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

The clinical import of the serum gamma-glutamyl transpeptidase (GGTP) level was evaluted in 162 prospectively studied patients. GGTP is helpful in determining the origin of alkaline phosphatase (AP); it clearly separates increased AP of bone and placental origin from that of liver origin. The GGTP level closely parallels the AP level in most instances, but it may be more sensitive in detecting liver disease in anicteric patients. The finding of significantly increased GGTP in patients with chronic aggressive hepatitis as compared to normal levels found in chronic persistent hepatitis may provide a prognostic clue in cases of unresolved hepatitis. The apparent specificity and sensitivity of the GGTP test, combined with ease of performance and low expense, make it a valuable addition to the evaluation of a patient with hepatic disease.
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PMID:Serum gamma-glutamyl transpeptidase: its specificity and clinical value. 3 71

A new antigen-antibody system was recently described in hepatitis B surface antigen (HBSAG(-positive sera. Despite indications of heterogeneity in specificity, the designations "e antigen" and "e antibodies" are used for the system as such in this articly. E'IGHT OF 17 long-term carriers of HBSAg with a histological picture of chronic persistent hepatitis or chronic aggressive hepatitis carried the e antigen, while none had demonstrable e antibodies in serum. Ten of 12 healthy carriers with e antibodies were blood donors who had donated 95 units of blood; none of these carriers was associeated with a reported case of posttransfusion hepatitis. In five individuals in the incubation stage of hepatitis B, e antigen appeared simultaneously with HBSAg but before the rise in transaminase levels. This finding further links e antigen to hepatitis B.
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PMID:A new antigen-antibody system. Clinical significance in long-term carriers of hepatitis B surface antigen. 4 64

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

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

Alpha-fetoprotein levels were measured by radioimmunoassay in 40 cases of acute viral hepatitis, 5 cases of chronic persistent hepatitis, 15 cases of chronic aggressive hepatitis and 5 cases of hepatic coma from fulminant viral hepatitis. Serum concentrations were increased in 55% of patients with acute viral hepatitis and in about 33% of patients with chronic aggressive hepatitis. Levels resulted markedly raised among the patients with coma from fulminant viral hepatitis who survived. The high aplha-fetoprotein values may reflect liver cell regeneration after necrosis of a critical mass of hepatic tissue.
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PMID:Serum alpha-fetoprotein in viral hepatitis and its complications. 6 58


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