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)

In experimental animals endotoxin administration causes increased levels of thromboxane B2 and prostaglandins. Liver cirrhosis is often complicated by endotoxemia. In sixteen patients with alcoholic liver cirrhosis, we measured plasma thromboxane B2 levels. In twelve patients we found on one or more occasions raised plasma thromboxane B2 levels. Raised plasma thromboxane B2 levels were associated with significantly higher serum levels of urea, alkaline phosphatase, gamma glutamyl transpeptidase and lower antiplasmin and antithrombin III levels. It is possible that some of the complications in patients with alcoholic liver cirrhosis are mediated by thromboxanes.
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PMID:Raised plasma thromboxane B2 levels in alcoholic liver disease. 657 82

A simplified method for the assay of antithrombin III (AT) with the highly reactive thrombin substrate 2AcOH X H-D-CHG-Ala-Arg-pNA (substrate Th-1) is described. The assay may be performed at either 30 degrees C or 37 degrees C, and alternatively with the substrate H-D-Phe-Pip-Arg-pNA (S-2238). The standard curve is linear in the 12.5-150% range. For routine assays, 3 standard dilutions of plasma are sufficient, and these may be stored at -20 degrees C for 3 weeks. As only the test plasma must be diluted prior to the assay procedure, the test is more rapidly performed than previous manual assays. In 80 patients plasma samples, with AT in the 19-108% range, there was a high correlation with the results of immunoquantification (r = 0.96). There was also a high correlation between the results obtained with the manual method and the automated version described using the Cobas-Bio Centrifugal Analyser and substrate Th-1 (r = 0.96). Low AT levels in hereditary deficiency (particularly during heparin treatment), in liver cirrhosis, in disseminated intravascular coagulation (DIC), and heparin-treated thrombosis were confirmed.
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PMID:Simplified assay for antithrombin III activity using chromogenic peptide substrate. Manual and automated method. 664 56

Liver diseases are associated with complex haemostasis defects, in which platelets, coagulation, and fibrinolysis may all be affected. The low plasma concentrations of clotting factors often found can be the result of many changes such as impaired synthesis, increased catabolism due to intravascular coagulation, or alternate distribution. In this study, we investigated the metabolism of purified human antithrombin III(AT III) labelled with 125I in 25 patients with histologically established liver disease and in nine control subjects. The results showed that, in general, low plasma concentrations of AT III in liver cirrhosis are not due to consumption in the central compartment but rather to altered transcapillary flux ratio. Such altered transcapillary flux ratios may already exist even with normal plasma AT III concentrations. Altered ratios are not only found for coagulation proteins but also for albumin and thus may be a general phenomenon of liver disease. In micronodular cirrhosis the alpha phase, the transcapillary efflux (k1, 2) and influx (k2, 1) were significantly increased compared with the normal subjects.
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PMID:Antithrombin III metabolism in patients with liver disease. 672

Twenty eight patients affected by liver cirrhosis were studied in comparison with 44 control subjects, matched for age. The following parameters were carried out: a) platelet aggregation (by Born's method) induced by increasing concentrations of ADP and epinephrine; b) PF3 ( Spaet - Cintron method) and antithrombin III, aPTT, prothrombin ratio, fibrinogen, platelet count. Platelet aggregation and availability of PF3 are lower in cirrhotic patients, suggesting an intrinsic defect of platelets. Moreover prolongation of aPTT and prothrombin ratio, lower levels of antithrombin III, fibrinogen and platelet count were detected.
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PMID:[Platelet aggregation and various coagulation parameters in liver cirrhosis]. 672 55

In order to detect impaired synthesis of blood coagulation factors associated to consumption coagulopathy, a simultaneous evaluation of factor II-related antigen (II rAg) and of antithrombin III (AT III) was carried out in 16 patients affected with severe defibrination. An in vitro preliminary study on plasma and serum demonstrated that the levels of II rAg and of AT III, assessed by the Laurell technique with Behring antisera, were not reduced by the coagulation process. The patients were, a posteriori, classified into two groups according to the absence (group A) or the presence (group B) of factors predisposing to liver failure such as metastasis, cirrhosis, and prolonged shock. II rAg and AT III levels are significantly correlated; they are in the normal range in group A but reduced in group B. Thus II rAg or AT III level determinations are useful markers in the detection of liver failure associated to the consumption phenomenon. These results also suggest that part of the decreased AT III levels reported in severe cases of disseminated intravascular coagulation may be the consequence of an associated liver failure.
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PMID:Factor II related antigen and antithrombin III levels as indicators of liver failure in consumption coagulopathy. 681 Apr 90

Blood coagulation and fibrinolysis before and after splenectomy was studied in 74 cases of liver cirrhosis. A hypocoagulable state was found before splenectomy, but the platelet count, and the levels of fibrinogen, plasminogen, alpha 2-macroglobulin and antithrombin III increased significantly after splenectomy (p less than 0.05 to p less than 0.001). A marked improvement was observed on the values of r (reaction time), k (clot formation time) and ma (maximal amplitude) of thrombelastograms (p less than 0.05 to p less than 0.001). The prothrombin time was reduced after the surgery, but not significantly (p less than 0.1, greater than 0.05). The levels of alpha 1-antitrypsin remained almost unchanged, while serum fibrinogen-fibrin degradation products (FDP) showed a slight decrease postoperatively. The immunohistologic study of the spleen excised from 7 cases with liver cirrhosis, with the use of the direct immunofluorescence technique, demonstrated the deposits of fibrin in the splenic cords in all cases. It was not recognized in the spleens of 4 cases without cirrhosis used as the control. A further study of the spleen weight and plasma fibrinogen level showed that a significant inverse correlation exists between these two parameters (p less than 0.01). These findings suggest that localized intravascular coagulation (LIC) occurs in the enlarged spleen associated with liver cirrhosis.
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PMID:Effects of splenectomy on blood coagulation and fibrinolysis in patients with liver cirrhosis: possible role of the spleen in haemostasis. 698 11

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

This study was designed to examine the effect of selective correction of antithrombin III activity on the increased turnover of fibrinogen, which occurs in patients with liver cirrhosis supposedly due to disseminated intravascular coagulation. Human antithrombin III concentrates were therefore transfused in seven patients with cirrhosis and antithrombin III deficiency (less than 80%). Fibrinogen half-life and the fractional catabolic rate constant were calculated from the turnover of 125I-fibrinogen which was represented by a two-compartment model. Prior to antithrombin III transfusion, 125I-fibrinogen half-life was 76.7 +/- 15.2 h and the fractional catabolic rate constant was 0.33 +/- 0.11 of the plasma fibrinogen pool per day. In six healthy adult controls these values were significantly different: 109.4 +/- 8.8 h and 0.19 +/- 0.01 respectively. Correction of antithrombin III activity with human antithrombin III concentrate reduced the increased turnover of radiolabelled fibrinogen to normal. The 125I-fibrinogen half-life became 108.4 +/- 17.6 h and the fractional catabolic rate constant decreased to 0.23 +/- 0.06. These observations indicate that decreased antithrombin III activity contributes in an important way to the increased 125I-fibrinogen turnover in patients with cirrhosis and this might reflect intravascular coagulation.
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PMID:Antithrombin III transfusion in patients with hepatic cirrhosis. 711 27

When compared to values obtained in healthy normolipidemic normal weight control subjects, the plasma antithrombin III level determined by immunological, clotting and thrombin-agarose diffusion techniques was found to be obviously decreased in patients with decompensated cirrhosis of the liver and slightly but significantly increased in hyperlipidemic and especially in hypertriglyceridemic subjects. Plasma antithrombin III was positively correlated with serum cholesterol level, the logarithm of serum triglyceride concentration and serum pseudocholinesterase activity. A weaker correlation between plasma fibrinogen and antithrombin III was noted in the investigated clinical material. It is suggested that the accelerated fatty acid and lipoprotein turnover occurring in many subjects with type IIb and type IV hyperlipoproteinemia might be accompanied by an enhanced hepatic protein synthesis involving various liver secretion enzymes and clotting factors as well as antithrombin III.
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PMID:Increased plasma antithrombin III level in hyperlipidemic subjects. 722 27

We performed coagulation profiles including a complete blood count (CBC), prothrombin time (PT), activated partial thromboplastin time (aPTT), and quantitation of fibrinogen, antithrombin III (AT III), plasminogen, and fibrin/fibrinogen degradation products (FDP) on 73 cancer patients. All had solid tumors with clinically documented metastases. Eleven patients had strong clinical and laboratory evidence of disseminated intravascular coagulation (DIC). Fifty-five of the remaining 62 patients had no clinical evidence of serious hemorrhage or thrombosis at the time of testing. Thirty-one (50%) non-DIC patients had no abnormal clotting tests. Our data indicate that a majority of cancer patients, with or without hepatic involvement, are able to maintain normal or near normal hemostatic function in vitro until advanced stage of disease. Deviation from normal for PT, aPTT, or TT, depressed AT III activity, or increased FDP signal the presence of complicating pathophysiologic events such as DIC or cirrhosis. Diminution of fibrinogen level or AT III activity and elevation of FDP are more sensitive indicators of DIC than prolongation of PT, aPTT, or TT.
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PMID:Hemostatic function in cancer patients. 739 48


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