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)

The activity of plasminogen (Pl) and proactivator of plasminogen (PPl) was studied in 812 patients, 682 of them sick with liver diseases and 130 healthy. A total of 419 patients with various clinical forms of viral hepatitis were covered: 35 patients with acute liver insufficiency, 39--with decompensated cirrhosis of liver, 16--cholangiohepatitis, 16--toxic hepatitis and 157 patients with mechanical jaundice. Coagulation micromethods were applied. The referentive values were derived: f for Pl--83-126%; for PPl--80-120%. The activity of Pl and PPl in jaundice with parenchymal nature was established to be, most frequently, reduced and correlated well with the severity and the phase of the morbid process--the lowest enzyme activity was established in acute liver insufficiency, decompensated liver cirrhosis and severe forms of vital hepatitis, at the earlier phases. Enzyme activity in mechanical jaundice is, most often, normal and rarely enhanced. The fibrinolytic enzymes obtained could help the differential diagnosis of jaundice and are of significance in the determination of the severity of the parenchymal liver diseases.
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PMID:[Potential fibrinolytic activity of the blood in jaundice of parenchymal and mechanical origin]. 654 67

Prekallikrein (Prekk), antithrombin III (ATIII), plasminogen and alpha 2-antiplasmin were evaluated in chronic active hepatitis and in liver cirrhotic patients and correlated with Normotest. Prekk, ATII and plasminogen were significantly decreased in chronic active hepatitis as well as in liver cirrhosis. Alpha 2-antiplasmin levels in chronic active hepatitis patients did not differ from controls; liver cirrhotic patients, on the contrary, showed significantly low values of alpha 2-antiplasmin, Prekk, ATIII and plasminogen were significantly correlated with Normotest in both groups, but when cirrhotic patients were divided into the compensated and decompensated state only Prekk was correlated with Normotest in the decompensated state. The investigation seems to suggest that Prekk could be a reliable index for protein liver failure.
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PMID:Prekallikrein behaviour in chronic active hepatitis and in cirrhotic patients. 656 63

A plasminogen activator, or class of activators, that absorbs to lysine-agarose is present in human plasma. We have developed a quantitative assay for this plasminogen activator. The assay involves removal of the activator from plasma with lysine-agarose affinity columns and subsequent measurement of the activity by the conversion of plasminogen to plasmin on standardized fibrin agar plates. Using this assay, we investigated three physiologic conditions that have in the past been associated with increased fibrinolytic activity to determine whether elevation of the LAPA was involved. Normal individuals undergoing strenuous physical exercise and others subjected to venous occlusion as well as patients with cirrhosis of the liver were examined. Treadmill exercise to maximal exertion produced up to 15-fold increases in the level of LAPA; venous occlusion produced similar elevation. Certain individuals did not show increase fibrinolytic activity in response to exercise or venous occlusion, as indicated by unchanged euglobulin lysis times. These fibrinolytic hyporesponders did not show an elevation of their LAPA levels. In the third group examined, patients with cirrhosis, 24 of 62 had elevated levels of LAPA. Supplementation of plasma from normal individuals with this plasminogen activator from exercised individuals and cirrhotics resulted in increased rates of clot lysis.
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PMID:A lysine-absorbable plasminogen activator is elevated in conditions associated with increased fibrinolytic activity. 678 11

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

To assess the nature of the hemostatic abnormalities associated with chronic liver disease, we have simultaneously evaluated the kinetic of radiolabeled platelets, fibrinogen, and plasminogen, together wit tests of platelet and fibrinogen function, and coagulation factors in 60 patients with documented, severe but stable cirrhosis of the liver. The mean platelet survival was substantially reduced (5.8 +/- 1.7 days compared with 9.5 +/- 0.6 days in normals, p less than 0.0001) and splenic sequestration of platelets was increased (mean recovery was 47% +/- 18 vs. 65% +/- 5 in normals, p less than 0.0001). Nevertheless the mean platelet count was nearly normal because platelet production was increased nearly twice normal values (mean turnover was 64,000 +/- 33,000 platelets/microliter/day; p less than 0.0001). The mean rate of fibrinogen removal was shortened (p less than 0.0001) and fibrinogen turnover increased about 20% (p = 0.008) while the mean fibrinogen concentration was not different from the results in normal control subjects (p = 0.212). Autologous and homologous fibrinogen disappeared from the circulation at equivalent rates (r = 0.751; p = 0.008), indicating that fibrinogen from cirrhotic patients was not kinetically different from normal fibrinogen. The mean plasminogen survival was significantly shortened (p less than 0.0001), but the mean plasminogen turnover was not increased (p = 0.388). Thus the plasminogen concentration was reduced (p less than 0.0001). For platelets, fibrinogen, and plasminogen, the production rate was the most important determinant of the concentration in the circulation. The administration of heparin to cirrhotic patients improved the survival of fibrinogen but not of platelets. LeVeen valve implantation generally resulted in parallel shortening of both the platelet and fibrinogen survivals and concentrations. Platelet function as assessed by template bleeding time, platelet retention by glass bead columns, and aggregation induced by ADP, epinephrine, and collagen was normal. Fibrinogen determinations by the Clauss and Jacobsson techniques were equivalent, indicating that the ability to polymerize fibrin monomer was not detectably altered. Sixty percent of patients had an abnormal prothrombin time and half that number had a prolonged partial thromboplastin time. Although most patients had a modest decrease in the prothrombin complex coagulation factors, fibrin degradation products were, in general, not elevated in the circulation. The wide range of values observed suggests that a number of different and complex processes may be ongoing in different patients. Overall, the kinetic data suggest that platelets are initially consumed, perhaps on incompletely endothelialized endovascular surfaces in the liver, and that fibrin subsequently forms secondary to local stasis. The absence of increased production of fibrinogen and plasminogen despite shortened survival times reflects the reduced capability of the cirrhotic liver to increase protein synthesis.
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PMID:Kinetic and functional studies of platelets, fibrinogen, and plasminogen in patients with hepatic cirrhosis. 706 18

Histidine-rich glycoprotein is a 3.8s alpha 2-glycoprotein of human plasma originally isolated in 1972 [1,2]. The biologic function of histidine-rich glycoprotein, however, is unknown. A recent report suggests that histidine-rich glycoprotein binds to the high-affinity lysine-binding sites of plasminogen and that histidine-rich glycoprotein may retard fibrinolysis by interfering with the binding of plasminogen to fibrin [3]. We have measured the plasma titers of histidine-rich glycoprotein in normal subjects and patients with advanced hepatic cirrhosis by single radial immunodiffusion with a monospecific antiserum. The levels in 22 patients were 7.0 +/- 2.5 mg/dl (mean +/- SD), whereas those in 20 control subjects were 11.8 +/- 2.7 (p less than 0.001). Upon two-dimensional crossed immunoelectrophoresis, the pattern of histidine-rich glycoprotein in liver cirrhosis was similar to that of normal histidine-rich glycoprotein. Since histidine-rich glycoprotein seems to function as an antifibrinolytic agent, the decreased titers in cirrhosis may be one factor contributing to the enhanced fibrinolysis commonly seen in this disorder.
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PMID:Reduced histidine-rich glycoprotein levels in plasma of patients with advanced liver cirrhosis. Possible implications for enhanced fibrinolysis. 711 73

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

The concentrations of 23 plasma proteins were measured by radial immunodiffusion in the plasma and ascites of 17 patients with cirrhosis and four patients with intraperitoneal malignancies, to learn whether there is a selectivity in the movement of proteins from plasma into ascites, analogous to that of proteinuria. Additionally, since some of the proteins are involved in coagulation, we hoped to clarify the coagulopathy frequently seen following peritoneovenous shunting of ascites. Analysis was by groups: group 1 consisted of nine patients with cirrhosis with an ascites-total protein content less than 2.5 g/dl; group 2 consisted of eight patients with cirrhosis with ascites-total protein content greater than or equal to 2.5 g/dl; and group 3 consisted of four patients with malignant ascites. The ratio of the plasma concentration/ascites concentration ([P]/[A]) for each protein was calculated for each patient. In each group the median [P]/[A] for each protein was plotted against the natural logarithm of its molecular weight (In MW). For 21 of the 23 proteins, [P]/[A] showed a close linear relationship to In MW. Fibrogen and plasminogen showed significant (p < 0.0002) elevation above the regression line relating [P]/[A] to In MW. This indicates depletion of fibrinogen and plasminogen in ascites. The ascites in group 1 showed moderate selectivity, defined as the slope of the regression line (1.59), while groups 2 and 3 were essentialy nonselective (0.35 and 0.50). Fibrin-split products were elevated in all ascites but not in plasma, indicating either fibrinolysis or fibrinogenolysis within the ascites. A normal ratio for prothrombin suggests fibrinogenolysis may be the dominant mechanism. Thus the coagulopathy induced by LeVeen valve insertion may be in part secondary to the infusion of plasmin or a plasminogen activator into the circulation.
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PMID:Analysis of Twenty-three plasma proteins in ascites. The depletion of fibrinogen and plasminogen. 744 27

The aim of this double-blind, placebo-controlled crossover study was to investigate the effect of 1-deamino-8-D-arginine vasopressin (dDAVP) on hemostasis in patients with chronic liver disease. Nine consecutive patients with biopsy-proven liver cirrhosis and related coagulation abnormalities received in a random order dDAVP, 0.5 microgram/kg, or saline intravenously. Blood samples were taken before dDAVP infusion and 30, 60 and 180 min after its end. dDAVP infusion induced a statistically significant shortening of the bleeding time from 9 min (range 6.5-15.5) to 6 min (range 4.5-9.5) at 1 h after the infusion. The activated partial thromboplastin time was significantly shortened at 30 and 60 min after dDAVP infusion. Plasma levels of factor VIII, XI and XII coagulant activities were significantly increased at all sampling times after dDAVP infusion. The maximum increase over basal values in plasma levels of factor VIII, XI and XII was 63, 22 and 40%, respectively. dDAVP did not induce any significant changes of prothrombin time, thrombin clotting time, fibrinogen, plasma levels of factor II, V, VII, IX, X, factor XII antigen, protein C (activity and antigen), antithrombin III, plasminogen and alpha 2-antiplasmin. Placebo infusion did not produce any significant changes in the evaluated parameters. We conclude that dDAVP can positively influence the hemostatic system in patients with liver cirrhosis. The clinical relevance of this hemostatic improvement deserves further evaluation.
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PMID:Effects of desmopressin on hemostasis in patients with liver cirrhosis. 748 63

Membranous obstruction of the inferior vena cava is a rare disease. The etiology of the membrane is believed to be thrombotic or congenital. In three of 11 siblings from a single family, symptoms of membranous obstruction of the inferior vena cava developed during early adult life. All had signs of more long-standing disease, as judged by the presence of collaterals, cirrhosis and, in one case, hepatocellular carcinoma. On family screening no further cases of membranous obstruction of the inferior vena cava were found. There was also no evidence of inherited defects in the natural coagulation inhibitors (protein C, protein S and antithrombin III) and plasminogen deficiency. This familial occurrence of membranous obstruction of the inferior vena cava supports a congenital etiology, although a thrombotic etiology cannot be totally excluded.
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PMID:Familial occurrence of membranous obstruction of the inferior vena cava: arguments in favor of a congenital etiology. 766 59


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