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)

During HBAg positive acute viral hepatitis transitory antibodies of a low titer against smooth muscle, vascular endothelium, nuclei, and liver cell membrane antigens (polygonal pattern of immunofluorescence) occur. In HBAg positive chronic aggressive hepatitis, sometimes antibodies against nuclei or smooth muscle are associated with HBAg. Their occurrence heralds an unfavorable prognosis. High titer antibodies against nuclei and smooth muscle - a typical serology finding in lupoid chronic aggressive hepatitis - and mitochondrial antibodies have not been observed in a HBAg positive hepatitis. Subdividing chronic hepatitis in six different groups is possible with HBAg and antibodies. The predominance of histocompatability antigen HLA 8 in lupoid hepatitis and a lack of this leukocyte antigen in HGAg positive chronic aggressive hepatitis suggests that in the various forms of hepatitis, a different susceptability and capability for immune response towards microorganism is reflected. It is postulated that for course and outcome of hepatitis, the type of immune reaction plays a decisive role.
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PMID:[Humoral immune phenomena in acute and chronic viral hepatitis (author's transl)]. 108 Oct 70

Adhesion to and penetration through the sinusoidal vascular endothelium is a mandatory step for leukocyte migration and accumulation at sites of liver inflammation. This leukocyte trafficking is controlled by interactions between adhesion molecules on leukocytes and corresponding ligands on endothelial cells. We have analyzed the in situ distribution of two recently described vascular adhesion molecules (i.e., endothelial leukocyte adhesion molecule-1 and vascular cell adhesion molecule-1) and of the lymphocyte "homing" receptor cluster of differentiation antigen-44 in normal and inflamed liver biopsy specimens. Endothelial leukocyte adhesion molecule-1 and vascular cell adhesion molecule-1 were absent from normal liver tissue, but they were strongly expressed on sinusoidal lining cells in inflammatory liver disease. Endothelial leukocyte adhesion molecule-1 expression predominated diffusely throughout the liver parenchyma in acute hepatitis; in contrast, vascular cell adhesion molecule-1 was mainly expressed in areas of periportal and intralobular inflammation in chronic active and persistent hepatitis. The "homing" receptor cluster of differentiation antigen-44 was weakly expressed on scattered mononuclear cells and on sinusoidal lining cells in normal liver tissue, but it was strongly up-regulated on mononuclear inflammatory cells and sinusoidal lining cells in acute and chronic hepatitis. In addition, reactivity for the cluster of differentiation antigen-44 was found on the membranes of variously sized clusters of hepatocytes in biopsy specimens with acute hepatitis. De novo or up-regulated expression of these adhesion molecules on sinusoidal lining cells in inflamed liver biopsy specimens indicates that these cells actively modulate their phenotype in response to environmental factors, thus playing a key role in the recruitment of leukocytes in acute and chronic liver inflammation.
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PMID:Vascular adhesion molecules in acute and chronic liver inflammation. 137 Sep 47

Intestinal lesions due to infection with an enterotropic strain of mouse hepatitis virus (MHV-Y) were found to be more severe and wide-spread in BALB/cByJ and Cr1:CD-1(ICR) mice than in SJL mice inoculated at 1 week of age, using nonparametric ranking analysis. Lesions and viral antigen were limited largely to the bowel, but also occurred in the liver and brain of some mice. BALB/cByJ mice developed a particularly high prevalence of brain infection, resulting in mortality after the enteric phase of infection had ceased. MHV-Y antigen was present in neurons, glia and vascular endothelium in a vascular distribution. Cr1:CD-1(ICR) pups inoculated with MHV-Y at 4 or 7 days of age developed severe typhlocolitis, enteritis and encephalitis with moderate mortality. Pups infected at 2 or 3 weeks of age had mild intestinal lesions with minimal alteration of mucosal architecture, no encephalitis and no mortality. These results demonstrate that host age and genotype influence the course of enterotropic mouse hepatitis virus, as has been shown previously with non-enterotropic, respiratory-type strains of mouse hepatitis virus.
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PMID:Host age and genotypic effects on enterotropic mouse hepatitis virus infection. 303 77

Of 1270 consecutive patients with liver diseases of various types we have examined the blood serum on autoimmune antibodies against cell nuclei (ANA), smooth muscle (SMA) and vascular endothelium. 98 patients (7.7%) had antibodies of one of the above. These patients were matched with patients with the same liver diagnosis without antibodies following the matched pair technique. 3-5 years later both were examined by the family doctor. It remained a collection of 58 pairs. The examined criteria were compared pair by pair. We conclude the existence of autoimmune antibodies from type ANA, SMA or vascular endothelium is without prognostic prediction. The outcome of chronic active hepatitis was in majority benign, but the outcome of alcohol-toxic hepatitis was bad, because the people were unable to stop the alcoholism.
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PMID:[Detection of tissue antibodies and long-term prognosis in liver diseases--a catamnestic matched-pair study]. 325 62

The histo-pathological lesions of hypersensitivity vasculitis (HV) consist in an inflammatory reaction to circulating immune complexes deposited on the vascular endothelium. A provocation test by intradermal injection of histamine was used to demonstrate HV in patients with chronic hepatitis. Three groups of patients were studied: 16 with chronic hepatitis and HV, 22 with chronic hepatitis without HV, 4 control subjects. Skin biopsy was performed before and 3 hours after intradermal histamine. The following markers were looked for in the serum, skin and liver of all patients with chronic hepatitis: HBV (HBs Ag and HBe Ag, anti-HBs, anti-HBe and anti-HBc in the serum, HBs and HBc Ag in the liver); non-A non-B (non-A, non-B Ag and antibody, anti non-A non-Bc in the serum, non-A, non-Bc Ag in the liver). Viral antigens were found in healthy skin in 2 cases (1 chronic A hepatitis, 1 vasculitis), and after injection of histamine in 9 cases (4 chronic A hepatitis, 5 vasculitis). Viral antigens were found on skin biopsy in 2 patients with negative sera. Significant skin changes after histamine were detected only in HV (75 p. 100) even in the absence of cutaneous vasculitis (6/12 positive cases). An intradermal histamine provocation test is a simple, non-invasive method for diagnosing HV.
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PMID:[Satellite vasculitis of B or non-A non-B hepatitis. Diagnostic value of a provocation test by intradermal injection of histamine]. 361 49

The pattern of tissue tropism for several prototype and uncharacterized strains of mouse hepatitis virus (MHV) was studied by intranasal inoculation of each virus strain into groups of neonatal Swiss mice under otherwise identical conditions. Mice were killed at intervals up to 18 days after inoculation, and their tissues were examined for the presence of MHV antigen by indirect immunofluorescence. Two patterns of infection were apparent. Prototype MHV strains 1, 3, A59, JHM, S and uncharacterized MHV strains Tettnang and wt-1 produced a respiratory pattern, in which nose and lung were consistently involved with dissemination to other organs in a vascular distribution. Pulmonary vascular endothelium and alveolar septal cells, but not airway epithelium, were infected. An enteric pattern was observed with MHV-Y and wt-2 in which MHV antigen was largely restricted to the nose and bowel, with limited dissemination to other abdominal organs but not lung. Intestinal lesions in these mice were severe compared to those manifesting the respiratory pattern of infection. These results indicate that, like coronaviruses of other species, different strains of MHV possess different primary and secondary organotropisms following a natural route of inoculation in a susceptible host.
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PMID:Mouse hepatitis virus strain--related patterns of tissue tropism in suckling mice. 633 43

Ninety-six liver biopsies [32 bone marrow transplant (BMT), 7 pre-BMT, and 57 non-BMT] are reviewed for histological evidence of graft versus host disease (GVHD), based on bile duct atypia and related inflammatory changes. In addition, the presence of cholestasis, piecemeal necrosis, and attachment of lymphocytes to vascular endothelium (endothelialitis) are evaluated. The 57 non-BMT biopsies include examples of viral hepatitis (acute and chronic), nonviral chronic hepatitis, extrahepatic biliary obstruction, cytomegalovirus hepatitis, primary biliary cirrhosis, and orthotopic liver transplant rejection. Although the sensitivity of bile duct damage as an indicator of GVHD appears high (only one probable false negative was noted), there is considerable overlap between the changes of GVHD and occasional cases of acute and chronic hepatitis and extrahepatic biliary obstruction. Nine of the 57 non-BMT biopsies (15%) were felt to be consistent with GVHD and represent "false positives". Despite this relative lack of specificity, analysis of several features in combination provided clues to improve accuracy of diagnosis. The findings of extensive bile duct damage with minimal inflammatory changes is characteristic of GVHD. Possibly more predictive is the presence of endothelialitis of portal or central veins, which was seen in only three non-BMT biopsies, being present in eight cases of GVHD.
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PMID:Hepatic graft versus host disease: a study of the predictive value of liver biopsy in diagnosis. 636 48

HBsAg has been detected by direct immunofluorescence in the small bowel biopsy specimen of a 16 a old male patient with diarrhoea and HBsAg seronegative (autoimmune) chronic aggressive hepatitis. HBsAg was localized focally in apical regions of intestinal crypts, in the cytoplasm, and on their cell membranes as well as in vascular endothelium. Pretreatment of the tissue sections with unlabelled anti-IgM, anti-IgG, and fresh human serum did not block the direct staining for HBsAg. Antisera to IgG, the complement components C1q, C4, and C5 as well as to fibrinogen and FITC-Staphylococcus protein A were bound in a similar manner. Therefore, it may be reasonable to assume, that hepatitis B virus can infect the human small intestine and could be regarded as one of rare gastroenteritic viruses.
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PMID:[Immunofluorescent optical detection of HBSAG in the human small intestine in chronic aggressive HBSAG-seronegative hepatitis with diarrhea]. 642 Oct 68

Serum samples from 35 female patients with and after acute non-A/non-B-hepatitis following application of human immunoglobulin "Anti-D (Rh0)" were tested for circulating antibodies against nuclei, smooth muscle, vascular endothelium connective tissue, mitochondria, ribosomes, endoplasmatic reticulum, stomach parietal cells, and other by indirect immunofluorescence and for circulating immune complexes by polyethylene glycol method. Tests were performed twice in the first weeks of illness and about 2 years after infection. 5 patients (14%) had increased levels of immune complexes, detected only in the early stage of illness. The most important early antibodies were low titre IgG-antibodies against smooth muscle antigens (68%), connective tissue (27%) and IgM-rat heart antinuclear factors (31%). 2 patients with recidival and chronic hepatitis had IgG-antimitochondrial antibodies 2 years after infection (titre I : 40 and I : 160). The results suggest, that special antibodies could be involved in the course of special form of non-A/non-B hepatitis.
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PMID:[Circulating autoantibodies and immune complexes in and after acute non-A/non-B hepatitis]. 645 99

Four groups of 6 pigs each were given 5 x 10(5) to 3 x 10(6) sporocysts of a Georgia isolate of Sarcocystis suicanis. Only the 6 pigs given 3 x 10(6) sporocysts became acutely ill at postinoculation days (PID) 12 to 15, and 3 of the 6 diet at PIG 14 or 15. Clinical signs included purpura of the skin of the ear, snout, and buttocks and dyspnea, muscle tremors, and severe locomotor difficulties. Clinical abnormalities were accompanied by laboratory findings of pyrexia, severe anemia, leukopenia, thrombocytopenia, megathrombocytosis, prolonged prothrombin time and activated partial thromboplastin time, and hypofibrinogenemia. Seemingly, excessive intravascular coagulation may be involved in the pathogenesis of this disease in swine. Pigs given 5 x 10(5) to 1 x 10(6) sporocysts did not exhibit clinical signs; however, leukopenia and thrombocytopenia were demonstrated in the pigs at all dosage levels. Growth rates were impaired in surviving pigs. Second-generation schizonts containing merozoites were found in vascular endothelium of pigs dying on PID 14 or 15. Nonsuppurative myocarditis and hepatitis were present. Numerous developing cysts were in the musculature of pigs enthanatized on PIG 35 to 52. Cyst dissolution and resorption occurred concomitantly, indicating that swine may be able to clear the infection.
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PMID:Experimental Sarcocystis suicanis infections: disease in growing pigs. 680 76


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