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)

Serum gamma-glutamyl transpeptidase (gamma-GT) level was estimated in 132 patients with different liver diseases (chronic persistent and chronic active hepatitis, postnecrotic cirrhosis, chronic alcholic hepatitis and alcoholic cirrhosis, cholestasis syndrome, fatty liver, Gilbert disease) and malignancies with and without liver involvement. The gamma-GT levels were compared with the values for serum bilirubin, transaminases (GOT, GPT) and alkaline phosphatase in the same patients. gamma-GT values were normal in chronic persistent hepatitis and increased in chronic active hepatitis. Very high activities were measured in chronic alcoholic cirrhosis in contrast to postnecrotic cirrhosis. gamma-GT proved to be more sensitive than alkaline phosphate as an index of cholestasis and liver involvement in malignancies. It is suggested that gamma-GT activity offers valuable aid in differential diagnostics of liver-diseases. gamma-GT being an inducible enzyme, its activity may be raised by enzyme inducing drugs also in subjects without liver disease.
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PMID:Serum gamma-glutamyl transpeptidase: its clinical significance. 2 44

A number of clinical, biochemical, immunological and morphological variables were recorded at first admission of 500 consecutive patients with biopsy verified acute viral hepatitis in the period February 1969-June 1972. In February 1973, 28 of these patients had a morphologically documented chronic liver disease: 4 cirrhosis of the liver, 15 chronic aggressive hepatitis, and 9 chronic persistent hepatitis. 74 patients were followed up until morphological normalization took place. The initially recorded variables in the two groups were compared, and the following factors were significantly higher in the group with subsequent development of chronic liver disease:--frequency of drug addicts, median of the highest gammaglobulin, ANA, SMA, partial destruction of the limiting membrane, incidence of piecemeal necrosis, and pronounced plasma cell infiltration in the portal tracts. These preliminary results suggest that factors in the initial phase of acute viral hepatitis can be helpful to some extent in predicting the course and prognosis of the disease.
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PMID:Acute viral hepatitis: factors possibly predicting chronic liver disease. 4 92

Chronic liver disease developing after acute hepatitis type B is well documented, but is not thought to occur after acute hepatitis due to other viruses. However, follow-up of 29 patients in a haemodialysis unit who contracted HBsAg-negative acute hepatitis during 1968-70 revealed 8 cases with raised serum-aminotransferase levels dating from that time. Liver biopsy in 7 of these disclosed chronic aggressive hepatitis in 3, of whom 2 had already progressed to advanced cirrhosis. Chronic persistent hepatitis was present in 2 others, and the remaining 2 had non-specific hepatitis in association with massive iron overload. Immunological studies demonstrated a higher frequency of cellular immunity to HBsAg in those who had previously had acute hepatitis than in those who had not, although the prevalence of humoral antibody was similar in the two groups. One possible explanation for these findings is the presence of immunological cross-reaction at a cellular level between the hepatitis B virus and that responsible for the initial outbreak.
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PMID:Chronic liver disease developing after outbreak of HBsAG-negative hepatitis in haemodialysis unit. 5 71

"e" is a serum antigen associated with type-B hepatitis. It is found only in hepatitis B surface antigen (HBsAg) positive sera, but is antigenically distinct from HBsAg. e antigen was not detected in the serum of any of 99 cases of acute type-B hepatitis who recovered normally. Its antibody, anti-e, was found in 14 (14%). The antibody usually appeared before clearance of HBsAg and before appearance of HBsAb. Serum e was not detected in any of 29 symptom-free carriers of HBsAg, but 21 (73%) showed anti-e. Serum e was found in chronic active hepatitis (44%) and chronic persistent hepatitis (31%). The antibody, however, was detected in only 2 of 79 patients with chronic active hepatitis but in 7 (44%) of chronic persistent hepatitis. Serum e was not found in 5 patients with primary liver-cell carcinoma or 5 with inactive HBsAg-positive cirrhosis. The antibody was, however, found in all 5 of those with inactive cirrhosis and in 4 of the 5 with primary cancer. These results suggest that the presence of e antigen is associated with active and usually continuing liver disease. Anti-e, however, is associated with inactive liver disease and asymptomatic carriage of HBsAg, and its presence must be regarded as a valuable sign in predicting those who will escape progressive chronic liver disease.
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PMID:Incidence and clinical significance of e antigen and antibody in acute and chronic liver disease. 5 57

Follow-up study of 40 children suffering from chronic hepatitis. The diagnosis was made by liver needle biopsy with the Menghini method, when clinical signs or laboratory data of liver disease had lasted for more than 6 months. 24 patients showed the histological pattern of the aggressiv type of chronic hepatitis according to the definition of the European Association for the Study of the Liver (1968). In this group only 5 children had autoantibodies in the serum (so-called lupoid hepatitis). The HBAg positive courses played the most important part in the chronic persistent group as well as in the aggressive one. According to literature only the patients with the aggressive type have been treated with prednison, because chronic persistent hepatitis has a good prognosis without any treatment. In nearly all cases high transaminases and gammaglobulin levels decreased during the treatment with prednison, whereas the histological signs of inflammation seldom changed. Cirrhosis of the liver has developed in 2 HBAg positive patients of the aggressive group, who had not consequently received their daily dose of prednison.
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PMID:[Studies on juvenile chronic hepatitis]. 5 74

One hundred liver biopsies from 100 patients with clinical presumptive diagnosis of hepatitis were examined by immunofluorescence for the presence of hepatitis B surface antigen (HBSAg) and hepatitis B core antigen (HBcAg). Of the 60 HBsAg-positive livers, 51 were diagnosed as chronic hepatitis on histological grounds, 6 as acute hepatitis, and 3 as "near-normal liver." From the 60 tissue-positive cases, 3 subjects were HBsAg seronegative. HBcAg was detected in 44 livers, all of which also had HBcAg in the localized in the cytoplasm and the membranes of the hepatocytes, and HBcAg in the nuclei and in 4 cases also in the cytoplasm. Predominant HBsAg expression in the cytoplasm was observed in near-normal liver, chronic persistent hepatitis, and cirrhosis with little activity. This correlated with the amount of ground glass hepatocytes in the biopsies. HBcAg and membrane-localized HBsAg were minimal in those conditions. HBcAg was most prevalent in patients with chronic aggressive hepatitis and active cirrhosis treated with immunosuppressive drugs, whereas the amounts of HBsAg and HBcAg in nontreated patients of those two groups and in acute hepatitis with signs of transition to chronicity were almost equal. HBsAg expression in liver cell membranes was most prominent in active forms of chronic hepatitis (chronic aggressive hepatitis and in active cirrhosis) and in acute hepatitis with signs of transition to chronicity. This observation correlated in the presence of HBcAg in the biopsies of those patients. In acute hepatitis both HBsAg and HBcAg were detected rarely and no membrane expression of HBsAg was observed. The over-all results show a significant relationship between the different degrees of accumulation of HBsAg and HBcAg in the liver and the various histological types of hepatitis and further suggest an interplay of both hepatitis B virus and host immune response in the development and pathogenesis of hepatitis B.
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PMID:Differential distribution of hepatitis B surface antigen and hepatitis B core antigen in the liver of hepatitis B patients. 5 75

Liver specimens from 103 patients with various hepatic diseases and from 297 consecutive liver biopsies examined routinely were stained with orcein after oxidation of the tissue sections with potassium permanganate. Orcein-positive dark brown cytoplasmic material could be demonstrated in 27 cases with long-standing cholestasis. These patients had either primary biliary cirrhosis, the cholestatic liver disease of ulcerative colitis or chronic active hepatitis, advanced alcoholic cirrhosis or secondary biliary cirrhosis due to extrahepatic biliary obstruction. Orcein-positive material could not be demonstrated in congenital disorders of bilirubin metabolism or in hemochromatosis. Similarly, it could not be found in acute, toxic, alcoholic or chronic persistent hepatitis.
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PMID:The occurrence of orcein-positive hepatocellular material in various liver diseases. 6 38

The serum alphafetoprotein level (AFP) was studies in 125 histologically verified cases of hepatocellular carcinoma, 66 other malignancies, 74 cases of cirrhosis of the liver, 60 of chronic aggressive hepatitis, 12 of chronic persistent hepatitis, 16 of subacute hepatitis, 36 of acute viral hepatitis, and 13 healthy hepatitis B-surface antigen (HBsAg) carriers. Double immunodiffusion and radioimmunoassay (RIA) were used in all cases. AFP greater than 10 ng-ml appeared in 90% of the cases, and was above 400 ng/ml in 69%. In 80% of those above 400 ng/ml, AFP could also be demonstrated by immunodiffusion. The AFP level in hepatocellular carcinoma was discovered to decline as the age increased. It also appeared to be related to the tumor cell type; the relatively immature cell type was more frequently associated with a higher AFP level. The presence of HBsAg did not influence the AFP level. Although the AFP in other malignancies and liver diseases ranged abnormally from 14 to 69%, the level did not exceed 400 ng/ml as in our cases of hepatocellular carcinoma (except in one case). Thus, this figure provides a diagnostic serum level of AFP for the identification of hepatocellular carcinoma.
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PMID:Serum alphafetoprotein in hepatocellular carcinoma. 7 Feb 68

Serum alpha-fetoprotein (AFP) levels were measured by radioimmunoassay in 89 healthy adult Chinese, 170 patients with histologically verified non-malignant liver diseases, and 14 hepatitis B surface antigen (HBsAg) carriers with normal liver histology. In 97% of the healthy adults, AFP levels were under 20 ng/ml, which is then regarded as the normal upper limit. Cases with supranormally elevated AFP levels ranged from 15-51% in chronic hepatic disorders and were 33% in acute hepatitis. None of the healthy HBsAg carriers had abnormal AFP level. HBs antigenemia was found to be related to AFP elevation in chronic active hepatitis, cirrhosis, and acute hepatitis but not in chronic persistent hepatitis and healthy HBsAg carriers. The correlation could be demonstrated only when the sensitive third generation test was employed to define seropositivity of HBsAg. Events after hepatic injury induced by hepatitis B virus, rather than the HBs antigenemia itself, are probably responsible for the association. Whether the association of HBsAg and elevated serum AFP in these nonmalignant hepatic disorders contributes to the higher risk of subsequent development of hepatocarcinoma in Taiwan is unknown and requires further long-term longitudinal study.
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PMID:Relationship of hepatitis B surface antigen to serum alpha-fetoprotein in nonmalignant diseases of the liver. 8 92

The concentration of beta 2-microglobulin in serum was determined in seventy-one patients with various liver disorders. Elevated values were found in most patients with chronic active or chronic persistent hepatitis and in over 80% of patients with alcohol-induced liver cirrhosis. In contrast, patients with alcohol-induced fatty liver, the serum beta 2-microglobulin concentrations were mostly within the normal range. Significant correlation (P less than 0.001) was noted between the elimination rate of galactose from blood and the serum beta 2-microglobulin concentration in patients with alcoholic liver damage but not in patients with chronic hepatitis. The reasons for the increased S-beta 2-microglobulin concentrations in liver diseases are unknown. Several explanations including a release of beta 2-microglobulin from necrotic liver cells or an increased synthesis of beta 2-microglobulin consequent to inflammation in the liver are possible. Alternatively, raised beta 2-microglobulin levels may reflect the hepatic synthesis during reparative growth.
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PMID:Serum beta2-microglobulin in liver disease. 9 2


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