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)

An in vivo murine model for immunodeficiency of both B and T cells is produced by continuous intraperitoneal infusion of 2'-deoxycoformycin (DCF), a specific tightly binding inhibitor of adenosine deaminase (ADase; adenosine aminohydrolase, EC 3.5.4.4). After DCF infusion, ADase of thymus, spleen, and lymph nodes was inhibited to varying degrees ranging from 57% to 100%. Immunodeficiency under these conditions was indicated by: (i) a striking decrease in lymphocyte response to the T-cell mitogens concanavalin A and phytohemagglutinin; (ii) an impairment of delayed hypersensitivity measured by the footpad reaction; (iii) a decrease in antibody production measured in both in vivo and in vitro plaque-forming cell assay; (iv) a significant prolongation of mouse skin allograft survival after transplantation into the C57BL/6J (H-2b) strain of skin from BALB/c (H-2d) mice; and (v) a marked lymphopenia. Histological examination indicated lymphoid degeneration in the thymus, lymph nodes, and spleen with no alterations in other tissues including bone marrow, kidney, lung, gastrointestinal tract, and liver except for the occurrence of hepatitis. A decrease in the number of Thy-1-positive cells in both spleen and lymph nodes further supported the fact of cytotoxicity of DCF to T cells. Anorexia and weight loss were observed within 5 days of continuous DCF infusion at 0.4 mg/kg body weight per day. These data indicate that this method provides an experimental model for future studies on the biochemical mechanisms responsible for the genetically determined severe combined immunodeficiency disease in man.
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PMID:Animal model for immune dysfunction associated with adenosine deaminase deficiency. 696 8

A systemic BCG infection in mice induced multiple small granulomas located mainly in the periportal areas of the liver. Following systemic challenge of such mice with purified protein derivative of tuberculin (PPD), a rapidly developing hepatitis with diffuse intralobular mononuclear cell infiltration was precipitated, accompanied by high levels of aspartate transaminase in peripheral blood, hypoglycemia, focal hepatocyte necrosis, and accumulation of fibrinogen in liver. Bacterial lipopolysaccharide (LPS) also provoked acute hepatic damage both in BCG-infected mice and in mice pretreated with Corynebacterium parvum. PPD was not active in the latter. There were also lymphoid cell destruction and fibrinogen accumulation in the spleen of BCG-PPD-treated mice. Possible involvement of inflammatory and hepatotoxic mediators is suggested, and a T-lymphocyte-macrophage regulatory role in the pathogenesis of hepatitis is discussed.
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PMID:Tuberculin hypersensitivity hepatitis in mice infected with Mycobacterium bovis (BCG). 702 5

Most previous studies of lymphocyte-mediated cytotoxicity to animal and human hepatocytes have not taken into account the ability to human lymphoid cells to kill spontaneously cultured cell lines, particularly those of malignant origin (the natural killer or NK effect). We have studied spontaneous killing to a human target (erythromyeloid cell line K562) in patients with biopsy-proven liver disease and from normal controls. Patients with chronic active hepatitis were shown to have a significant reduction in NK activity unrelated to immunosuppressive therapy (P less than 0.01). Other groups showed normal values. These results imply that cytotoxic effectors reported active in chronic liver disease are K cells and not NK cells, with which they share many characteristics, and suggest that a cytotoxic mechanism considered to be of importance in immunosurveillance may be reduced in chronic aggressive hepatitis.
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PMID:Natural killer activity in patients with biopsy-proven liver disease. 731 58

The course of experimental hepatitis B in chimpanzees was studied, and two biochemically, serologically, and histopathologically distinctive types were identified. The first type was self-limiting, rapidly resolving hepatitis with spiking and short-term elevation of SGPT starting at around 5 weeks after the appearance of HBs antigenemia. The second type was smoldering and persistent hepatitis with low-plateau-forming persistent transanimase abnormality developing around 10 weeks after the appearance of HBsAg. Anti-HBc became positive before the transaminase elevation in the second type, while in the first type it became positive after the SGPT elevation. Histologically, the second type was characterized by marked infiltration of lymphoid cells in portal areas with lymphoid follicles. This was seen even before the histologic manifestations of liver cell injury and the elevation of SGPT in two cases. The portal inflammatory cell infiltration became evident at 6 to 9 weeks after the HBsAg appearance and became increasingly more severe thereafter. The intralobular changes remained mild, with rare liver cell necroses. Chronic hepatitis developed subsequently in two cases. In the first type, the portal changes developed almost simultaneously with intralobular changes and were not prominent. In contrast to the second type, the intralobular changes with multiple liver cell necrosis were more severe.
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PMID:Two distinct types of hepatitis in experimental hepatitis B virus infection. 737 87

The syndrome of nodular lymphoid hyperplasia of the small bowel with hypogammaglobulinemia is one of the hypogammaglobulinemic enteropathies. Chronic diarrhea and malabsorption are the most characteristic features of this disease, and they are frequently associated to hypogammaglobulinemia of various types (acquired, congenital non sex-linked) and to selective IgA deficiency. The immunological deficiency gives rise to the more characteristic features of the disease, namely: a) hypogammaglobulinemia; b) respiratory infections and dental caries; c) Giardia lamblia infestation of the small bowel; d) the characteristic radiological features; and, e) the histological aspect of the intestinal mucosa with absence of plasma cells. Periodical follow-up is needed because of the increased incidence of tumors in immunological deficiency states. A new case of nodular lymphoid hyperplasia associated to hemolytic anemia and granulomatous hepatitis is reported, and its possible pathogenesis is discussed.
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PMID:[Nodular lymphoid hyperplasia of the small bowel with IgA deficiency and hemolytic anemia (author's transl)]. 742 63

The primary biliary cirrhosis (PBC) is characterized by lymphoid infiltrates in the portal tracts of the liver and occurrence of antimitochondrial autoantibodies (AMA) in serum directed against the pyruvate dehydrogenase complex or other enzyme complexes that are located on the inner mitochondrial membranes. The destruction of the biliary tracts is thought to be mediated by autoreactive liver infiltrating T-cells. In this study we demonstrate the reactivity of peripheral and liver-infiltrating T-cells against a crude preparation of human liver subcellular fractions measured by the tritium-thymidine uptake. Peripheral blood mononuclear cells (PBMC) from 13 of 15 patients with PBC and from 3 of 9 patients with chronic autoimmune hepatitis recognized human liver mitoplasts, i.e. mitochondria depleted of their outer membranes. PBMC from patients with chronic viral hepatitis B and C or with extrahepatic cholestatic icterus and PBMC from healthy controls did not recognize this antigen. Monoclonal antibodies against HLA-class II molecules blocked this proliferative response. Clonal analysis of 115 liver-infiltrating T-cells derived from two diagnostic liver biopsies of patients with PBC revealed a predominance of activated CD4+CD8- T helper cells. Six CD4- positive T-cell clones were reactive to the HLM preparation when the antigen was presented by autologous B cell lines. MAb against HLA-class II or HLA-DR inhibited the response whereas mAb against HLA-DP did not. These clones did not respond to other subcellular fractions of human liver tissue. We conclude that among liver-infiltrating T-cells in PBC autoreactive T-cells exist that recognize some epitopes on the inner mitochondrial membranes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Infiltrating T-cells in primary biliary cirrhosis recognize mitochondrial epitopes]. 748 31

Since the introduction of screening for hepatitis C virus (HCV) in donated blood, the risk of contracting posttransfusion hepatitis has been greatly reduced and the test has led to the recognition of asymptomatic blood donors positive for anti-HCV antibodies. Following confirmation of the HCV status with second generation RIBA testing followed by counselling, 55 patients had full investigations, including liver biopsy. These were classified by the traditional chronic hepatitis system and were graded according to the Knodell and Scheuer histological activity indices. Seven of the biopsies were normal (12%), apart from minor degrees of steatosis in two. Eleven cases (20%) were in the chronic lobular hepatitis category without portal inflammation, while 37 cases showed portal inflammation, including 20 (36%) cases where chronic persistent hepatitis was the predominant feature and 17 cases (31%) where there was chronic active hepatitis with piecemeal necrosis. Features which have previously been described in chronic HCV-associated hepatitis were noted: portal lymphoid aggregates (58%), lymphoid follicles with germinal centres (15%), bile duct damage (11%), lobular inflammation (80%), sinusoidal mononuclear cell infiltration (26%), acidophil body formation (11%), and steatosis (47%). Fibrosis was present in 46% of cases but was generally of mild degree; 9% of biopsies demonstrated bridging fibrosis but no cases of cirrhosis were present. Even though serum transaminase levels correlated well with the presence of chronic hepatitis and with the Scheuer and Knodell activity indices, a proportion of patients with significant liver damage had normal transaminase levels, and this study suggests the need for liver biopsy in the evaluation of asymptomatic HCV-positive blood donors.
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PMID:The histopathological features of asymptomatic hepatitis C virus-antibody positive blood donors. 752 Apr 12

The correlation between histological features of liver biopsy specimens before interferon (IFN) treatment and the clinical effect of IFN administration on chronic hepatitis C was investigated. The changes in the biopsy specimens were graded on the basis of different histological features. The degree of portal fibrosis adversely affected the rate of normalization of ALT levels in the patients treated with IFN. During IFN treatment, the group of chronic hepatitis C patients who showed marked piecemeal necrosis and less lymphoid follicle formation in the liver specimens, showed abnormal ALT values even after disappearance of hepatitis C virus RNA in the sera, suggesting that functions of IFN other than antiviral effect, including enhancing interaction between lymphocytes and hepatocytes, sometimes induce exacerbation of hepatitis.
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PMID:[Correlation between histological features of liver biopsy specimens and clinical effect of interferon on patients with chronic hepatitis C]. 752 16

The pathogenesis and perpetuation of hepatocellular injury in hepatitis C viral infection remains unclear. It has been proposed that a direct viropathic effect, the host immune response, or both mediate cell damage. To address this issue, the immunophenotype of the inflammatory infiltrate in the liver of 18 patients with abnormal liver function tests and serologically detectable hepatitis C virus antibodies was compared with seven control patients (three cases with hepatitis B virus infection, two with alcoholic hepatitis, and one patient each with primary biliary cirrhosis and autoimmune hepatitis). The immunohistochemical markers included UCHL1, L26, Ham-56, Mac-387, CD68, Leu-M1, and cathepsin B. We found that T cells represent the predominant cell type in both histopathologic patterns of hepatitis C, ie, chronic active hepatitis and chronic persistent hepatitis, but the intensity of the T-cell infiltrate displayed marked differences. B-cell infiltrates were only seen in the germinal centers of lymphoid follicles in portal tracts. Furthermore, significant numbers of CD68-positive macrophages/monocytes were seen in the more aggressive form of hepatitis C viral infection. These data suggest that the T-lymphocyte-mediated host immune response is similar in chronic active and chronic persistent hepatitis patterns of hepatitis C viral infection, but varies in its intensity. In addition, macrophages/monocytes may play a role in hepatocyte and bile duct injury in chronic hepatitis C.
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PMID:Chronic hepatitis C. Analysis of host immune response by immunohistochemistry. 753 56

Most histologic studies of cryptogenic chronic liver disease were done before the discovery of hepatitis C, and therefore encompass the histologic spectrum of this disease. The authors report the histopathologic findings of 18 liver biopsies of presumed cryptogenic chronic liver disease patients and compared them to chronic autoimmune hepatitis and hepatitis C virus biopsies. Severe bridging fibrosis or cirrhosis was present in 55%. Eighty percent of biopsies had minimal necroinflammatory activity including those with cirrhosis; 20% had moderate activity. Histologic distinction from chronic hepatitis C was difficult in the minimally active cryptogenic chronic liver disease biopsies because 20% of biopsies had portal lymphoid follicles and 33% had macrovesicular steatosis. Chronic autoimmune hepatitis had more parenchymal necroinflammatory activity and plasma cells than did either cryptogenic chronic liver disease or chronic hepatitis C biopsies. These findings suggest that one form of cryptogenic chronic liver disease is a persistent, low grade hepatitis that can progress to cirrhosis despite an innocuous histopathologic appearance. Pathologists should be aware that cryptogenic chronic liver disease biopsies may have minimal histologic abnormalities. These biopsies should not be reported as normal. Such cases require long-term clinical follow-up.
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PMID:Histologic spectrum of cryptogenic chronic liver disease and comparison with chronic autoimmune and chronic type C hepatitis. 757 18


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