Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 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

"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

Liver biopsies from 18 patients with primary biliary cirrhosis (PBC) and from 25 patients with chronic active hepatitis (CAH) were stained by orcein after oxidation of the tissue sections with potassium permanganate. In 15 out of the 18 cases which could be classified on clinical, biochemical and immunological basis as PBC, the hepatocytes, usually periportally, contained cytoplasmic stainable material. 5 out of the 25 CAH patients contained the same material, but four of these patients were clinically atypical and showed features of cholestatic form of CAH and features crosslinking with PBC. All patients in both groups were serologically hepatitis-B antigen negative. The orcein staining method seems to be a reliable addition to differentiating histologically between PBC and CAH.
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PMID:Orcein positive hepatocellular material in histological diagnosis of primary biliary cirrhosis. 5 54

F-antigen is a liver-specific antigen detected with antibody, raised in allogeneic (CBA) mice, to BALB/c mouse liver extract. The authors have confirmed the hepatic specificity of this antigen by showing it to be absent in extracts of extrahepatic organs of mouse and human origin. It is present in liver extracts of guinea pigs, rats, and rabbits, as well as in liver extracts from mouse and human sources. The antigen was present in the circulation of rabbits with acute carbon tetrachloride-induced hepatocellular injury. It was also demonstrated in the sera of 3 of 8 patients with acute hepatitis B antigen-positive hepatitis and in 1 of 4 patients with chronic active hepatitis. It was absent from the sera of 121 other patients with a variety of hepatic and nonhepatic diseases, and from the sera of 20 healthy subjects. The antigen is immunologically distinct from hepatitis B antigen, from the liver-specific lipoprotein antigen LP-2 of Meyer zum Buschenfeld, and from each of 15 individual human serum proteins tested.
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PMID:F-antigen: nature, liver specificity, and release in experimental liver injury. 5 3

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

Testing for e antigen and antibody (anti-e) was performed by immunodiffusion and counterelectrophoresis in patients with polyarteritis nodosa fulminant hepatitis, and chronic active hepatitis (CAH), in 59 asymptomatic carriers of hepatitis B surface antigen (HBsAg) who underwent liver biopsy, and in 150 carriers followed with sequential SGPT determinations. Counterelectrophoresis was more sensitive that immunodiffusion. Neither e antigen nor anti-e was found in the absence of HBsAg. Among HCsAg-positive patients with polyarteritis nodosa and CAH, e antigen was found in 16 of 18 and 13 of 22, respectively. It was not found in any of 43 patients with fulminant hepatitis, of whom 24 were HBsAg-positive. The e antigen was detected in none of 13 biopsied carriers with normal histology, 4 of 28 with nonspecific changes of 11 of 18 with CAH or chronic persistent hepatitis. Conversely, anti-e was present in 9 of 13 with normal biopsy, 7 of 28 with nonspecific changes, and none of 18 with CAH or chronic persistent hepatitis. The e antigen was found more commonly in nonbiopsied carriers with elevated SGPT, and anti-e in those with normal SGPT. Six carriers whose antigenemia terminated spontaneously had anti-e. The presence of e antigen correlated with a high titer of HBsAg, and with immunofluorescent detection of hepatitis B core antigen in the nuclei of hepatocytes. Conversely, anti-e was associated with significantly lower titers of serum HBsAg (P less than 0.001) and lack of detectable hepatitis B core antigen in the liver.
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PMID:Detection of e antigen and antibody: correlations with hapatitis B surface and hepatitis B core antigens, liver disease, and outcome in hepatitis B infections. 6 Nov 46

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

A young women with clinical and histological features of chronic active hepatitis was noted to have extremely high levels of immunoglobulin (14.6 g per dl). This was associated with the hyperviscosity syndrome, diffuse coagulation abnormalities, and renal insufficiency in the absence of severe liver disease. Correction of these features occurred with plasmapheresis before corticosteroid therapy was begun. A similar group of persons with very high gamma-globulin levels, described previously under the heading of "plasma cell hepatitis," may form a distinct and rare subgroup of chronic active hepatitis patients.
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PMID:Hyperviscosity syndrome attributable to hyperglobulinemia in chronic active hepatitis. 7 88


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