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Query: UMLS:C0019158 (hepatitis)
30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The surface (HBsAg) and core (HBcAg) antigens of hepatitis B virus (HBV) have been searched by optic microscopy in the liver specimens from patients hospitalized for various conditions and from 38 HGsAg chronic carriers. The study was done blindly using Shikata et al.'s orcein staining on fixed and frozen material and direct immunoperoxidase on frozen material with antisera specific for surface (anti-HBs) and core (anti-HBc) antigens of HBV. No liver staining could be found in the 98 HBsAg seronegative patients. Among the 28 HBsAg seropositive patients, only 3 showed positive staining: 1 patient with acute viral hepatitis showed nuclear staining with anti-HBc; 2 patients with postnecrotic cirrhosis showed cytoplasmic staining with anti-HBs and/or orcein, and one of them also showed nuclear staining with anti-HBc. In contrast, among the 38 chronic carriers, 25 showed positive cytoplasmic staining with anti-HBs and/or orcein, while one of them (with chronic aggressive hepatitis) also showed nuclear staining with anti-HBc. Anti-HBs and orcein staining are equally sensitive and specific for the detection of HBsAg in hepatocytes; discrepant results can be attributed to sampling error of distribution of HBsAg in small liver fragments.
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PMID:Detection of surface and core antigens of hepatitis B virus in the liver of 164 human subjects. A study by immunoperoxidase and orcein staining. 5 2

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

Determination of the complement titer in the serum and plasm of 120 patients with chronic liver diseases showed that in eight (7%) patients with cirrhosis of the liver, chronic active or chronic inactive hepatitis complement in the serum was less than half in the plasma. The dissociation of complement serum and plasma was due to cold activation of the classical pathway of complement in vitro since serum drawn from these patients at 37 degrees C lost hemolytic activity in 4 hours when transferred to a cold environment. Neither HB antigen nor cryoglobulin participated in this phenomenon. The activation of complement in the cold could be prevented by increasing the ionic strength, or by adding vitamin E or, to a lesser extent its vehicle HCO-60, while heparin, Trasylol, soybean trypsin inhibitor, or hirudin had no effect. Trans-AMCHA prevented activation in one case. It is speculated that a factor appearing as a result of blood clotting is able to activate the classical pathway of complement in the cold; it is probably not related to Hageman factor (factor XII), factor VII, thrombin, kallikrein.
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PMID:Cold activation of complement i. presence of coagulation-related activator. 5 81

Using the single radial immunodiffusion method, the serum levels of IgG, IgA, Ig M, transferrin, haptoglobin, alpha2-macroglobulin, alpha1-antitrypsin and alpha1-acid glycoprotein were estimated in healthy subjects and patients with liver diseases consisting of chronic active and inactive hepatitis, incipient cirrhosis, cirrhosis and primary liver cancer. The results obtained from the statistical analysis of the data were as follows: i) Immunoglobulins and alpha2-macroglobulin in all diseases were higher than those of healthy subjects. ii) The increased transferrin levels were found in chronic active and inactive hepatitis, and the increased alpha1-antitrypsin levels were observed in chronic inactive hepatitis, in incipient cirrhosis in cirrhosis and in primary liver cancer was higher than those of the other liver diseases. iii) Haptoglobulin levels in all diseases except for chronic inactive hepatitis were decreased. iv) alpha1-acid glycoprotein in chronic active hepatitis, in incipient cirrhosis and in cirrhosis were lower than that of healthy subjects. The evaluation of significance for difference of each protein level among disease groups clarified that the decrease of haptoglobin in cirrhosis and the increase of alpha1-antitrypsin in primary liver cancer were characteristic change respectively.
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PMID:The serum protein profile in chronic hepatitis, cirrhosis and liver cancer. 6 35

The authors studied 496 patients with chronic persistent or aggressive hepatitis, and active or non-active hepatic cirrhosis, and 396 non-hepatic patients. AgHB was detected in the serum by immuno-electrophoresis and by immuno-diffusion and, in the liver, by needle biopsy, using immuno-fluorescence. The liver diagnosis was made histologically. AgHB was found in 34.2% of patients, more often in chronic active hepatitis (53.7%) than in inactive forms (23.2%). This finding may be interpreted as a sign of severity, chronic aggressive hepatitis is more frequently caused by B virus and by its persistence in the liver. In all cases of chronic, aggressive hepatitis studied with AgHB in the serum, AgHB was detected in the nuclei of the liver parenchyma cells. It should be emphasized that there is no significant difference from the immunological point of view, between patients with AgHB and the others, the levels of gamma-globulin and immunoglobulin were higher in the former. The increased frequency of AgHB in the active forms of the disease compared with stabilised forms, reinforces its physiopathological, diagnostic and prognostic significance.
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PMID:[Significance of the AgHB and of the immune reaction in chronic hepatitis]. 6 14

Progression of acute type B hepatitis to chronic liver disease and cirrhosis is well recognized, whereas no progression of acute type A hepatitis has as yet been documented. The natural history of acute non-A, non-B hepatitis has not been previously characterized. Ten cases of chronic liver disease were identified in 44 cases of acute non-A, non-B post-transfusion hepatitis. Age, sex, severity of acute illness, and prevalence of preoperative antibodies to known hepatitis-producing agents did not differ between the group whose hepatitis progressed to chronicity and the group whose hepatitis resolved. Less progression of acute hepatitis to chronic liver disease was seen in those patients receiving immune serum globulin preoperatively than in those receiving an albumin placebo (P = 0.009). Only 3 patients had clinical symptoms of hepatitis at the time of liver biopsy, and elevations of liver enzymes and gamma-globulin were mild. However, liver biopsy specimens in 8 of 10 patients showed chronic active hepatitis and an additional biopsy specimen showed cirrhosis. Acute non-A, non-B post-transfusion hepatitis often progresses to chronic active hepatitis. Preoperative gamma-globulin prophylaxis significantly reduces this progression. Identification and characterization of this viral agent(s) will further aid in the prevention of this undesirable complication of blood transfusion.
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PMID:Development of chronic liver disease after acute non-A, non-B post-transfusion hepatitis. Role of gamma-globulin prophylaxis in its prevention. 6 67

In an attempt to determine the frequency of liver injury in adult coeliac disease (A.C.D.) the case records of 74 consecutive patients were examined. In 13 cases histological sections of the liver were available and in 5 of these there were signs of reactive hepatitis. Histological signs of distinct hepatic injury with cirrhosis and/or chronic active hepatitis were found in 7 other patients. In 5 of these serum-IgA was normal, whereas 16 out of 20 control patients with liver cirrhosis not associated with A.C.D. had raised serum-IgA. Serum-aspartate-aminotransferase and serum-alanine-aminotransferase were determined in 53 patients; 29 had raised concentrations. In 19 patients serum-aminotransferases were repeatedly determined before and during the dietary regimen and there was a significant reduction in enzyme concentrations during treatment. The median concentration of serum-alkaline-phosphatase was also reduced during treatment but not significantly. The histological evidence of liver injury in 16% and the abnormal liver-function tests in 39% of the patients indicate that hepatic injury is common in A.C.D. Since liver-function tests or liver biopsy specimens were available for only about two-thirds of the patients, liver damage in A.C.D. may be more common than indicated by these results. The effect of a gluten-free diet on aminotransferase concentrations indicates that the liver injury may be reversible and suggests that in some A.C.D. patients progressive liver damage may be prevented by suitable treatment. Since A.C.D. is not always recognised, the diagnosis should be considered in patients with liver disease of unknown aetiology.
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PMID:Hepatic injury in adult coeliac disease. 6 80

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

In the liver needle biopsy specimens of 45 patients with hepatitis chronica persistents, hepatitis chronica aggressiva and cirrhosis of the liver the number of lymphoid cells and fibroblasts, and in the serum of the same patients concentration of IgG, IgA, IgM, alfa-2-macroglobulin and coeuroplasmin was examined. It was established that 1. the number of lymphoid cells and fibroblasts in the liver tissue of patients with hepatitis chronica aggressiva and cirrhosis of the liver increases significantly, 2. there exists a correlation between the number of lymphoid cells and the concentration of IgG, 3. the serum level of the alfa-2-macroglobulin increases parallely with the number of fibroblasts of the liver in hepatitis chronica aggressive and in cirrhosis of the liver.
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PMID:[Serum immunoglobulin and glycoprotein concentration and mesenchymal reaction in chronic hepatitis and liver cirrhosis]. 7 28

We have measured the plasma levels of alpha-1 fetoprotein (AFP) and carcinembryonic antigen (CEA) by RIA in 98 chronic liver diseases (20 chronic aggressive hepatitis and 75 cirrhosis), in 46 subjects with several varieties of malignant neoplasias and in 30 normal controls. In cirrhosis levels higher than the media +/- 2 DS of controls were found in 25.3% for AFP (Max. value 250 ng/ml) and in 36.0% for CEA (Max. value 150 ng/ml). Only in 6 cases of cirrhosis we found high levels of AFP and CEA contemporaneously. High levels of AFP were found in 10/13 primary liver cancers and only in 1 patient with colonic carcinomata. High levels of CEA were found in 4/13 primary liver cancers (1 AFP positive too), 3/4 metastatic liver cancers, 7/17 colonic primary cancers, 3/6 bronchogenic carcinoma, and 3/6 other malignancies.
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PMID:[Comparative study of the plasma levels of alpha-1 fetoprotein and carcinoembryonic antigen in chronic liver diseases and malignant neoplasias (author's transl)]. 7 37


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