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)

Serial determinations of titers of binding antibodies to single stranded DNA were performed over a period of three years in 43 type B hepatitis patients with persisting HBsAg who had either developed chronic hepatitis or were asymptomatic carriers. Patients with histopathological diagnosis of chronic active or chronic persistent hepatitis, with or without clinical symptoms, showed high titers of anti-DNA throughout the course of the disease, whereas in most of these patients the serum alanine transaminase and bilirubin levels fluctuated widely and were often normal; in such cases the elevation of anti-DNA was frequently the only positive sign present. On the other hand anti-DNA titers were within the normal range in chronic asymptomatic HBsAg carriers who showed no histopathological or biochemical changes. Anti-DNA determinations are proposed as a reliable diagnostic aid to supplement current procedures for assessment of the disease status during the course of chronic hepatitis B virus infections.
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PMID:Antibodies to single stranded DNA: a diagnostic aid in chronic hepatitis B virus infections. 31 70

The occurrence of anti-HBcAg antibodies in the blood as determined by indirect immunofluorescence and its relation to the occurrence of HBsAg in the cytoplasm and of HBcAg and IgG in the nuclei of hepatocytes were studied in the following groups of patients (total of 123 biopsies): I. 64 HBAg-negative patients with various liver diseases; II. 51 HBAg-positive patients without therapeutical immunosuppression (6 acute hepatitis, 10 nonspecific reactive and 10 chronic persistent hepatitis, 19 chronic aggressive hepatitis, 6 "Hippie"-hepatitis); III. 8 kidney transplant recipients. It could be shown that nuclear IgG is found only if both parameters can be demonstrated at the same time: HBcAg in liver cell nuclei and anti-HBcAg antibodies in the serum in titers higher than 1:64. Accordingly, all types of hepatitis with excess formation of nuclear HBcAg (early phase of acute hepatitis, chronic aggressive hepatitis and chronic non-aggressive forms with generalized core formation, i.e. carrier state or chronic persistent hepatitis of the HBc type) may show nuclear fluorescence for IgG. All forms of hepatitis B without detectable core formation (acute hepatitis in the elimination phase, chronic non-aggressive hepatitis with isolated HBsAg expression, i.e. carrier state or chronic persistent hepatitis of the HBs type, posthepatitic phase) do not present nuclear IgG despite eventual anti-HBcAg formation. Finally, lack of anti-HBcAg or very low titers associated with lack of IgG in hepatocytic nuclei do not exclude generalized core formation in liver cell nuclei in chronic persistent hepatitis of effectively immunosuppressed patients. Although the demonstration of nuclear IgG has several diagnostic and prognostic consequences in common with the demonstration of HBcAg, a specific search for the core antigen in the tissue is needed for the correct appraisal of the HBcAg- and HBsAg tissue expression pattern and the associated disease.
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PMID:Nuclear fluorescence of liver cells for IgG in viral hepatitis B: significance and relation to hepatitis B-core and anti-hepatitis B-core formation. 32 65

The characterisation of lymphocytes from liver biopsies indicates that 'activated' T lymphocytes are present in the liver in alcohol induced hepatitis, chronic active hepatitis (HBS+ve and -ve), and in primary biliary cirrhosis but not in inactive cirrhosis, chronic persistent hepatitis, extrahepatic and drug induced cholestasis. A greater percentage of lymphocytes bear Fc-receptors in chronic active hepatitis than in alcohol induced hepatitis or cholestatic liver disease. The concentration of 'activated' T cells in the peripheral blood in all groups studied was within the normal range, suggesting that the 'activated' T cells found in the liver were reacting to either native or foreign antigens within the liver. The data on Fc-receptor bearing cells are consistent with the involvement of antibody assisted K cell mediated cytotoxicity in chronic active hepatitis.
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PMID:Lymphocyte populations in liver biopsy specimens from patients with chronic liver disease. 32 39

The purpose of this study was to determine the frequency of liver involvement in malignant lymphomas. Non-specific liver changes were also registered. Percutaneous liver biopsy was performed on 120 patients with untreated malignant lymphomas. There were 38 patients with Hodgkin's disease, 42 with histiocytic and 40 with lymphocytic lymphomas. All the biopsy specimens were histologically and cytologically analyzed. Positive liver findings (lymphomatous infiltration) were observed in 27.5% of patients with lymphocytic, 23.8% with histiocytic lymphomas, and 7.8% with Hodgkin's disease. Liver involvement in non-Hodgkin's lymphomas was significantly higher (P less than 0.025) than in Hodgkin's disease. In the whole group of patients, there were non-specific liver changes: 23 chronic persistent hepatitis, 5 aggressive hepatitis, 9 liver steatosis and 4 liver hemosiderosis. Based on these results, it can be concluded that liver involvement with lymphomatous tissue is more common in non-Hodgkin's lymphomas. Knowledge of this is relevant for clinical staging and the treatment program. These findings also confirm that percutaneous liver biopsy is a valuable diagnostic procedure in the staging of malignant lymphomas.
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PMID:Histologic and cytologic liver changes in 120 patients with malignant lymphomas. 34 9

The classification, clinical course, etiology and treatment of chronic hepatitis are discussed. The clinical manifestations of chronic hepatitis are of limited diagnostic use. Diagnosis must be made by liver biopsy. The disease is classified as chronic persistent or chronic active hepatitis. The prognosis for chronic persistent hepatitis is excellent, and no treatment is required. Chronic active hepatitis may progress to cirrhosis and is associated with a poor prognosis if untreated. Recognized causes of chronic active hepatitis are hepatitis-B virus infection, post-transfusion hepatitis not associated with hepatitis-B virus, and certain drugs. For drug-induced hepatitis, discontinuation of the medication is indicated. For other types of chronic active hepatitis the recommended treatment is prednisone 10 mg and azathioprine 50 mg daily.
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PMID:Drug therapy reviews: chronic hepatitis. 35 29

The 'e antigen' (eAg) is specifically associated with hepatitis B virus infections and appears to be a marker for the infectivity and a prognostic indicator of the chronicity of liver disease. Therefore we examined by immunodiffusion the presence of eAg in the seum of HBsAg-positive patients on maintenance dialysis. The dialysis patients had a significantly higher incidence of positive eAg compared with a group of unselected HBsAg-positive patients without renal failure. In most of the dialysis patients the microscopic findings in the liver revealed only 'minimal changes'. Three eAg-positive patients received a renal transplant. Afterwards they displayed an appreciably increased eAg-yield on immunodiffusion and histology revealed chronic persistent hepatitis. It is assumed therefore that the immunodeficiency of patients undergoing chronic haemodialysis is possibly a supporting factor in the synthesis of eAg, and will perhaps induce a more subscute and prolonged course of hepatitis. The synthesis of eAg after renal transplantation may be enhanced by the additional immunosuppressive therapy.
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PMID:E antigen in the serum of HBs antigen-positive patients on maintenance dialysis and after transplantation. 36 77

Single liver biopsies from 102 clinically diagnosed hepatitis patients were examined by immunofluorescence for the presence of hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg), complement and immunoglobulin deposition, and for their capacity to fix human complement in vitro. Of the sixty-five HBsAg positive livers, fifty-three were histologically diagnosed as chronic hepatitis, three as acute hepatitis, five as acute hepatitis with signs of transition to chronicity, and four as 'near normal liver'. In the group with chronic hepatitis, HGcAg was observed in thirty-nine livers, all of which also had HBsAg. Thirty-five of these thirty-nine cases also had the ability to fix complement in vitro in the hepatocyte nuclei and/or cytoplasm. Of these thirty-five cases, twenty-nine were positive for immunoglobulin deposition on the nuclei. All of these cases had antibody to HBcAg in the blood, but only five had anti-HBs. The frequency of in vitro complement fixation and immunoglobulin deposition was higher in active forms of the disease, such as chronic aggressive hepatitis and active cirrhosis, than in non-active disease such as chronic persistent hepatitis and mild cirrhosis. By the application of double fluorescent staining techniques, complement fixation was observed in some HBcAg-positive nuclei. In the 'near normal liver' cases there was no intrahepatic accumulation of HBcAg, and despite the presence of anti-HBc in the blood, in vitro complement fixation and immunoglobulin deposition were both absent. The group of three HBsAg ositive 'acute hepatitis with signs of transition to chronicity' cases behaved similarly to those with chronic aggressive hepatitis and had circulating anti-HBc, in vitro complement fixation and immunoglobulin deposition in the hepatocytes. None had circulating anti-HBs. In the group sith HBs-positive acute hepatitis, anti-HGc in the blood was the only other evidence of hepatitis B virus infection.
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PMID:Hepatitis B core antigen immune complexes in the liver of hepatitis B patients. 38 86

Serological markers for hepatitis virus B (HBV) infection and the occurrence of hepatopathies were analyzed in 152 patients during the hemodialysis period and on average 3.8 years after receiving a renal allotransplant. At the beginning of hemodialysis, 25% of the patients showed signs of an ongoing or past infection with HBV (10% hepatitis virus B surface-antigen [HBsAG] positive and 15% anti-HBsAG positive). At the time of transplantation, 20% of the patients were positive for HBsAG and 25% had detectable anti-HBs. At the end of the study, 31% of the patients were positive for HBsAG and 25% had detectable anti-HBs. In 21 patients (14%) inflammatory liver disorders were observed: transitory hepatitis (7 patients), chronic persistent hepatitis (7 patients), chronic aggressive hepatitis (3 patients) and active cirrhosis (2 patients). Two patients had died in liver coma. All 21 patients with inflammatory hepatopathy had detectable HBsAG at the time of diagnosis, and all patients with chronic inflammatory liver disease were HBs carriers. In most of these patients the carrier state had been present for more than 3 years before diagnosis.
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PMID:[Hepatitis virus B infection and hepatopathy after kidney transplantation]. 39 Jun 93

Histological examination of liver tissue from 3 patients who died 6, 4, and 9 days, respectively, after an intramuscular injection of 3 +/- 0.5 mg of hycanthone per kg of body weight for schistosomiasis, showed features of a toxic hepatitis with massive hepatic necrosis, many acidophil bodies and minimal inflammatory response in 2 patients, and confluent necrosis with early fibrosis in 1. Liver cells showed prominent fatty change. The former 2 patients had evidence of schistosomal granulomatous hepatitis. A follow-up liver biopsy in a 4th patient who had had hycanthone hepatitis with liver failure 1 year before showed good recovery with features of chronic persistent hepatitis.
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PMID:Liver pathology in hycanthone hepatitis. 40 Oct 84

Among 4903 liver biopsies were found 96 cases (241 biopsies) of non-active hepatitis persisting for longer than one year (up to 12 years). Three forms of the course of chronic persistent hepatitis could be delimited in morphological terms taking into account clinical laparoscopic and clinical chemical data. The type Ia presents the picture of a largely subsided, lobular accentuated acute virus hepatitis. The type Ib corresponds to a chronic inflammation with emphasis on the portal system without destruction of the limiting plate, without fibrosis and with only slight intralobular involvement. The type Ic is characterized by a portal and slight septal fibrosis with round-cell infiltrates and a slight facultative periportally active inflammation as well as a moderate intralobular mesenchyme reaction. The typing permits a clear subdivision and a differentiated prognosis: 10% of the cases of type Ic pass into an active chronic hepatitis of the type IIa.
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PMID:[Chronic persistent hepatitis. Histological and clinical study of different forms of the course of CPH]. 41 96


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