-Turcotte severity stages A to C.
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PMID:The behaviour of lipoprotein(a) in patients with various diseases. 786 33

We previously studied fibrinolysis and fibrinogenolysis by analyzing fragments of fibrin/fibrinogen degradation products (FDP) employing sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting. In this report, we characterized the fragments of FDP in three patients with increased serum FDP, that were caused by various diseases. In the patient suffering from tuberculous constrictive pericarditis (case 1), the most part of the FDP fragments were DD and D. In the patient suffering from infection in addition to liver cirrhosis (case 2), the most part of the FDP fragments were high molecular weight (HMW) and D. In case 1 and 2, serum FDP levels were increased in parallel with the elevations of CRP levels. Although DD and HMW fragments were remarkably increased in case 1 and 2 with our immunoblotting analysis, DD levels assayed with LPIA system were much lower than FDP levels. The reason this discrepancy was explained by the observation that affinities of the monoclonal antibody used in LPIA system with DD and HMW fragment were markedly lower than that to DD-E fragment. In the patient suffering from deep vein thrombosis probably caused by steroid therapy of nephrotic syndrome (case 3), the most part of detected FDP fragments were DD and HMW in the period when APTT was shorter than normal, whereas D was mainly observed in the period when APTT was normal. In case 3, FDP and DD levels were increased in parallel with the shortening of APTT. In these non-DIC patients, increased serum FDP levels were induced by the presence of ascites and/or pleural effusion plus infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Studies on the fragments of FDP in 3 non-DIC patients with increased FDP levels in the sera]. 836 Oct 25

Ninety-seven patients undergoing elective liver resection through a subcostal incision were assigned to large-dose aprotinin treatment or placebo in a double-blind, prospective, randomized fashion. Randomization was stratified by diagnosis: (a) cancer in cirrhosis, (b) cancer in healthy liver, and (c) benign tumor in healthy liver. Intraoperative blood loss, percentage of transfused patients, and total transfusion requirement per group were significantly lower in the aprotinin group than in the placebo group (1217 +/- 966 mL vs 1653 +/- 1221 mL, P = 0.048; 17% vs 39%, P = 0.02; 30 vs 77 red blood cell packs, P = 0.015, respectively). Assessment of hematological markers (a) prior to surgery, (b) at the end of surgery, and (c) 24 h after surgery showed an identical intraoperative increase in thrombin-antithrombin III complexes in patients of both groups (P = 0.86), which indicates a similar activation of coagulation. Intraoperative hyperfibrinolysis was significantly less pronounced in the aprotinin group than in the placebo group (P = 0.0002 and P = 0.004 for D-dimers and fibrinogen, respectively). No adverse drug effects were detected (circulatory disturbances, deep venous thrombosis, increase in serum creatinine). These results suggest that aprotinin significantly reduces blood loss and transfusion requirement in patients undergoing elective liver resection through a subcostal incision.
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PMID:Aprotinin reduces blood loss in patients undergoing elective liver resection. 908 74


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