Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many reports have demonstrated an elevation of circulating carcinoembryonic antigen (CEA) in the majority of patients with alcoholic liver disease and, less frequently, in patients with nonalcoholic liver disease. Several explanations for this finding have been proposed, eg, increased production or release of CEA by the damaged liver, decreased hepatic metabolism, or diminished excretion of CEA of extrahepatic origin. In an attempt to clarify the mechanism of CEA elevation in liver disease, we have compared the CEA plasma level as measured by radioimmunoassay with CEA demonstrable in liver tissue by the indirect fluorescent antibody technique in 7 patients without significant changes in the liver biopsy specimen, 23 patients with alcoholic liver disease, and 16 patients with miscellaneous liver diseases such as acute or chronic nonalcoholic hepatitis or extrahepatic biliary obstruction. The mean CEA plasma level in patients with alcoholic liver disease was significantly higher than in patients with nonalcoholic liver disease (8.8 +/- 9.5 vs 2.7 +/- 2.5 ng/ml; P less than 0.02). In normal liver tissue, CEA was observed in the apical cytoplasm and along the luminal surface of bile duct epithelial cells, suggesting that under normal conditions CEA accumulates in and is excreted by bile ducts. In patients with alcoholic hepatitis and/or cirrhosis there was marked bile ductular proliferation and prominent cytoplasmic CEA-specific staining and both were associated with elevated CEA plasma levels in more than 80% of cases. In the group of miscellaneous liver diseases, bile ductule counts and CEA-specific staining did not correlate with CEA plasma levels. These observations suggest that proliferating bile ductules contribute to elevated plasma CEA in alcoholic patients.
 ...
PMID:Carcinoembryonic antigen in normal and diseased liver tissue. 35 25

Chronic alcohol consumption results in early biochemical and ultrastructural alterations of the hepatocyte which in turn may lead to alcoholic fatty liver as well as alcoholic hepatitis and via the central hyaline sclerosis to fibrosis and cirrhosis of the liver. Already at the stage of the alcoholic fatty liver an isolated increase of serum gamma-glutamyltransferase activity can often be observed; it results from hepatic microsomal enzyme induction and may facilitate early recognition of alcoholic liver injury. To establish the diagnosis, however, a histological examination of the liver is necessary. The therapy of alcohol-induced liver injury is based upon an absolute alcohol abstinence since alcohol itself or one of its metabolites are hepatotoxic.
 ...
PMID:[Clinical aspects of alcohol induced liver injury (author's transl)]. 35 67

Sera of twenty-five patients with alcoholic liver disease and forty normal control sera were screened for circulating immune complexes by means of the anti-antibody neutralization test and by Raji-cell membrane immunofluorescence assay. IgG-containing immune complexes were detected in thirteen out of twenty-five patients with alcoholic liver diseases and in one out of forty normal individuals; in addition, IgA-containing complexes were demonstrated in seven out of thirteen sera positive for IgG complexes. The presence of immune complexes was restricted to alcoholic hepatitis and active cirrhosis, thus indicating a relationship with disease severity.
 ...
PMID:Detection of circulating immune complexes in alcoholic liver disease. 37 31

The relative importance of malnutrition and alcohol toxicity in the pathogenesis of cirrhosis has been controversial. In epidemiological studies the incidence of cirrhosis can be correlated with the duration and amount of alcohol imbibed. The importance of nutrition has been discounted. In these studies few analyses of dietary intake were included. Diets of patients with alcoholic cirrhosis characteristically are poor. Furthermore, alcohol toxicity impairs nutrition by interfering with absorption, transport, and utilization of essential nutrients. Patients with cirrhosis respond favorably to nutritious diets despite the concurrent intake of alcohol, although in lesser amount than their usual intakes. In long-term studies highly nutritious diets have protected rats against cirrhosis from alcohol. However, in acute experiments with "loading" doses there was evidence of direct hepatotoxicity in animals and man. Recently, cirrhosis has been produced in baboons with alcohol and a diet considered adequate. The findings are important, but there is some question whether dietary factors (imbalance) may have played a role. Also of recent interest has been the occurrence of lesions simulating alcoholic hepatitis and cirrhosis after jejunoileal bypass surgery. The evidence suggests that malnutrition may have been a major factor in this disease. The roles of alcohol toxicity and of malnutrition in the pathogenesis of cirrhosis are not fully understood. Further studies are needed to clarify these relationships.
 ...
PMID:Alcohol, malnutrition, and alcoholic cirrhosis. 37 14

Alcoholic steatosis was associated with sclerosis around the terminal hepatic venules in liver biopsies of 40% of chronic alcoholics but not in those of moderate drinkers. To determine whether this sclerosis could be a precursor lesion of cirrhosis, controlled studies were performed in animal models. In the alcohol-fed baboons that developed fibrosis or cirrhosis, progressive perivenular sclerosis invariably started at the fatty liver stage before or even more commonly in the absence of alcoholic hepatitis. No sclerosis occurred in controls or in alcohol-fed baboons and rats that did not progress beyond the fatty liver stage. The clinical and experimental data indicate that sclerosis around the terminal venules, a common but often overlooked complication of alcoholic fatty liver, reflects heavy prolonged drinking, and may identify those patients who are susceptible to develop the more advanced lesions of alcoholic liver injury upon continued drinking.
 ...
PMID:Early perivenular sclerosis in alcoholic fatty liver: an index of progressive liver injury. 40 18

Ninety patients with chronic diffuse liver disease were evaluated with free hepatic venography, wedge hepatic venography, hepatic vein pressure measurements, and liver biopsy. Free hepatic venograms were normal and minimally pruned in patients with hepatic sarcoidosis and fatty liver due to alcohol, and their biopsies showed little or no fibrosis. Pruning of hepatic vein branches on free hepatic venography correlated well with the corrected wedged hepatic vein pressure and with the degree of fibrosis in patients with alcoholic hepatitis, alcoholic cirrhosis, and postnecrotic cirrhosis. Free hepatic venography correlated better with hemodynamic measurements and fibrosis than did wedge hepatic venography. Free hepatic venography is a reliable predictor of the presence and degree of hepatic fibrosis and may be a useful alternative to liver biopsy in patients with clotting disorders.
 ...
PMID:Hepatic venography and wedge hepatic vein pressure measurements in diffuse liver disease. 40 97

In two simultaneously-taken needle biopsies of the liver from 70 consecutive patients, a number of changes were evaluated semiquantitatively and compared in n x m tables. The lesions examined were steatosis, Mallory's hyalin, alcoholic hepatitis, cirrhosis and cholestasis; furthermore the size, amount of inflammatory cells, connective tissue and bile-duct proliferation of the portal tracts and finally focal necroses and acidophilic bodies in the lobules were recorded. Cirrhosis, cholestasis and steatosis showed a high correlation, while the agreement between the two interdependent biopsies, especially concerning acidophilic bodies and bile-duct proliferation, was low. Possible reasons for the variation in the agreement of the lesions are discussed.
 ...
PMID:The variation of pathological changes in the liver evaluated by double biopsies. 42 6

Sampling variability of liver biopsy was determined in three consecutive biopsy specimens obtained from each of 118 patients immediately prior to autopsy. No sampling variability was found for fatty liver, alcoholic hepatitis, nonspecific hepatitis, fulminant hepatitis, leukemic infiltrate, and venous congestion. Cirrhosis was diagnosed in 80% of cases at the first biopsy but in all cases after three biopsies. Chronic aggressive and chronic persistent hepatitis were diagnosed correctly in two of three cases each at the first biopsy, and in all cases after three biopsies. Metastatic carcinoma was detected in 46% of cases at the first biopsy and in 69% after three biopsies. Granulomas were missed once on the first biopsy, but found on a subsequent biopsy. The amounts of fat and fibrosis in the biopsy specimens often were not representative of the amounts present at autopsy.
 ...
PMID:Sampling variability on percutaneous liver biopsy. 44 70

Chronic hepatitis is one of liver diseases with arguments from the clinical and histopathological aspects. Histopathological examinations were made on 687 biopsy cases clinically diagnosed as chronic hepatitis. Histopathological classification was based on our own criteria by referring to discussions in the series of Inuyama symposia on hepattis and others. The correlation between histological diagnosis and clinical data was also examined. Histopathological diagnoses made of the 687 cases were classified as follows; normal liver or liver with no pathognomonic changes of 77 cases (11.2%), non-specific reactive hepatitis of 56 cases (8.0%), viral hepatitis of 488 cases (71.0%), alcoholic hepatitis of 25 cases (3.6%), fatty liver of 23 cases (3.3%), massive liver necrosis of 3 cases, liver fibrosis of 2 cases, congestive liver of 1 case, and unclassified 12 cases due to inadequate specimens or other reasons. Among 488 viral hepatitis cases, histological stages were as follows; acute hepatitis (38 cases, 7.8%), persistent hepatitis (23 cases, 4.7%), chronic inactive hepatitis (142 cases, 29.1%), chronic active hepatitis (165 cases, 33.8%), chronic hepatitis with subloblar necrosis (33 cases, 6.8%), precirrhosis (51 cases, 10.5%), cirrhosis (27 cases, 5.5%). The relationship between histological aspects and clinical features was discussed by sex, age, and others. Of 41 follow up cases, significant values of histological type, presence of HB ag., or alcoholic were discussed as for the causative factors evolving liver cirrhosis.
 ...
PMID:[Chronic hepatitis--clinicopathological studies of 687 cases (author's transl)]. 46 98

Thirty patients with alcoholic cirrhosis, ascitic during 13.6 +/- 13 months (mean +/- S.D.) were cured of ascites and followed up during 2 to 9 years (4.3 +/- 2.7 years). Twenty six were compared with a same number of cirrhotics, matched for age and sex, who died during the year after the first admission. Many biological data show statistical difference. Nevertheless no valuable prognosis can be predicted in an individual case. The clinical improvement is associated with major, sometimes total biological recovery. Other complications of cirrhosis (gastro-intestinal bleeding, hepatoma) may occur (7 cases with 5 deaths) or alcoholic hepatitis if alcohol withdrawal is stopped (3 cases, 2 deaths). Some associated diseases look unexpectedly frequent: diabetes (4 cases), obesity (9), nodular lipomatosis (14 cases) whose frequency looks higher than that can be calculated for a similar group of healthy subjects.
 ...
PMID:[Recovery after treatment for cirrhotic ascites : a study of 90 cases. Frequency of arterial hypertension (author's transl)]. 49 44


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>