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)

Mitochondrial phosphorylative activity was measured in the livers of various shunted or pancreatectomized dogs. In simple portal vein branch-ligated dogs, the mitochondrial phosphorylative activity in the nonligated lobe, which was supplied with excess portal blood, increased to approximately 150% of control values. In splenocaval-shunted or totally pancreatectomized dogs, the mitochondrial phosphorylative activity did not increase even in the nonligated lobe. However, the mitochondrial phosphorylative activity in the nonligated lobe increased to 120% of control in 80%-pancreatectomized and 150% in 50%-pancreatectomized dogs. In distal splenorenal-shunted (Warren-shunted) dogs, the mitochondrial phosphorylative activity increased to 150% of control values. Thus, the Warren's shunt operation is considered to be the more reasonable procedure for treatment of liver cirrhosis with esophageal varices, from the point of view of hepatic functional reserve based on the energetic metabolism of the liver.
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PMID:Role of portal venous blood supply from the pancreas in maintaining hepatic functional reserve. Appraisal of Warren's shunt operation. 68 95

The question is still open, whether a pathologic formation of fibrinogen or an insufficient stabilized fibrin are causative factors within the complex disorders in hemostasis in patients with liver cirrhosis. Thus, 45 patients with liver cirrhosis, which was proven by liver biopsy, were investigated by means of sodium-dodecyl-sulfate (SDS) polyacrylamidgel-electrophoresis in order to evaluate, whether the liver produces a pathological fibrinogen or whether the formation of fibrin from fibrinogen is defect. The fibrin stabilizing factor (factor XIII) was measured by immunological methods. In order to have a mean of the stage of the disease, 37 patients were subdivided by the extend or their porto-caval collateral circulation and further 8 patients were investigated having bleeding from esophageal varices. By the results evidence accrued that in advanced stages of liver cirrhosis and a marked porto-caval collateral circulation polymerization of fibrinogen was insufficiently, especially, the formation of alpha-chains was altered, whereas the formation of gamma-dimers, the separation of fibrinopeptides from fibrinogen, and the aggregation of fibrinmonomers were normal. This defect in fibrin structure was positive correlated with the stage of liver cirrhosis, which correlated negative with the plasma activity of factor XIII. In vitro, the defect in fibrin formation, from fibrinogen was abolished by adding factor XIII to the assay. Thus, in liver cirrhosis fibrin formation is altered because of factor XIII deficiency, but a normal fibrinogen is synthesized by the liver. In consequence, the administration of factor XIII preparations is suggested as one clinical action among others to benefit the hemostatic disorders, especially in patients with bleeding from esophageal varices.
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PMID:[Fibrinogen and fibrin structure in patients with cirrhosis of the liver (author's transl)]. 70 17

The results of surgical treatment of 100 patients with hemorrhage from the upper digestive tract (except gastric cancer and hepatic cirrhosis, complicated with bleeding esophageal varices) are discussed. The role of gastrotomy is emphasized, while vagotomy and drainage operations do not seem to be greatly warranted in treatment of chronic and acute gastroduodenal ulcers complicated with bleeding.
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PMID:[Surgical tactics in hemorrhage from the upper segments of the digestive tract]. 78 94

The prognosis of 97 patients with congenital biliary atresia treated by hepatic portoenterostomy was studied. In 37 of 97 patients (38%), good bile excretion was observed after surgery, and jaundice cleared. Sixteen of the 37 patients developed ascending cholangitis; 11, esophageal varices; and nine died. Seven died of ascending cholangitis and two of hepatic failure. Fourteen patients had an uneventful course. In the remaining 60 patients, bile excretion was scanty, and the disease progressed to biliary cirrhosis; 52 died. Causes of death were hepatic failure (53%), intracranial hemorrhage (16%), rupture of esophageal varices (12%), severe dehydration (9%), and postoperative complications (9%). The age at death ranged from 2 to 52 months, with an average at 16 months.
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PMID:Congenital biliary atresia. Analysis of 97 cases with reference to prognosis after hepatic portoenterostomy. 82 37

Percutaneous transhepatic catheterization of the portal vein was performed in 21 patients with liver cirrhosis and esophageal varices. Coronary and short gastric veins were selectively catheterized and obliterated. The examination was performed to stop bleeding in 6 patients and was successful in 5. Follow-up examination showed recanalization of previously obliterated veins in 13 of 16 patients.
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PMID:Follow-up of patients with portal hypertension and esophageal varices treated with percutaneous obliteration of gastric coronary vein. 83 Mar 54

A case is presented which, 9 years after surgical removal of a scirrhous breast cancer, exhibited morphologically atypical metastasis in the liver with fibrosis and reduction of liver parenchyma, as well as typical features of cirrhosis including portal hypertension and esophageal varices. Problems posed by the differential diagnosis and pathogenesis of this rare type of metastasis (known in the literature as metastatic carcinomatous cirrhosis) are briefly discussed.
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PMID:[Liver cirrhosis due to a breast neoplasm metastasis. So-called metastatic-carcinomatous cirrhosis]. 83 63

Bleeding esophageal varices and severe portal hypertension developed in a patient with capillary hemangiomatosis of the spleen. No signs of cirrhosis were found at postmortem examination, and preoperative celiac angiography suggested an intrasplenic shunt as the cause of the high portal pressure. Although a very rare condition, this possibility should be considered in the differential diagnosis of esophageal varices.
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PMID:Portal hypertension and esophageal varices in hemangiomatosis of the spleen. 84 25

Thirty-five Black patients with cirrhosis of the liver were admitted to the professorial unit over a 1-year period and were included in a carefully planned prospective study. Men predominated over women in a ratio of 3:1. Alcohol consumption in the form of African beer was significantly higher in cirrhotic patients than in a control population. The clinical picture was neither predominantly that of alcoholic nor of cryptogenic cirrhosis. Hepatomegaly, porphyria cutanea tarda, ascites, splenomegaly and oesophageal varices were common. There was a complete absence of gynaecomastia, spider naevi and liver palms. Histologically, the majority of patients had macronodular cirrhosis, and only 1 patient had micronodular cirrhosis and minimal fatty change. Hepatitis B surface antigen (HbsAg) was not detected in any patient, despite a positive HbAg rate of 4% in Black African blood donors, determined by means of the same laboratory technique.
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PMID:Cirrhosis of the liver in Rhodesian Blacks. 88 20

Two patients with hepatorenal syndrome were treated by insertion of a peritoneovenous shunt. The renal deficit was corrected rapidly in both cases. A 62-year-old woman with a slow onset syndrome with urine output of 100 to 150 ml/day and urinary sodium excretion of 1 mEq/day responded with large volume urinary output and sodium excretion. She is alive with minimal ascites 18 months after shunt. A 53-year-old man with severe nutritional cirrhosis, alcoholic hepatitis, and eventual massive necrosis was treated for bleeding esophageal varices by portacaval shunt. Postoperative massive ascites progressed to acute hepatorenal syndrome. Insertion of a peritoneovenous shunt reversed the renal deficit. HE eventually exsanguinated due to a hemorrhagic diathesis caused by massive hepatic necrosis.
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PMID:Hepatorenal syndrome: reversal by peritoneovenous shunt. 88

16 patients with acute hepatitis, 18 patients with cirrhosis and a total of 21 volunteers and patients with normal liver function received 7.32 mg/kg hexobarbital by linear intravenous infusion within 60 min. Hexobarbital was determined gaschromatographically in serial blood samples and the hexobarbital-clearance was calculated from the plasma concentration curve versus time. Additional experiments were performed in rats suffering from so called "galactosamine hepatitis". In half of the patients with acute hepatitis a normal hexobarbital clearance could be found. In the other patients this was distinctly reduced but not correlation was found to other liver function tests. Patients with cirrhosis were subdivided into two groups. The patients in group 1 were well compensated. The patients in group 2 had a decompensated state with ascites and oesophageal varices. In nearly all patients with cirrhosis the hexobarbital-clearance was diminished. This was more pronounced in group 2. Ketohexobarbital excretion in healthy subjects was in the range of 40-60% of dose. Patients with acute hepatitis excreted only 10-20% of dose and patients with liver cirrhosis only about 5% of dose. In rats with "galactosamine hepatitis" hexobarbital clearance in vivo was distinctly reduced and this could be explained by diminished microsomal cytochrome p 45- and hexobarbital oxidation rate.
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PMID:[Metabolism of hexobarbital in patients with acute hepatitis and cirrhosis (author's transl)]. 88 88


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