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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Alcoholic liver damage is associated with the development of portal hypertension quite early, as a result of increasing fibrosis. By means of laparoscopic transhepatic manometry (LTM) in the branches of the portal and hepatic veins, we measured the pressure levels in 15 patients with early and transitional-stage alcoholic injury extending to cirrhosis of the liver, and compared them with histological and laboratory investigation criteria. We discovered that parenchymal damage with portal and centrolobular fibrosis already gave rise to some portal hypertension which, compared to a group showing histological changes of remodelling or cirrhosis, constantly increased. In completely developed alcoholic cirrhosis (n = 41), the pressure levels reached a peak. Despite this fact, bleeding from oesophageal varices cannot be predicted. Over the period of observation of 33 months, 4 deaths occurred (portal vein pressure between 4.5 to 5 kPa = 34.0 to 38.8 mm Hg), and three variceal bleedings we were able to manage were seen (pressures between 3.6 to 4.3 kPa = 27.0 and 32.0 mm Hg). Compared to hepatitic cirrhosis the prognosis was slightly more favourable.
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PMID:[Portal hypertension associated with alcoholic liver damage (author's transl)]. 9 37

In 1896, when he was 63 years old, Johannes Brahms, who had always been demonstrably in good health, developed an icterus of increasing intensity together with a considerable enlargement of the liver and loss of weight. Since infectious hepatitis could scarcely come into the question, from the medical point of view a neoplasm in the region of the liver as well as cirrhosis of the liver were considered. While hepatic carcinoma is a relatively rare disease in Europe even today and Brahms, on the other hand, had consumed copious quantities of concentrated alcoholic drinks during his lifetime, cirrhosis of the liver is the most probable diagnosis, especially as at the end hemorrhages from esophageal varices and the lower intestinal segments occurred.
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PMID:[How Johannes Brahms died]. 11 Oct 50

The relationships among collateral veins, gastroesophageal varices, extrahepatic shunting, and free portal pressure were studied by percutaneous transhepatic portography in 57 patients with cirrhosis of the liver. The size of esophageal varices was related to the size of the coronary and short gastric veins and to the portal pressure. The size of gastric varices was related to cephalad collaterals from the spleen and splenic vein, but not to portal pressure. Portosystemic shunting was associated with collaterals in the lower abdomen, but not with varices or portal pressure.
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PMID:Percutaneous transhepatic portography. III. Relationships between portosystemic collaterals and portal pressure in cirrhosis. 11 3

The clinical picture of liver disease in endemic areas of Schistosomiasis mansoni differs in many ways from that observed in alcoholic and other types of cirrhosis. In hepatosplenic schistosomiasis there is predominance of the clinical manifestations of portal hypertension, e.g., bleeding esophageal varices, while ascites, jaundice, and hepatic precoma or coma are much less common. Ammonia tolerance is usually normal and helps explain the low mortality rate during bleeding. Of special interest is the observation of a high incidence of persistent hepatitis B surface antigenemia among patients with hepatosplenic schistosomiasis, suggesting increased susceptibility of such patients to the development of virus-induced chronic active hepatitis.
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PMID:Clinical aspects of hepatosplenic schistosomiasis: a contrast with cirrhosis. 12 11

A sonographic procedure is described which permits accurate determination of liver volume by simple means. Comparison between the sonographic measurements and volume determinations at autopsy carried out by water displacement of the isolated organ showed a statistical error of +/- 1.58% and for average liver volumes of 1,800 ml and 95% limits of confidence of -84 to +20 ml. Quantitation of liver size may be an important clinical measurement, e.g. in assessing the possibility of shunts in the lieno-portal system in portal hypertension with recurrent bleeding from oesophageal varices due to cirrhosis of the liver, for evaluating liver atrophy after shunts affecting the liver, for demonstrating liver size in right heart insufficiency and congestive states or for the control of the effectiveness of cytostatic drugs in lymphatic or haematological disease.
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PMID:[Sonographic determination of liver volume. Problems, methods and practical significance of liver volume measurements (author's transl)]. 16 Dec 56

The authors report their experience of 210 fiber endoscopies carried out as an emergency for upper digestive hemorrhage. They emphasize the necessity of early examination and only consider here examinations carried out within 12 hours from the start of the hemorrhage. In 91.4 % of cases, a correct diagnosis was possible. More than 20% of the patients had at least two lesions liable to cause hemorrhage. In cirrhosis, esophageal varices were the cause of hemorrhage in only 50% of cases.
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PMID:[A propos of 210 emergency endoscopies in upper digestive hemorrhage]. 17 29

Although there have been isolated reports of an acquired abnormal fibrinogen in patients with liver disease, its frequency and clinical significance is not known. In this study 121 consecutive patients with a wide spectrum of hepatic disorders were screened for abnormal fibrin polymerization. A simple colorimetric method using Reptilase was employed. Of 32 patients with proven cirrhosis, 16 (50%) showed abnormal fibrin polymerization. The incidence in decompensated alcoholic cirrhosis was particularly high. The abnormality was also detected in all patients with acute liver failure and seven of 15 with chronic active liver disease. Clinical improvement often correlated with its disappearance. Two patients with primary liver cell tumours demonstrated the abnormal polymerization. In patients with bleeding oesophageal varices the detection of abnormal fibrin polymerization was associated with a poor prognosis. None of the patients with surgical obstructive jaundice (26) or miscellaneous liver disorders (37) had abnormal fibrin polymerization. The occurrence of abnormal fibrin polymerization in liver disease is more frequent than previously suspected and usually signifies severe primary hepatocellular dysfunction. Evidence is presented to support the presence of a primary abnormality of fibrinogen as the cause of impaired fibrin monomer polymerization.
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PMID:Abnormal fibrin polymerization in liver disease. 18 92

The chief causes of liver disease in Ethiopia are reviewed, considering hospital data on admissions for hepatitis, cirrhosis, ascites and hepatoma. Liver diseases account for 11.4% of all medical admissions in 3 medical wards in Addis Ababa. The causes are viral hepatitis, post- hepatic and post necrotic and mixed cirrhosis and hepatocellular carcinoma. Alcoholic cirrhosis is rare. Viral hepatitis with shivering, rigor and fever and elevated direct bilirubin levels are common in Ethiopians, especially in child-bearing women. The hepatitis B surface antigen (HBsAg) is often associated with hepatitis. The disease may be transmitted by several species of mosquitoes, placental transmission, or feces, urine, saliva or semen. Blood products are not screened for hepatitis B. Cirrhosis is common, and causes significant mortality, usually from esophageal varices and hepatic coma. Chronic active hepatitis patients may live for a time, especially if they are near a hospital and are treated with steroids. In Ethiopia presenting symptoms for hepatoma are anorexia, weight loss, persistent, burning, right upper quadrant pain, and a hard, nodular, tender RUQ mass. Over 5% of malignancies seen are primary hepatocellular carcinomas. 50% have HBsAG, compared to 3.8% of controls. 65% have alpha-fetoglobulins. It is suggested that some viral hepatitis cases progress to cirrhosis, of which some go on to hepatocellular carcinoma. Herbal medicines, aflatoxins and other toxins may also contribute to liver disease.
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PMID:Current views on liver diseases in Ethiopia. 20 62

Seven patients with compensated liver cirrhosis and esophageal varices, all with a base line wedge hepatic vein pressure greater than 20 cm H2O, received 1-mg doses of vasopressin hormonogen (tGLVP) intravenously. There was a significant mean decrease in wedge pressure of 32%, which lasted for at least 20 min (the duration of measurement), with no change in cardiac output measured. The only cardiac response was a 10 to 20% bradycardia at the height of the moderate pressor response-otherwise the ECG was without change. In 5 patients who received the same tGLVP dose during surgery, direct measurements of portal venous pressure showed the same degree of decrease within 10 min of intravenous injection. Fifteen patients with liver cirrhosis and severe bleeding from esophageal varices were treated conservatively with blood transfusion and tGLVP as the only major drug aside from antibiotics. A nonrandomized control group of 13 patients with the same age distribution, stage of disease, number of previous bleeds, etc., was treated conservatively in the same manner, except that they received either no hemodynamically active drugs or short acting neurohypophysial peptide preparations such as Pitressin. In the control group there was a 61.5% total mortality, a 53.8% mortality directly related to uncontrollable bleeding, and a mean duration of the bleeding episode of 11 days. In the tGLVP-treated group total mortality was 20%, mortality directly related to uncontrollable bleeding was 13.3%, and mean duration of the bleeding episode was 2.9 days. These results appear to justify a large scale clinical trial of the vasopressin hormonogen in this disease.
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PMID:Action of the triglycyl hormonogen of vasopressin (glypressin) in patients with liver cirrhosis and bleeding esophageal varices. 30 62

In the 10 year period from 1964 through 1973, 25 patients bleeding from esophageal varices underwent ligation procedures coupled with splenectomy rather than a shunt. These procedures included the transesophageal and transgastric approaches and extragastric ligations. For patients with normal liver function, the risk of this urgent or emergency surgery is comparatively low (two of 12 patients died). The chance of recurrent hemorrhage is high (nine of nine surviving patients), as is the need for subsequent surgery (eight of nine patients). Nevertheless, despite these drawbacks, nine of these 12 patients (75 percent) are alive, and seven have survived 5 or more years. In patients with cirrhosis, the initial operative mortality rate (three of 12 patients) and the subsequent mortality rate (five additional patients) reflect the greater risk because of liver disease. Only five of 13 patients (38 percent) survive, three of whom are alive 5 or more years. In patients with cirrhosis, the initial operative mortality rate (three of 12 patients) and the subsequent mortality rate (five additional patients) reflect the greater risk because of liver disease. Only five of 13 patients (38 percent) survive, three of whom are alive 5 or more years after their initial surgery. These results indicate that there are situations when ligation procedures are valuable, especially in the noncirrhotic patient.
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PMID:Ligation procedures in the management of portal hypertension. 30 May 9


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