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 well defined liver diseases in 69 alcoholics and in 71 patients without history of alcoholism the enzymatic findings were compared. Also a group of 43 alcoholics with praedelirium or delirium tremens were examined. In steatosis due to alcohol, the average of GGTP (145 U/l) attains values two times higher than in comparable cases of non-alcoholic origin (73 U/l). In cirrhotics with alcoholism, the average GGTP levels (477 U/l) exceed those obtained in patients with cirrhosis of other origin (110 U/l), four times more. Similar or higher GGTP values were found only in primary biliary cirrhosis. After a period of at least 3 months of abstinence, GGTP values had decreased (to 68 U/l) in the average). The highest values of GGTP were found in acute alcoholic hepatitis and in chronic alcoholics with praedelirium or delirium tremens. GGTP accords diagnostic hints in comparison with other enzymes, as shown by a quotient of GGTP-GPT. GGTP is very helpful for differentiation and long time observation of alcoholic liver disease, especially with regards controlling abstinence of alcohol.
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PMID:[Gamma-glutamyl-transpeptidase in alcoholic liver diseases]. 1 29

Mononuclear-cell responses to liver extracts were studied by a migration-inhibition assay in patients with alcoholic liver disease, viral hepatitis, chronic alcoholism without evidence of liver disease, and in healthy individuals. Patients with acute alcoholic hepatitis demonstrated liver-antigen-induced inhibition of migration (migration index [M.I]equal 0-58 plus or minus 0-08, mean plus or minus S.D.), while patients with cirrhosis, alcoholism, and acute viral hepatitis, as well as healthy volunteers, did not demonstrate such a response (M.I. 0-92 plus or minus 0-13, 0-90 lus or minus 0-10, 0-86 plus or minus 0-18, 0-99 plus or minus 0-04, respectively). It is concluded that cell-mediated immunity to normal or damaged liver tissue may act to perpetuate alcoholic hepatitis and thereby contribute to the development of cirrhosis.
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PMID:Cell-mediated immunity to liver in patients with alcoholic hepatitis. 4 24

A group of 18 chronic alcoholic patients who had sclerosing hyaline necrosis in noncirrhotic livers was compared with a group of 12 similar individuals with acute alcoholic hepatitis, but no centrilobular fibrosis. In cases with sclerosing hyaline necrosis, the most characteristic features were portal hypertension with very large, tender livers and unusually high glutamic-oxalacetic transaminase values; these were associated with centrilobular fibrosis and abundant alcoholic hyalin. Three of these patients died within two years and in two of these, early cirrhosis was found at necropsy. In the cases of acute alcoholic hepatitis, hepatomegaly was the most conspicuous finding, and only a single patient died; death here was unrelated to hepatic disease, the liver being unremarkable at necropsy. Patients who had sclerosing hyaline necrosis tended to remain ill for significantly longer periods. These observations, in conjunction with evidence gathered from the literature, seem to suggest that sclerosing hyaline necrosis is an obligatory step in the natural evolution of alcoholic hepatic disease, especially in cases that evolve into cirrhosis.
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PMID:Sclerosing hyaline necrosis in noncirrhotic chronic alcoholic hepatitis. 6 9

Liver biopsies from 60 patients with acute alcoholic hepatitis (AAH) developing against the background of steatosis, chronic hepatitis and cirrhosis were studied histologically, histochemically and electron microscopically. AAH is characterized by necrosis of hepatocytes with deposition of alcoholic hyalin, obesity of the organ, and polymorphonuclear leukocyte infiltration. Hyperplasia of the smooth endoplasmic reticulum, the appearance of megamitochondria, and an increased amount of peroxisomes reflect the participation of MEOS and the catalase system in alcohol metabolism with a progressive decrease in the activity of alcoholdehydrogenase. Acute alcoholic hepatitis is a connecting link between steatosis and cirrhosis of the liver in which the accompanying autoimmune mechanism and microcirculation disorder followed by activation of lipofibroblasts are conducive to the progression of the pathologic process.
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PMID:[Morphological characteristics of acute alcoholic hepatitis]. 7 56

The results of liver biopsy in 100 patients with tuberculosis are reported. In 8 patients, biopsy only occurred secondarily, during liver disease which appeared during antituberculous treatment. In five cases, the association of rifamycin and isoniazid was probably responsible and the mild histological signs noted suggested a favourable course after stopping one of the drugs or simply reducing the dose. The 3 other patients had virus hepatitis and biopsy was of prognostic interest by revealing the onset of post-hepatic cirrhosis. In 92 cases, liver biopsy was carried out before treatment. In 34 cases the liver was normal, in 38 patients there were hisotlogical changes which did not suggest tuberculosis but, probably, alcoholism. These were : steatosis, in 21 cases, cirrhosis in 8 cases, a mixture of steatosis and cirrhosis in 4 cases, and acute alcoholic hepatitis in 5 cases. Finally, in 20 cases, biopsy revealed an appearance of granulomatous hepatitis. Although this lesion is significant in the development of the disease, it is not characteristic of tuberculosis unless there is caseous necrosis, as in 2 cases, and unless culture of the biopsy material is positive, as in one case out of 9, i.e. the diagnostic interest of liver biopsy is not very great compared with prognostic interest. By determining the anatomical condition of the liver, often not obvious when simple liver function tests are carried out, it permits one to forsee to some extent the tolerance of the liver to antituberculous treatment, especially in alcoholics.
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PMID:[Information obtained by liver biopsy in 100 tuberculous patients]. 17 Jun 85

The present study reported a group of 168 chronically alcoholic patients with a daily ingestion superior to 80 grams. Twenty of these patients (10 percent) did not have liver disease, and 148 (68.5 percent) had different forms of liver disease classified by histopathologic examination. Considering a 97 fi MCV as macrocytosis, we have found in the group of alcoholics without hepatopathy a 50 percent rate of macrocythemia with a mean value of 97.9 fl. In the group of chronic alcoholics with liver disease there was a 64.2 percent macrocytosis with a mean value of 100 fl. We have also studied 43 (21.5 percent) patients with cryptogenetic cirrhosis with a 32.6 percent macrocytosis and a mean value of 93.9 fl. With respect to the alcoholic hepatopathy subgroups, macrocytosis is more frequent in portal fibrosis and acute alcoholic hepatitis, the mean value being higher in the latter. We consider macrocytosis to be frequent among alcoholics, and a good persistence indicator of alcoholic ingestion, pathogenically linked to the now proven dyserythropoietic factor of the alcohol upon the bone marrow. There is no statistically significant correlation between anemia and reticulocytes. We consider macrocytosis to be a more precocious data, and believe that the positive correlation with certain intraerythrocitary enzymes in the juvenile population of red cells corroborates this fact. With respect to the rest of parameters studied there was a correlation with gammaglutamiltranspeptidase, glutamic-oxalacetic transaminase, and the value of prothrombin. The values of mean macrocytosis and elevations of gammaglutamiltranspeptidase and glutamic-oxalacetic transaminase are good persistence indicators of alcoholic ingestion.
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PMID:[Macrocytosis in chronic alcoholism (author's transl)]. 52 26

We have studied the cytotoxicity against rabbit liver cells of lymphocytes from the peripheral blood of 71 patients with various liver diseases. The group with chronic active hepatitis and three patients with acute alcoholic hepatitis showed significantly higher mean values of lymphocytotoxicity (P less than 0.001) compared with the other patients with chronic persistent hepatitis, post-necrotic fibrosis and cirrhosis. Wilson's disease, and prolonged viral hepatitis. The mean cytotoxicity of these last groups did not differ significantly from controls. In four out of six patients with chronic active hepatitis a significant decrease of lymphocytotoxicity was found after immunosuppressive therapy with oral prednisolone. A good correlation between the lymphocytotoxicity test and histological signs of activity suggests that a cell-mediated immune aggression is present in this disease.
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PMID:Lymphocytotoxicity test against rabbit hepatocytes in chronic liver diseases. 63 39

Approaches for the diagnosis of alcoholic cirrhosis of the liver at the dissecting table are given on the basis of the analysis of autopsy materials and liver biopsies. The etiological verification of cirrhosis is based on the peculiar morphological lesions of the liver and other organs. The liver is enlarged, its surface micronodal; histologically, an attack of acute alcoholic hepatitis is found not infrequently: necroses of hepatocytes, predominantly neutrophilic infiltration of the stroma and necrotic zones, alcoholic hyalin. Due to autolysis, alcoholic hyalin in the autopsy material changes somehow and is hardly detectable. A combination of alcoholic cirrhosis of the liver with alcoholic cardiopathy and/or chronic calcifying pancreatitis is typical.
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PMID:[Diagnosis of alcoholic liver cirrhosis during autopsy]. 72 69

Acute alcoholic hepatitis is an anatomical (fatty liver with sclerosing hyaline necrosis) and a clinical (hepatomegaly with a variety of symptoms of hepatic failure) entity arising out of chronic alcoholism, and of a typically 'pre-cirrhotic' state. Although fatal in 25% of acute cases due to failure of homeostasis, it often leaves a centrilobular scarring necrosis which in more than 60% of cases progresses to nodular cirrhosis. Continued alcoholism worsens the prognosis. Alcoholic hepatitis may be confused with acute abdominal catastrophes or with a hepatoma. The characteristic Mallory bodies found on liver biopsy are found rarely in non-alcoholic hepatitis. There is no effective treatment for this disease except reduction of alcohol intake; indeed, the disease may become self-perpetuating.
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PMID:[Acute alcoholic hepatitis]. 92 58

A total of 42 biopsy specimens of the liver (blind and spot) in 32 patients with alcoholic cirrhosis of the liver were investigated. Morphological, portal, postnecrotic, and mixed types of cirrhosis were established. The portal type of cirrhosis is most common. On the basis of repeated analyses of biopsy materials of the liver it may be assumed that the development of cirrhosis of the liver of alcoholic etiology is connected with multiple attacks of acute alcoholic hepatitis. Abstention from alcohol consumption resulted in stifestations of exacerbation of cirrhosis. On the other hand, continuation of alcohol consumption contributed to progressing of cirrhosis, which following several attacks of alcoholic hepatitis, may change its morphological type: portal cirrhosis "transforms" into the postnecrotic or mixed type. The data obtained clarified the role of ethanol in progressing alcoholic cirrhosis of the liver, which according to the initial mecranisms of its development in postnecrotic, since every attack of acute alcoholic hepatitis is accompanied by coagulative (fields of alcoholic hyaline, or Mallory's bodies), or by colliquative (balloon dystrophy) necrosis of hepacytes.
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PMID:[The morphology and morphogenesis of alcoholic cirrhosis of the liver]. 127 77


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