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)

Kininogen level, that of active kinins and kininase activity in the plasma of patients suffering from cirrhosis of the liver and of healthy people were studied. The kininogen content was determined by different available methods i.e. the trypsin and acetone techniques and by means of the plasma and glandular kallikrein preparation. An increase in kininase activity and a lowered kininogen level as determined by all the methods were found in the sick persons. The maximal decrease in the kininogen level determined by means of the plasma kallikreins is substantiated in connection with the increased fibrinolytic activity of the plasma of the patients with hepatic cirrhosis.
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PMID:Studies of the plasma kinin-forming system in cirrhosis of the liver. 16 51

Serum angiotensin I converting enzyme, identical with kininase II, was measured fluorometrically in patients with acute viral hepatitis (n=18), liver cirrhosis without (n=44) and with (n=19) ascites. In all groups of patients the enzyme was significantly elevated as compared to 44 healthy controls (p less than 0.001). No correlation could be found between angiotensin I converting enzyme activity and liver function tests (serum glutamic oxalacetic transaminase, serum glutamic pyruvic transaminase, total protein, albumin, bilirubin) or other parameters (serum potassium, serum sodium). High serum converting enzyme activity in chronic liver diseases might originate primarily from an altered pulmonary circulation and indicates higher conversion rate of angiotensin I by passage through the lungs as well as increased bradykinin degradation. The reason for the enzyme liberation in acute viral hepatitis is as yet uncertain.
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PMID:Changes of serum angiotensin I converting enzyme in patients with viral hepatitis and liver cirrhosis. 22 16

Abnormalities of Hageman factor dependent pathways have been described in a wide variety of human disease states. Congenital deficiencies of factor XII (Hageman trait) prekallikrein (Fletcher trait) and high molecular weight kininogen (Williams, Fitzgerald and Flaujeac traits) although resulting in profound in vitro changes, do not cause in vivo difficulties. In contrast, deficiency of C1 esterase inhibitor (hereditary angioedema) results in significant morbidity and mortality. Acquired diseases may exhibit decreased synthesis of these three proteins in cirrhosis and dengue fever. In vivo activation of factor XII initiated pathways occur in septic shock, disseminated or localized intravascular coagulation, typhoid fever, polycythemia vera, hyperbetalipoproteinemia, coronary artery disease, nephrotic syndrome, transfusion reactions, hemodialysis and extracorporeal bypass. Activation of both the intrinsic system and tissue mediators contribute to the vasomotor phenomena in carcinoid syndrome and postgastrectomy dumping. Roles for factor XII, prekallikrein and kininogen have been suggested in gouty arthritis, allergic disorders and cystic fibrosis but the evidence is not yet convincing in these disorders.
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PMID:Participation of Hageman factor dependent pathways in human disease states. 34 10

Different causal factors have been speculated about in regard to hemodynamic changes (hyperdynamic circulation) in liver cirrhosis. Effects of various vasoactive substances upon the increased arterio-venous intrapulmonary shunting in cirrhosis have been demonstrated, including reduced ferritin, bradykinin, prostaglandins, VIP and parenterally applied histamine. In cirrhotic patients pre- and posthepatic plasma concentrations of histamine are definitely elevated, and elimination of histamine by the liver is reduced. It is speculated, that elevated plasma concentrations of endogenous histamine may contribute to hemodynamic changes in liver cirrhosis.
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PMID:[Plasma histamine concentration and hemodynamic changes in liver cirrhosis (author's transl)]. 63 19

A specific, sensitive, and reproducible radioimmunoassay for human plasma thromboplastin antecedent (PTA, factor XI) has been developed with purified PTA and monospecific rabbit antiserum. Precise measurements of PTA antigen were possible for concentrations as low as 0.3% of that in normal pooled plasma. Normal plasma contained approximately 6 microgram PTA/ml. A good correlation (correlation coefficient 0.68) existed between the PTA procoagulant assays and radioimmunoassays among 50 normal adults (25 males and 25 females). PTA antigen was markedly reduced in plasma of 13 patients with congenital homozygous PTA deficiency (range less than 0.003-0.128 U/ml) and 9 patients with hepatic cirrhosis (0.35+/-0.17 U/ml), but was normal in those of 9 patients under treatment with warfarin, 8 patients with disseminated intravascular coagulation and 16 patients with other congenital clotting factor abnormalities, including prekallikrein deficiency (Fletcher trait) and high molecular weight kininogen deficiency (Fitzgerald trait).
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PMID:Plasma thromboplastin antecedent (PTA, factor XI): a specific and sensitive radioimmunoassay. 88 16

Fitzgerald factor (high molecular weight kininogen) is an agent in normal human plasma that corrects the impaired in vitro surface-mediated plasma reactions of blood coagulation, fibrinolysis, and kinin generation observed in Fitzgerald trait plasma. To assess the possible pathophysiologic role of Fitzgerald factor, its titer was measured by a functional clot-promoting assay. Mean +/- SD in 42 normal adults was 0.99+/-0.25 units/ml, one unit being the activity in 1 ml of normal pooled plasma. No difference in titer was noted between normal men and women, during pregnancy, or after physical exercise. Fitzgerald factor activity was significantly reduced in the plasmas of eight patients with advanced hepatic cirrhosis (0.40+/-0.09 units/ml) and of ten patients with disseminated intravascular coagulation (0.60+/-0.30 units/ml), but was normal in plasmas of patients with other congenital clotting factor deficiencies, nephrotic syndrome, rheumatoid arthritis, systemic lupus erythematosus, or sarcoidosis, or under treatment with warfarin. The plasmas of 21 mammalian species tested appeared to contain Fitzgerald factor activity, but those of two avian, two repitilian, and one amphibian species did not correct the coagulant defect in Fitzgerald trait plasmas.
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PMID:Fitzgerald factor (high molecular weight kininogen) clotting activity in human plasma in health and disease in various animal plasmas. 100 85

Changes of high molecular weight kininogen (HMW-K) clotting activity, antigen and cleavage in the plasma in the health and various diseases were studied. In 20 healthy individuals clotting activity of HMW-K, as measured by APTT one stage method, was 99 +/- 12% (male) and 84 +/- 15% (female). Antigen as measured by Laurell method were 106 +/- 24% (male) and 91 +/- 21% (female). In 35 patients with disseminated intravascular coagulation (DIC), both activity (78 +/- 33%) and antigen (69 +/- 31%) were statistically lower than those in normal individuals (p less than 0.01). In DIC both activity and antigen of HMW-K was correlated with serum albumin level. These results suggest that the cause of the lower level of HMW-K in DIC especially with septicemia is the result of lower production rather than consumption. In vivo cleavage of HMW-K was detected in plasma of a patient with septicemia and DIC by immunoblotting. The change of HMW-K was also assessed in other pathological states including liver cirrhosis, collagen disease, cardiopulmonary bypass and pregnant women.
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PMID:[Changes of high molecular weight kininogen in various states]. 259 37

To clarify the role of endotoxaemia and congestion of the stomach in the development of acute haemorrhagic gastritis in cirrhotic patients and to investigate the mechanisms of gastric mucosal haemorrhage, the present study was undertaken using rats. Congestion of the stomach was produced by the ligation of gastric veins. Congestion of the stomach or endotoxaemia could not produce gastric mucosal haemorrhage by itself. However, petechial haemorrhage was induced when endotoxin was given to the rats with congestion of the stomach, and the gastric mucosal haemorrhage was largely prevented by administration of gabexate mesilate, an anti-kallikrein drug. Administration of bromelain, which releases prekallikrein and high molecular weight kininogen, instead of endotoxin, also induced gastric mucosal haemorrhage. These findings suggest that the cause of acute haemorrhagic gastritis may be the coexistence of endotoxaemia and congestion of the stomach due to liver cirrhosis and portal hypertension. The mechanisms of the haemorrhage may be as follows: Endotoxin-induced bradykinin acts on the dilated capillaries and small veins in the mucosa and markedly increases their permeability.
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PMID:An experimental study into the cause of acute haemorrhagic gastritis in cirrhosis. 309 56

The activities of Hageman factor, high molecular weight kininogen (HMWK), and prekallikrein were studied in patients who had chronic active hepatitis and cirrhosis. Serum HMWK and prekallikrein activities were decreased in chronic active hepatitis and cirrhosis, but Hageman factor activity was low in cirrhosis only. The reduction of prekallikrein, HMWK, and Hageman factor was dependent on the degree of liver failure. Similar prekallikrein values were found in serum samples, activated or not, with an excess of Hageman factor and HMWK, which suggests that the decrease of prekallikrein in liver disease is not influenced by the simultaneous decrease of Hageman factor and HMWK.
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PMID:Hageman factor, high molecular weight kininogen, and prekallikrein in chronic liver disease. 363 88

Because of an increasing interest in the determination of prekallikrein a kit was made for the determination of this plasma proenzyme. The kit consists of 1) a prekallikrein activator of the cephalin-ellagic acid type containing Factor XII and HMW-kininogen to ensure a total activation of the prekallikrein even in pathological plasmas, 2) a buffer which is optimal for both activation and substrate hydrolysis and 3) the chromogenic substrate S-2302. A control plasma is also included. This kit was evaluated by thirteen research groups as well as by ourselves. Both normal and patient plasmas were analyzed. Good correlations were obtained for prekallikrein levels in plasma samples between the kit method and two other methods (immunochemical and functional). As well as in deficiency states the prekallikrein level was low in pancreatitis (n = 20), cancer (n = 16), early pregnancy with gestosis (n = 15), cirrhosis (n = 9) and cases with thromboembolic disorders (n = 5). The prekallikrein level was high in late pregnancy (n = 4).
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PMID:Description and evaluation of a new chromogenic substrate assay kit for the determination of prekallikrein in human plasma. 364 42


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