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 a prospective study 148 consecutive patients with biopsyproved acute viral hepatitis were observed serially and followed for 5 years. They were divided into three groups on the basis of being treated with high or low doses of gamma globulin and compared with a control group, not treated. As the efficacy of gamma globulin for the prophylaxis or modification of infectious hepatitis has been well documented by many investigators during the past 25 years, we were interested in evaluating the therapeutic effect of gamma globulin on the course of viral hepatitis. The purpose of the study was to determine the comparative efficacy of various doses of gamma globulin in preventing complications and in influencing the severity and the length of time of acute viral hepatitis and in preventing the development of chronic hepatitis and cirrhosis. For controlling the clinical, biochemical and histopathologic course 12 functional parameters were repeatedly measured under stable clinical conditions and 3--12 liver biopsies were performed in an individual patient using the Menghini needle with an intercostal approach. During the 5-year trial an overall of 825 liver biopsis were performed with this 148 patients. We conclude from this study, that in about 80% of patients with acute viral hepatitis recovery is complete, but takes several month's. A protracted course of 4 month's duration until recovery was found in 45 patients (30,4%), persistent hepatitis with recovery after 1--4 years duration occurred in 37 patients (25%), global liver necrosis with hepatic coma in 3 (2,3%), chronic hepatitis in 22 (14,8%), 8 of them as chronic aggressive hepatitis and cirrhosis in 3 (2,3%). The study demonstrated no therapeutic efficacy of gamma globulin in modifying the course or preventing complications of both AuAg+ and AuAg-neg. acute viral hepatitis in man. There was no striking difference in the groups treated with various doses of gamma globulin compared with a control group.
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PMID:[Gamma globulin therapy of acute viral hepatitis. Studies on the therapeutic effect of gamma globulin on the course and late prognosis of manifested acute viral hepatitis in man]. 5 14

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

A new precipitating antigen-antibody system possibly was demonstrated by immuno-diffusion in the serum of patients suffering from non A-non B hepatitis. The antigen appears during the first four weeks of transaminases elevation. In acute cases was transient antigenemia (average 3 weeks). Antibodies appeared rapidly after the disappearance of antigen. The same antigen was also detected, by immunodiffusion and by immunofluorescence, in the liver nuclei of infected hepatocytes. This antigen specific appears for non A-non B hepatitis since it is neither found in the serum of normal subjects nor in that of patients with cirrhosis toxic or viral that hepatitis A or B. The hypothesis of a virus associated antigen is the most likely explanation.
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PMID:[Demonstration of a serum and liver antigen in acute or chronic non A-non B viral hepatitis]. 12 Sep 41

Serum vitamin B12 and vitamin B12 binding proteins (transcobalamins, TCS) were determined in patients with malaria, amoebic liver abscess, carcinoma of the liver, infectious hepatitis, cirrhosis and chronic myelocytic leukemia (CML) as well as in 60 blood donor subjects. Serum vitamin B12 in patients with infectious hepatitis, cirrhosis and CML were higher than that of the normal subjects. The values of unsaturated vitamin B12 binding capacity (UBBC) in patients with carcinoma of the liver, infectious hepatitis, cirrhosis were lower while that of patients with CML were higher than that of the normal subjects. A markedly increased TCI and decreased TCII was observed in patients with CML while these changes was much less in patients with other liver diseases. The difference was possibly due to a flooding of vitamin B12 from damaged liver cells into the circulation and the decreased synthesis of transcobalamins in patients with liver diseases while the increased granulocytes, the source of TCI, was much increased in patients with CML.
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PMID:Vitamin B12 and vitamin B12 binding proteins in liver diseases. 60 23

329 patients with acute ouvert viral hepatitis which occurred in the Hannover area 1975 were classified according to virological data. The proportions of type A and type non A - non B hepatitis were each approximately 20 percent of the total cases (n = 60). Viral hepatitis B was the most frequent type of viral hepatitis (n = 209). 174 individuals of the 329 hepatitis patients were reexamined serologically two years after the onset of the acute disease. 7 out of 105 patients with hepatitis B (6,7%) and 5 out of 40 patients with hepatitis non A - non B (12,5%) revealed a serological pattern compatible with chronic hepatitis. In contrast none of 29 patients with hepatitis A indicated chronic liver disease. The frequency of anti-HAV was also determined in 41 patients with HBsAg positive and HBsAg negative histologically proven chronic hepatitis or liver cirrhosis. All patients were under 35 years of age. An equal proportion of anti-HAV was found in both groups. These results suggest that hepatitis A practically never results in chronic hepatitis, while hepatitis non A - non B can run a chronic course with a frequency similar to that of hepatitis B.
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PMID:[Chronic hepatitis as sequela of acute viral hepatitis A and hepatitis non A - non B (author's transl)]. 74 46

The heterogeneity of the clinical responses to hepatitis A and B infection is well known, and may in part relate to different etiologic agents (hepatitis A, B, "C", etc.) as well as to the individual hosts' immune responses. The spectrum of disease ranges from anicteric asymptomatic infections to fulminant hepatic necrosis with hepatic failure and death. Although the clinical presentation is varied, there are essentially two patterns of necrosis that can be seen histologically during the first few weeks of clinical symptoms. The more common pattern is focal, and necrosis is scattered throughout the hepatic lobule. Less commonly, zones of necrosis that bridge between the portal--portal or portal--central areas of the lobule develop. When the latter process (bridging necrosis) is extensive, confluent lobules may be destroyed. Patients with focal patterns of necrosis eventually recover without sequelae, whereas a sizable proportion (30-60%) of patients who have bridging or multilobular necrosis progress to chronic active hepatitis, postnecrotic cirrhosis, or progressive hepatocellular failure. There is increasing evidence that these widely differing clinical and histologic responses to hepatitis infection may be related to differences in the immune response.
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PMID:The diagnosis and pathogenesis of clinical variants in viral hepatitis. 80 49

Oral glucose tolerance tests (100 g glucose) and the intravenous tolbutamide test were carried out. The glucose tolerance was seen to be disordered even in acute infectious hepatitis, but returning to normal when cured. If chronic hepatitis develops, however, the proportion of manifest diabetes increases to 7.2% in chronic persistent hepatitis and to 16.3% in chronic progressive hepatitis, while 30% each have latent diabetes. The glucose tolerance is most impaired in fatty liver (stage III) and in active cirrhosis of the liver with portal hypertension, where more than half of all patients present manifest or latent diabetes. Conversely, glucose tolerance improves even in chronic hepatitis and in cirrhosis of the liver as the inflammatory activity subsides. The main cause for the development of "liver diabetes" is therefore likely to be the activity of the inflammatory process, the extent of portal hypertension, disorders of glucose regulation in the liver and the increased insulin inactivation in the cirrhotic liver.
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PMID:[Disorders of glucose tolerance in 2600 histologically confirmed acute and chronic liver patients (author's transl)]. 81 Jun 95

Using a micromethod, hepatic bilirubin UDP-glucuronyl transferase has been assayed in percutaneous needle biopsy samples obtained from patients with infectious hepatitis, postnecrotic cirrhosis, Gilbert's disease, noncirrhotic portal fibrosis (NCPF), granuloma of the liver, and extrahepatic portal vein obstruction. The results were compared with those obtained from 10 control subjects. Patients with cirrhosis and infectious hepatitis revealed normal bilirubin transferase levels, whereas those with Gilbert's disease showed significantly low enzyme levels. Many patients with NCPF, some with extrahepatic portal vein obstruction, and patients with granulomatous involvement of the liver demonstrated significantly low levels. This low hepatitic-enzyme activity was not associated with hyperbilirubinemia. The mechanism of such low values in NCPF and other disorders is not known. It is postulated that low heaptic-enzyme activity in noncirrhotic portal fibrosis is due to sparse smooth endoplasmic reticulum. This study also emphasizes that serum bilirubin may remain normal with very low hepatic-enzyme activity. Although induction of the microsomal enzyme bilirubin transferase was observed following phenobarbitone administration in noncirrhotic portal fibrosis, this was not apparent in patients with cirrhosis, possibly due to maximal enzyme induction having been achieved by endogenous substrate.
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PMID:Estimation of hepatic bilirubin UDP-glucuronyl transferase in patients with noncirrhotic portal fibrosis and liver disease: Significance and limitations. 81 Nov 12

It is reported on the dispensary care of 789 patients suffering from infectious hepatitis. Of these patients 92.86% healed completely of hepatitis during observation. 2.91% developed sequels after hepatitis, among them 1.03% a posthepatitic hyperbilirubinaemia, 1.03% a chronic persistent hepatitis, 0.17% a chronic aggressive hepatitis, 0.34% a liver cirrhosis, 4.25% had concomitant diseases, such as fatty degeneration of the liver, diseases of the bile duct, pancreatitis, and ventricular ulcer. The probable associations of these diseases with infectious hepatitis are discussed. Three patients suffered from diabetes mellitus. One of these patients developed a chronic aggressive hepatitis and finally an incipient cirrhosis.
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PMID:[Results of 10 years hepatitis follow-up]. 87 28

40 patients with infectious hepatitis, 25 with chronic aggressive hepatitis, 25 with compensated liver cirrhosis, and 10 with decompensated liver cirrhosis were submitted to examination. The following abnormalities depending upon the stage and severity of hepatic diseases were found: a) disturbances of total lipids, cholesterol, phospholipids, beta-lipoproteids, glycerin, glycerides and neutral fats concentrations; b) marked disorders of glucose tolerance as indicated by the difference between plasma and erythrocyte glucose levels increasing in proportion to the degree of liver damage; c) a fall in plasma and erythrocyte magnesium reflecting the degree of hepatic parenchyma damage; d) a decrease of the albumin/gamma-globulin ratio in proportion to the degree of the impairment of hepatic cells. The presented fat, carbohydrate, magnesium and protein balance indices yield better criterions for the differential diagnostics of hepatic diseases than the routine investigations, and they also make possible objective prognosis.
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PMID:Disturbances of fat, carbohydrate, magnesium and protein balance in liver diseases. 88 63


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