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)

Determination of the complement titer in the serum and plasm of 120 patients with chronic liver diseases showed that in eight (7%) patients with cirrhosis of the liver, chronic active or chronic inactive hepatitis complement in the serum was less than half in the plasma. The dissociation of complement serum and plasma was due to cold activation of the classical pathway of complement in vitro since serum drawn from these patients at 37 degrees C lost hemolytic activity in 4 hours when transferred to a cold environment. Neither HB antigen nor cryoglobulin participated in this phenomenon. The activation of complement in the cold could be prevented by increasing the ionic strength, or by adding vitamin E or, to a lesser extent its vehicle HCO-60, while heparin, Trasylol, soybean trypsin inhibitor, or hirudin had no effect. Trans-AMCHA prevented activation in one case. It is speculated that a factor appearing as a result of blood clotting is able to activate the classical pathway of complement in the cold; it is probably not related to Hageman factor (factor XII), factor VII, thrombin, kallikrein.
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PMID:Cold activation of complement i. presence of coagulation-related activator. 5 81

Sodium and water retention is constant in decompensated cirrhosis with ascites and edema. Sodium retention is due to several factors. Renal hemodynamic disturbances appear first: decrease in glomerular filtration and renal plasmatic perfusion, redistribution of renal perfusion to the juxtamedullar area where the longer nephrons reabsorb more sodium. Metabolic disorders of estrogens, natriuretic hormonal factor, prostaglandins and the kallikrein-kinin system contribute to greater sodium retention. Water retention is secondary to greater sodium reabsorption and to hyperactivity of the antidiuretic hormone. Sodium and water retention, associated with portal hypertension, with reduced oncotic pressure and with dynamic lymphatic insufficiency, is responsible for the production of ascites. The latter results in a decrease in the effective plasmatic volume, with non-suppression of the renin-angiotensin system, increased aldosterone production and additional sodium retention.
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PMID:[The physiopathology of ascites]. 46 62

Plasma prekallikrein (kallikreinogen) and kallikrein inhibitor, assayed with the kaolin activable esterase method, have been evaluated in 20 patients with hepatic cirrhosis, in 12 cases with jaundice from acute viral hepatitis, and in 9 normal. A significant reduction of the plasma prekallikrein in cirrhosis has been found. A lowering of plasma prekallikrein has also been observed in viral hepatitis; in this condition, however, the modifications were less important than those obtained in cirrhosis. In three cases of hepatitis, the behaviour of the plasma prekallikrein and kallikrein inhibitor have been controlled during the period of the disease and compared with the behaviour of some conventional parameters, such as serum transaminases and bilirubin. An important increase of the prekallikrein level has been observed during the improvement of hepatitis. These data confirm the implication of the prekallikrein-kallikrein system in severe liver diseases, and indirectly points out the role of the liver in maintaining the physiological balance of the kallikrein system.
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PMID:Prekallikein and kallikrein inhibitor in liver cirrhosis and hepatitis. 108 79

The pathogenesis of salt and water retention in cirrhosis remains unclear. Systemic and portal hemodynamic parameters, including cardiac output, portal pressure gradient and systemic vascular resistance, were measured in six patients with untreated ascites and in six patients with hepatic cirrhosis with no history of ascites. Renal blood flow, urinary volume, and humoral factors, including plasma renin, aldosterone, angiotensin II, and urine kallikrein, were measured. Significant differences were seen between the two groups in urine volume, urine sodium and fractional sodium excretion, plasma angiotensin II, and the ratio between plasma renin activity and urinary kallikrein excretion (PRA:UKallV). A strong correlation existed between urinary sodium excretion and the PRA:UKallV ratio. No significant differences were detected between the groups in portal, renal, and systemic hemodynamics. The present results suggest that humoral changes occur early in ascites. Altered relationships between intrarenal hormone systems, such as the renin-angiotensin and kallikrein-kinin systems, may be important in salt and water retention.
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PMID:Portal and systemic hemodynamics and humoral factors in cirrhosis with and without ascites. 141

DIC in patients affected by cirrhosis, accompanied by portal hypertension and splenomegaly, has been suspected in the past. The main aim of this study is to ascertain the incidence of this phenomenon. We carried out coagulation and fibrinolytic tests in 113 cirrhotic patients and 20 healthy control persons. We found chronic consumption coagulopathy at analysis level in 28 cases (24.8%) with a decrease of fibrinogen, factor V, kallikrein, platelets, prothrombin complex activity, increase of PDF, partial thromboplastic time and euglobulin lysis. 25 cases had active cirrhosis, with ascites, variceal bleeding and/or hepatic encephalopathy; 3 were non-active cirrhosis. Only 7 patients had clinical DIC. We observed that coagulation disorders increased with more active cirrhosis.
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PMID:[The incidence of consumption coagulopathy in liver cirrhosis]. 256 20

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 urinary excretion of aldosterone, kallikrein and prostaglandin E2 (PGE2) was studied in sodium-retaining (RC) and nonretaining (NRC), nonascitic cirrhotic rats, under basal conditions and after an oral sodium load (5 mmol). The glomerular synthesis of PGE2 was measured in RC rats under the same conditions. Both groups of cirrhotic animals showed a decreased urinary excretion of PGE2. Isolated glomeruli of RC rats produced less PGE2 than those of the control animals, both under basal conditions and after the sodium load. The NRC group was the only one able to increase the urinary excretion of kallikrein in response to the sodium load. These findings could contribute to explain the early physiopathological events of hepatic cirrhosis.
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PMID:Urinary excretion and glomerular synthesis of prostaglandin E2 and prostaglandin F2 alpha in cirrhotic, non-ascitic rats: the effects of sodium overload. 316 14

Urinary kallikrein excretion was found as compared with 22 normal subjects (0.88 +/- 0.05 mumol/min/day) to be significantly reduced in 15 cirrhotics without ascites (0.42 +/- 0.04; p less than 0.01) and in 23 cirrhotics with ascites (0.15 +/- 0.02; p less than 0.01), and further, showed a significant difference between the two groups (p less than 0.01), but did not significantly change in 14 patients with chronic active hepatitis. Urinary kallikrein excretion in cirrhotics showed a positive correlation with serum albumin, indocyanine green disappearance rate, cholinesterase, and prothrombin, and an inverse correlation with bilirubin. After indomethacin administration to 13 cirrhotics with ascites, not only plasma renin activity and plasma aldosterone decreased significantly (p less than 0.01), but urinary kallikrein excretion also showed a small but statistically significant decrease (p less than 0.05). These results suggest that urinary kallikrein excretion decreases almost parallel to the severity of liver damage and is mediated via prostaglandins or the renin-angiotensin-aldosterone system, which may be involved in the reduction of renal blood flow in patients with liver cirrhosis.
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PMID:Urinary kallikrein excretion in chronic liver disease and effect of indomethacin. 351 May 29

A study of 93 patients with liver cirrhosis showed that the most important blood coagulation disorder in this pathology resulting in hypocoagulation, was not decreased synthesis and deficit of the prothrombin complex factors but disturbance of the final stage determined by afibrinogenemia. Considerable depression of XIIa-kallikrein-dependent fibrinolysis and marked increment of an antiplasmin level in the plasma were noted. Positive paracoagulation tests were revealed in 57% of the patients, and as other signs typical of the lingering DIC-syndrome were absent, they were interpreted as the "hypercoagulation syndrome" or "pre-DIC syndrome". The problem of possible relationship of development of both thromboses and hemorrhages with acquired afibrinogenemia in liver cirrhosis was discussed.
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PMID:[Role of dysfibrinogenemia and disorders of fibrinolysis in the pathogenesis of hemostatic pathology in liver cirrhosis]. 357 61

Increased renal production of prostaglandins are thought to be important for the maintenance of kidney blood flow in advanced cirrhosis. In alert, unanesthetized dogs with chronic cirrhosis and ascites, produced by bile duct ligation, we measured inulin and p-aminohippurate (PAH) clearance before and after the intravenous administration of 2 mg/kg indomethacin, an inhibitor of prostaglandin production. Inulin and PAH clearance declined by 42 and 43%, respectively. This decline in renal perfusion was not associated with changes in blood pressure or cardiac output. If portal hypertension was prevented by creating an end-side portacaval anastomosis at the time of bile duct ligation, indomethacin was without effect on renal perfusion whether or not the dog had ascites. If ascites was completely mobilized in cirrhotic dogs with portal venous hypertension with the aid of a LeVeen valve, indomethacin depressed inulin and PAH clearance as usual during the steady-state period once all ascites had been removed. An attempt was made to determine some of the factors mediating the apparent increase in renal prostaglandin synthesis by administering various pharmacological antagonists. The inhibition of angiotensin effect with saralasin and the inhibition of kallikrein with aprotinin prevented the usual indomethacin effect. It is concluded that portal hypertension, but not a "sick liver per se, in cirrhosis activates the renin-angiotensin system to both produce renal vasoconstriction and stimulate prostaglandin synthesis, thereby normalizing renal perfusion. Renal kallikrein also appears to play a role, probably by augmenting renin release.
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PMID:Renal perfusion in dogs with experimental hepatic cirrhosis: role of prostaglandins. 635 40


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