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 eight patients with cirrhosis of the liver and portal hypertension an intravenous infusion of lysine vasopressin induced a rapid increase in the plasma level of the fibrinolytic proenzyme plasminogen activator. In contrast, triglycyl lysine vasopressin (glypressin; GVP), in a dose known to lower portal venous pressure, produced no fibrinolytic response. This lack of fibrinolytic response represents an advantage of GVP over lysine vasopressin in addition to its longer in vivo half-life and lower cardiotoxicity. Clinical trials of GVP in the treatment of bleeding oesophageal varices are needed.
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PMID:Effects of lysine vasopressin and glypressin on the fibrinolytic system in cirrhosis. 48 51

184 autopsy cases with liver diseases were examined clinicopathologically with special reference to the incidence and distribution of microthrombi and classic thrombi in various organs. Microthrombi and/or classic thrombi were found in one or more organs in 50.0% to 59.4% of the patients with various liver diseases. But only 4 among 184 patients had many microthrombi in more than three organs and the incidence of disseminated intravascular coagulation seemed to be low in autopsy cases with liver diseases. Incidence of microthrombi showed no significant difference in the groups with and without portal vein thrombosis. Hemorrhage in the upper alimentary tracts of the patients with liver cirrhosis did not seem to develop by disseminated intravascular coagulation. Consumption of clotting factors in liver diseases seemed to occur by thrombus formation in portal vein and esophageal varices and by hemorrhage in various organs.
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PMID:Intravascular coagulation in autopsy cases with liver diseases. 50 65

Twenty patients with portal hypertension due to cirrhosis were examined by esophagoscopy and percutaneous transhepatic esophageal phlebography. Esophageal varices were found in 18 cases at endoscopy and in 19 cases at esophageal phlebography. There was little correlation between the findings of the two methods with respect to the size and number of esophageal varices. At endoscopy the subepithelial and submucosal varices were reliably detected. At esophageal phlebography differentiation between intrinsic (i.e. subepithelial and submucosal veins) and peri-esophageal veins was not possible. Negative findings at esophageal phlebography do not rule out esophageal varices.
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PMID:A comparative study of esophageal varices by endoscopy and percutaneous transhepatic esophageal phlebography. 51 Aug 67

In 93 patients with cirrhosis of the liver and portal venous hypertension the main tributaries of the portal vein were examined by percutaneous transhepatic catheterization. The appearance and degree of porto-systemic collaterals were analysed. Esophageal varices were demonstrated in 82 patients. No correlation was found between the portal venous pressure and the extent of porto-systemic communications.
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PMID:Porto-systemic collaterals in cirrhosis of the liver. Selective percutaneous transhepatic catheterization of the portal venous system in portal hypertension. 54 69

Regencrative nodular hyperplasia (RHN) is a rare condition, the diagnosis of which is based upon histological findings. It is seen in Felty's syndrome with portal hypertension (PHT), as was the case in the patient reported here. This was a 72-year-old man, with long standing rheumatoid arthritis, hepatosplenomegaly, a neutrophil leucopaenia and oesophageal varices responsible for recurrent haematemeses. Despite a portocaval anastomosis, the patient died from postoperative acute hepatic failure. Histological study revealed changes in the hepatocytes and the reticulin system typical of RNH without cirrhosis. The relationship between Felty's syndrome and RHN, as well as the mechanism of the hypertension, are discussed in the light of cases from the literature.
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PMID:[Anatomo-clinical study of a case of regenerative nodular hyperplasia of the liver with Felty's syndrome and portal hypertension]. 54 55

The frequent occurrence of abnormal fibrin polymerisation in patients with liver disease has recently been reported. To investigate this further, fibrin polymerisation was studied in 68 patients with cirrhosis or chronic active liver disease. Thirty-three of these patients demonstrated impairment of this phase of blood coagulation. When other tests of liver function were compared in patients demonstrating this abnormality and those in whom fibrin polymerisation was normal, it was found that the former group demonstrated significantly reduced albumin concentrations (p less than 0.0002), raised bilirubin and aspartate aminotransferase levels (p less than 0.0006 and less than 0.003 respectively), and greater prolongation of the one-stage prothrombin time (p less than 0.001) with more marked reduction in factor VII levels (p less than 0.002) compared with the latter patients. It is concluded that defective fibrin polymerisation occurring in patients with liver disease indicates the presence of severely impaired hepatocellular function. This might account for the grave prognosis reported in cirrhotic patients with abnormal fibrin polymerisation who also suffer bleeding from gastro-oesophageal varices.
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PMID:Association of abnormal fibrin polymerisation with severe liver disease. 59 Aug 52

A case of hepatic artery portal fistula, presenting with bleeding esophageal varices five months following a liver biopsy for cirrhosis, is presented. The angiographic features of the lesion are illustrated and the pertinent literature concerning etiology of hepatic arterioportal shunts is reviewed.
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PMID:Hepatic arterioportal fistula related to a liver biopsy. 61 27

A new operation for selective or total decompression of the portal venous system in cases of intrahepatic portal hypertension is described. It involves interposition of a large-caliber Dacron graft between the splenic vein and the inferior vena cava. The graft-interposition splenocaval shunt is performed readily and quickly, satisfying the variable hemodynamic needs of patients with portal hypertension. It can be either selective (S-SCS) or total (T-SCS) from the beginning, or a T-SCS may be converted subsequently to a S-SCS should surgically induced hepatic decompensation supervene. It is less demanding technically than distal splenorenal shunt (D-SRS). The S-SCS conserves portal venous perfusion of the liver, preserves hepatocellular function and architecture at the preoperative levels, avoids precipitation of postshunt portal-systemic encephalopathy, and decompresses gastric-esophageal varices with prevention of further variceal bleeding even better than D-SRS. One hundred percent graft patency has been obtained, and the surgical results have been superior to those following portacaval shunt in patients with large liver blood flow and relative benignity of the liver disease, be it cirrhosis or noncirrhotic portal fibrosis. In patients with advanced cirrhosis, variceal bleeding, and small liver blood flows, T-SCS would be indicated. Patients of this category obtained inferior surgical results and had operative deaths (16.7%) following S-SCS. The concept of the operation has merits and deserves further evaluation.
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PMID:Graft interposition splenocaval shunt for total or selective decompression of portal hypertension. 62 91

A variety of indirect techniques has been claimed to provide evidence of spontaneous reversal of portal blood flow in hepatic cirrhosis but the existence of the phenomenon has been doubted by some who do not accept the validity of the indirect evidence. There are few reports of the demonstration of hepatofugal portal flow by selective hepatic arteriography, which is the only acceptable technique. We report three patients with histologically confirmed cirrhosis in whom hepatofugal portal blood flow was unequivocally demonstrated by arteriography, in whom no surgical portosystemic shunt had been performed and in whom there was no evidence of the Budd-Chiari Syndrome or hepatoma, situations accepted as associated with reversed portal blood flow. Theoretical considerations suggest that shunt surgery for bleeding esophageal varices should not be ruled out on the grounds of hepatofugal portal flow. However, end-to-side portacaval anastomosis and distal splenorenal shunt might predispose to the early redevelopment of esophageal varices when reversed portal flow is present. Side-to-side portacaval and conventional splenorenal shunts might be preferable in having less effect on hepatic parenchyma perfusion than when orthograde portal flow in the case.
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PMID:Hepatofugal portal blood flow in hepatic cirrhosis. 62 19

Congenital membranous obstruction of the inferior vena cava is a rare phenomenon resulting from failure of anastomosis between the right subcardinal vein and the liver. A case is reported in which the presenting symtpom was bleeding from esophageal varices. Cirrhosis was present and other signs of vena caval obstruction were minimal. The diagnosis was made only after an ineffective mesenterico-caval shunt had been performed. Venacavography or pressure measurements in the inferior vena cava are mandatory before attempting a porta-systemic shunt operation.
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PMID:Congenital membranous obstruction of the inferior vena cava. 64 Aug 19


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