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)

Peripheral blood and hepatic tissue T- and B-lymphocyte distributions, serum alpha fetoprotein (AFP) concentrations, and hepatic AFP were studied in 46 patients undergoing diagnostic percutaneous liver biopsy. The patients included 26 with alcoholic liver disease, 13 with nonalcoholic hepatitis or cirrhosis, and 7 with either normal histology or minor nonspecific changes. Serum AFP was determined by radioimmunoassay and hepatic tissue AFP by indirect immunofluorescence. Peripheral blood T lymphocytes were identified by the sheep red-cell rosette technique; and B lymphocytes by fluoresceinated anti-immunoglobulin antisera and IgG aggregates. Tissue identification of T lymphocytes was accomplished using an extensively absorbed rabbit antihuman thymocyte antiserum and indirect immunofluorescence; tissue B lymphocytes were identified using pepsin F (ab')2 fragments of rabbit IgG antibodies to human immunoglobulins. T lymphocytes predominanted in hepatic lymphoid infiltrates from patients with alcoholic liver disease (91+/-4%), whereas in patients with chronic active or chronic persistant hepatitis, viral hepatitis, or cryoptogenic cirrhosis proportions of T and B lymphocytic infiltrates were similar (50+/-15%). Hepatic tissue AFP was detected in 9 of 18 patients with alcoholic hepatitis; serum AFP concentration was increased in only 1 of these 9 patients. Tissue AFP was not observed in the remaining biopsy material nor were serum AFP concentrations increased. Peripheral blood T-cell numbers were significantly decreased in patients with alcoholic liver disease (P less than 0.01) and in nonalcoholic hepatitis or cirrhosis (P less than 0.025). A close relationship between peripheral blood T-lymphocytopenia and hepatic T-cell infiltrates was observed in patients with alcoholic liver disease; this relationship was less apparent in patients with nonalcoholic hepatitis or cirrhosis.
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PMID:Localization of T and B cells and alpha fetoprotein in hepatic biopsies from patients with liver disease. 5 55

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

Acute viral hepatitis has several identifiable morphologic components but the major categories are (1) cytopathic, (2) inflammatory, and (3) regenerative. Each category has independently variable characteristics. Extreme alterations related to severity of disease, alteration of immune response, or pre-existing liver disease may result in diagnostic difficulties for the pathologist. In contrast to the usual concept, patients who survive fulminant viral hepatitis rarely, if ever, develop cirrhosis and those who have severe hepatic necrosis from hepatitis also do not usually develop serious sequelae of that disease except in the older age group where the difficulty is in impaired regeneration (IR). The usual criteria for the diagnosis of chronic active hepatitis or chronic aggressive hepatitis need a thorough review since many of the variations of acute viral hepatitis result in histologic patterns that might be considered to be chronic aggressive hepatitis using the previous definitions; yet such patients recover without developing chronic liver disease. Chronic active hepatitis, a progressive hepatic disorder, is characterized by changes in the distribution of necrosis and regeneration within the lobule from that usually observed in acute viral hepatitis. Persistent viral hepatitis, a development in 10 to 12 per cent of adult patients after icteric acute disease, is characterized by a "cobblestone" hepatocellular change that resembles continued regeneration, focal hepatocytolysis, and often portal lymphoid hyperplasia. Apparently with time, these histologic features fade and the incidence, in type B PVH, of "ground glass" HBs Ag laden cells increases. This may reflect a continued adaptation of host and virus to one another.
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PMID:Viral hepatitis: a pathologic spectrum. 17 49

Type-8 avian adenoviruses were isolated from chickens in a commerical flock suffering an outbreak of inclusion body hepatitis. Serum-neutralizing titer to this type, but not to 7 other types of avian adenovirus, was more than 4 times as high in convalescing chickens as in chickens from the flock bled 2 weeks previously, during the disease outbreak. A disease similar to that in the commercial flock and to inclusion body hepatitis as described in the literature was produced by intra-abdominal inoculation of a type-8 isolant, AMG 5 (2a), into 1-day-old specific-pathogen-free chicks. Pathologic features of the disease included necrotizing hepatitis, pancreatitis, and severe lymphoid depletion of the bursa of Fabricius, thymus, and spleen. It was concluded that type-8 avian adenoviruses were involved in the etiology of the naturally occurring outbreak of inclusion body hepatitis.
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PMID:Involvement of a type-8 avian adenovirus in the etiology of inclusion body hepatitis. 19 Sep 94

Twenty 1-day-old specific-pathogen-free chickens each were given an intraabdominal inoculation of either a type-8 avian adenovirus, [AMG 5 (2a], or a type-5 avian adenovirus, inclusion body hepatitis virus (IBHV). The diseases produced were similar. High (60-100%) mortality and statistically significant depression of body weights occurred in both infections. There were necrotizing hepatitis and pancreatitis, lymphoid depletion in the spleen, bursa of Fabricius and thymus, hydropericardium, nephritis and enteritis. Intranuclear inclusions occurred in affected organs. Fluorescent-antibody staining, the Feulgen reaction for deoxyribonucleic acid and electron microscopic studies, as well as studies from the literature, indicated that basophilic inclusions consisted of assembled adenovirions.
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PMID:Comparative study of experimental inclusion body hepatitis of chickens caused by two serotypes of avian adenovirus. 20 21

Two-day-old mice were inoculated orally with a mouse hepatitis virus which had been isolated from a suckling mouse with fatal diarrhea, and a systemic infection was shown to be established, though enterotropism of the isolate was evident. Significant viral growth and syncytium forming lesions were first detectable in the intestines at day 2 postinoculation, followed by the development of focal necrotic hepatitis. The virus titer in both liver and intestine attained maximum levels at days 4 to 5. Death occurred at day 5 or later, and 60 to 100% mice died during the first 2 weeks of life. Before death, some mice showed neurologic signs with high titered viruses recovered from the brain. The necrotizing lesions were also demonstrated in the lung and lymphoid organs.
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PMID:Pathology of diarrhea due to mouse hepatitis virus in the infant mouse. 22 29

Aleutian disease is a chronic persistent viral infection of mink characterized by hypergammaglobulinema, generalized plasmacytosis, sclerosing glomerulonephritis, polyarteritis, and plasma cell hepatitis with bile duct proliferation. The development of hepatic lesions was studied both light- and electron-microscopically in mink experimentally infected with Aleutian disease virus. Fifteen normal and 99 mink experimentally infected with Aleutian disease virus were used. Experimental mink were killed in intervals from 3 weeks to 23 months after infection, and liver sections were processed for both light- and electron-microscopic studies. Experimentally infected mink developed portal and intralobular lymphocytic and plasmacytic infiltrates in the liver 3 weeks after infection. Four to five weeks after infection there was evidence of early bile duct proliferation that began as an outgrowth of the portal bile ducts. Three to five months after infection a marked bile duct proliferation was present in some of the portal triads and adjacent liver lobules; but there was no tendency of these lesions to progress into biliary cirrhosis. Ultrastructural characteristics of proliferating bile duct cells were marked deformation, formation of multiple cell layers, reduction in the number of microvilli and desmosomes, and infiltration of the epithelial cells by lymphoid cells and plasmacytes. The hepatic lesions either develop by direct virus stimulation or by the deposition of virus-antibody complexes.
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PMID:[Pathogenesis of aleutian mink disease. VII. Chronic hepatitis with bile duct proliferation]. 24 13

Medical histories of themselves and their first-degree relatives were obtained from parents of 82 leukaemic children (54 acute lymphoblastic (ALL), 28 acute myeloblastic (AML)) and from control couples matched for age. The possibility of a primary familial immunological abnormality as an aetiological factor in childhood leukaemia was suggested by binding some infections significantly more frequently reported in parents than in controls, but more strongly supported by the finding of a significantly (P less than 0.02) increased prevalence of disorders associated with autoimmunity (but not of other conditions such as peptic ulceration, infective hepatitis, tuberculosis or malignancy) amongst members of ALL families compared to those of controls. Analogy with Down's syndrome and the strain of NZB mice, in which diminished T-cell function is associated with autoimmune disease and lymphoid neoplasia, is discussed. Varicella and herpes zoster occurred respectively in 2 ALL mothers during their pregnancies involving the patients and in none of the other 388 pregnancies here reported. This supports previous evidence that antenatal varicella infections may be of aetiological importance in some cases of ALL.
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PMID:Family studies in acute leukaemia in childhood: a possible association with autoimmune disease. 28 5

The study of human lymphoid cell differentiation markers has recently yielded many insights into the pathogenesis of certain diseases which primarily affect the immune system. The application of these markers has, however, generated a host of new questions. Both technical difficulties and uncertainties concerning the significance of particular markers limit their routine application at the present time. Indeed, many studies in the literature, both in the diseases reviewed above, and perhaps to a greater degree in other conditions ('autoimmune' diseases, sarcoidosis, hepatitis and various infections) require re-evaluation in the light of recently increased sophistication about cell surfaces. Because of these qualificatins, the application of multiple characterizations of lymphoid cells using independent methodologies is necessary before any firm conclusions can be drawn in a particular clinical or experimental situation.
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PMID:Human lymphocyte differentiation markers and their application to immune deficiency and lymphoproliferative diseases. 33 21

A characteristic alkaline phosphatase (orthophosphoric monoester hydrolase, alkaline pH optimum, EC 3.1.3.1) was detected in the sera of most patients with infectious mononucleosis, acute and chronic lymphatic leukaemia, non-Hodgkin's lymphoma, Burkitt's lymphoma and nasopharyngeal carcinoma. The enzyme was also present in the sera of nine out of 26 patients with cancer of the cervix. N-APase in these cases counted 30-100% of the total alkaline phosphatase activity. N-APase was absent from the sera of healthy individuals and of patients with acute and chronic granulocytic leukaemia, breast cancer, colon cancer, rheumatoid arthritis, ulcerative colitis, systemic lupus erythematosis, hepatitis and obstructive jaundice. Only three of 22 patients with Hodgkin's disease showed n-apase activity in the serum. In infectious mononucleosis the presence of N-APase activity was well correlated with the clinical course. In 13 cases studied, the clinical improvement was associated with the decrease or disappearance of N-APase activity. N-APase activity could not be detected in white cells of acute myeloid leukaemic patients, nor in the cells of myeloid blastic crisis of chronic granulocytic leukaemia. It was present in the cells of lymphoid blastic crisis of chronic granulocytic leukaemia.
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PMID:N-alkaline phosphatase: a potential disease marker for lymphoproliferative disorders. 43 2


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