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)

Tissue samples from 180 unselected necropsy cases of various forms of hepatitis were examined by histopathology and immunofluorescence. The hepatitis forms studied included acute fulminant hepatitis (28 patients), subacute hepatitis (48 patients), acute fatal hepatitis (24 patients), chronic aggressive hepatitis (26 patients), liver cirrhosis (49 patients), and "minimal" hepatitis (5 patients). Hepatitis B surface antigen and hepatitis B core antigen were detected in 101 patients (56.1 per cent). In these, lesion-bound immune complexes of hepatitis B surface antigen were found in the liver and extrahepatic locations in 77 patients (76.2 per cent). The latter included activated germinal centers of lymph nodes and spleen, focal hyaline lesions of splenic and renal arterioles, necrotic and/or proliferative lesions of small and medium-sized arteries, and kidney glomeruli with mild proliferative and degenerative lesions. There was an inverse relation of the approximate amounts of hepatitis B surface antigen in the liver and the liver damage, the latter being directly proportional to the amount of HBS Ag immune complexes in the liver and indirectly proportional to their amount in extrahepatic locations and to the severity of lesions at these sites.
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PMID:Immunopathological aspects of hepatitis type B. 1 54

A study of 221 patients revealed that detectable hepatitis B surface antigen (HBS Ag) was found in 16.3% of 49 patients who had hepatoma associated with cirrhosis. None of the 8 hepatoma patients without cirrhosis had detectable HBS Ag in the serum. When known causes of cirrhosis were excluded, HBS Ag was present in 18% of 22 patients. Positive alpha-1-fetoprotein (AFP) was found in 25 of 49 cases (51%) of hepatoma with cirrhosis but was found only in 1 of 8 cases (12.5%) of hepatoma without cirrhosis. Of 25 patients whose AFP was positive, HBS Ag was also present in 7. The latter was detected in only 1 of 24 patients in whom AFP was not detected. This study suggests that HBS Ag is closely associated with hepatomas in cirrhotic patients but not in noncirrhotic patients with hepatoma.
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PMID:Relationship of hepatitis B antigen in cirrhosis and hepatoma in Thailand. An etiological significance. 4 28

"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

Additional antigenic sites, distinct from those present on spherical 20 nm diam. particles of hepatitis B surface antigen (HBsAg), are exposed on the surface of Dane particles and tubular forms of HBsAg. The immunological relationship of these sites to e-antigen, an antigen detected earlier in HBsAg-positive sera from patients with chronic hepatitis, cirrhosis or acute hepatitis but not in healthy HBsAg-carriers, was established by immune electron microscopy and affinity chromatography. These findings suggest that e-antigen may be potentially useful in active immunization against hepatitis B.
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PMID:Identification of additional antigenic sites on Dane particles and the tubular forms of hepatitis B surface antigen. 5 22

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

Two hundred seventy-nine patients who died of hepatocellular carcinoma were autopsied at Los Angeles County--USC Medical Center and the John Wesley--USC Liver Unit from 1949 through 1974, and tissues from 168 of these cases were available for staining for hepatitis B surface antigen (HBSAg). Twenty-one per cent of the livers had stainable HBSAg. There were prominent increases both in total numbers of hepatic cancers and in the percentages that were HBSAg-positive beginning about 1970, but the numbers of hepatocellular carcinomas arising in noncirrhotic livers also increased. From 1969 to 1974, 73% of those who had hepatocellular carcinomas arising to nonalcoholic but cirrhotic livers were HBSAg-positive. Racial differences in the incidences of cirrhosis, the incidences of hepatocellular carcinomas associated with HBSAg were found. The incidences of cirrhosis were: Caucasian 11%; Mexican 12.2%; Negro 5.7:; Oriental 10%. Hepatocellular carcinomas arose in 3.2% of Caucasians who had cirrhosis; 3.6% of Mexicans; 8.3% of Negroes; 47% or Orientals. Ten per cent of Caucasians who had hepatocellular carcinomas in cirrhotic livers were HBSAg-positive; 25% of Negroes; 12% of Mexicans; 47% of Orientals.
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PMID:The changing incidence of association of hepatitis B with hepatocellular carcinoma in California. 6 78

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

Paraffin sections of liver on 227 autopsy cases were stained by a modified orcein method of Shikata et al (14) in order to detect hepatitis B surface antigen (HBsAg). Blood of all the 227 cases obtained at autopsy were tested for HBsAg by immune adherence hamagglutination method (7) and for antibody to HBsAg (anti-HBs) by passive hemagglutination method (6). Cases of seropositive in HBsAg but negative in anti-HBs group showed orcein-positive hapatocyte in 13 (68%) of 19 cases of cirrhosis with hepatoma, in 2 (67%) of 3 cases of cirrhosis without hepatoma, and in 2 (67%) of 3 cases of non-cirrhotic neoplastic diseases other than hepatoma. Cases of seronegative in both HBsAg and anti-HBs group showed orceinpositive hepatocyte in 4 (17%) of 24 cases of cirrhosis with hepatoma, in 2 (11%) of 19 cases of cirrhosis without hepatoma, and in 3 (5%) of 60 cases of non-cirrhotic neoplastic diseases other than hepatoma. Cases of seronegative in HBsAg but positive in anti-HBsAg but positive in anti-HBs group showed orcein-positive hepatocyte in 1 (17%) of 6 cases of cirrhosis with hepatoma and in 1 (5%) of 21 cases of non-cirrhotic neoplastic diseases other than hepatoma. Cases of seropositive in both HBsAg and anti-HBs group showed orcein-positive hepatocyte in 1 (33%) of 3 cases of cirrhosis with hepatoma. No orcein-positive hepatocyte was detected in cases of hepatoma without cirrhosis and in cases of non-cirrhotic non-neoplastic diseases in any serological groups.
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PMID:Orcein staining of hepatitis B surface antigen in paraffin sections of liver on autopsy cases. 7 35

In 31 patients with an initial diagnosis of cirrhosis or chronic hepatitis hepatocellular carcinoma (HCC) was detected after a clinical follow-up of 8 months to 14 years with an average of 59 months. They had had no scintigraphic and biochemical abnormalities suggestive of HCC at the beginning. The follow-up period before the detection of carcinoma was shorter in patients positive for hepatitis B surface antigen compared with those negative for hepatitis B surface antigen. Analyses of clinical data during the follow-up and liver scans made shortly before tumor detection suggested that in most of these patients HCC became discernible relatively early in the course of cirrhosis or long before cirrhosis reached an advanced stage. A sharp rise in serum alpha-fetoprotein level proved highly diagnostic in 11, it remained low throughout in 7, and tumor was already unresectable in the majority. Although continuous and regular check for alpha-fetoprotein is imperative in patients with chronic liver disease, particularly in those with hepatitis B surface antigenemia, additional diagnostic tools are necessary for the detection of small HCC in its resectable stage.
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PMID:Detection of hepatocellular carcinoma during a clinical follow-up of chronic liver disease: observations in 31 patients. 7 17

The prevalence of serological markers of active of past hepatitis-B virus (H.B.V.) infection was determined in 80 Greek patients with primary hepatocellular carcinoma (P.H.C.), 160 age and sex matched controls and 40 patients with metastatic liver cancer (M.L.C.). The relative risk of the various patterns of H.B.V. serological markers for P.H.C. was calculated. Active H.B.V. infection, as indicated by positive tests for hepatitis-B surface antigen (HBsAg), or antibody to hepatitis-B core antigen (anti-HBc) without antibody to HBsAg) (anti-HBs), was associated with P.H.C. (relative risk 10.4) but not with M.L.C. (relative risk 1.2). Patients without markers and those who had recovered from hepatitis B (anti-HBs-positive) had approximately the same low risk for P.H.C. (relative risk 0.8). Active infection was more common in P.H.C. patients with co-existing cirrhosis than in those without cirrhosis (67% versus 26%). Thus the relationship between active hepatitis B and P.H.C. seen in African and Asian populations is now seen in a European Caucasian population with different racial, environmental, and dietary circumstances.
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PMID:Hepatitis B and primary hepatocellular carcinoma in a European population. 8 32


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