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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of duck hepatitis B virus (DHBV) DNA in liver and serum and its state (integrated vs. free) were studied in 23 ducks from Chi-tung county in China by spot hybridization and Southern blot hybridization, respectively. In 16 of 23 (70%), DHBV DNA was detected in serum and/or in liver tissue. These infected ducks showed a variety of pathological changes including advanced chronic disease in the liver. In contrast, none of the virus-negative ducks had advanced hepatic changes. One DHBV DNA-seropositive duck had a large hepatocellular carcinoma. Southern blot analysis demonstrated integrated DHBV DNA in neoplastic tissue and abundant episomal DHBV DNA in non-neoplastic tissue of the liver. In one noninfected duck with a small adenoma, no viral DNA was detected in tumor or non-neoplastic tissue. The detection of integrated DHBV DNA in hepatocellular carcinoma suggests that DHBV behaves like human and woodchuck hepatitis viruses in relation to chronic liver disease and hepatocarcinogenesis.
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PMID:Duck hepatitis B virus DNA in liver and serum of Chinese ducks: integration of viral DNA in a hepatocellular carcinoma. 386 Aug 52

Of 560 hepatitis B surface antigen-positive patients who were tested for antibody to hepatitis delta-antigen by blocking radioimmunoassay, 29 (5%) were seropositive. Patients with chronic active hepatitis had a greater frequency of seropositivity than those with chronic persistent hepatitis (26% vs. 0%, p less than 0.05), and patients with symptomatic chronic disease harbored the antibody more commonly than asymptomatic counterparts (14% vs. 2%, p less than 0.01) or patients with acute hepatitis (14% vs. 1%, p less than 0.02). Of 8 patients with acute fulminant hepatitis, including 6 who died of liver failure, none were seropositive. Antibody was detected in drug users, dialysis patients, hemophiliacs, and transfusion recipients; in 17 patients, however, including 3 homosexuals, it occurred sporadically. Samples harvested in 1969 contained delta-antibody. Antibody was found in most ethnic groups, including Orientals, where it occurred only in relocated Vietnamese. We conclude that delta-antibody is detected infrequently in a diverse referral population within the United States. Seropositivity is associated with symptomatic chronic disease and histologic findings of chronic active hepatitis. Homosexuals and resettled Vietnamese are susceptible to sporadic delta-infection.
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PMID:Frequency and significance of delta antibody in acute and chronic hepatitis B. A United States experience. 405 16

The sensitivity of mice to mouse hepatitis virus 3 (MHV3) varies according to strain, age, and immune status of the animals. In semisusceptible strains, mice surviving the acute phase of infection develop a chronic disease characterized by the occurrence of paralysis, virus persistence, and immunodeficiency. Persistent MHV3 infections established in vitro in YAC and RDM -4 mouse lymphoid cell lines were characterized by virus production, presence of cytoplasmic viral antigens, and cell lysis. The occurrence of cell "crisis" in YAC cells was manifested by a sharp increase in cell lysis and in the number of fluorescent cells and, concomitantly, by a marked decrease in virus titers. A relationship was observed among the percentage of fluorescent cells, cell lysis, and virus yield and was modulated by renewal of culture media, change in temperature, or inhibition of cellular RNA synthesis. Cell cloning and antibody treatment experiments indicated that viral transmission was performed by viral infection of newly permissive cells produced by the division of uninfected cells in the culture and not by transmission of viral information by infected dividing cells. The biological and biochemical properties of MHV3 variants derived from persistently infected YAC lymphoid cells were characterized. Thermosensitivity and thermolability of cloned viruses originating from persistently infected YAC cells, as well as parent virus suspensions, were studied. A similar heterogeneity was observed when YAC-derived cloned substrains (YAC-MHV3) were compared with parent-derived cloned viruses, indicating that no selection of temperature-sensitive mutants was induced in persistently infected YAC cells. However, the capacity of MHV3 to induce a lethal acute disease when injected into susceptible mice was lost very rapidly. The absence of pathogenicity was related to the induction of a subclinical infection which elicited defense mechanisms. These data suggest, therefore, that MHV3 replication in lymphoid cell lines leads to induction or selection of variants which maintain pathogenicity in vitro but display reduced pathogenic effects in vivo.
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PMID:Persistent infection with mouse hepatitis virus 3 in mouse lymphoid cell lines. 632 31

The material of 100 punch liver biopsies from patients with a secondary nonspecific reactive hepatitis as a complication of chronic disease of the alimentary canal (gall bladder, pancreas, stomach and intestine) was studied. The criteria of morphological diagnostics of this hepatitis were elaborated. It is established that the morphology of the nonspecific reactive hepatitis depends on the pathogenesis and clinical course of the underlying disease. The response of liver macrophagal system is a basis of inflammatory changes.
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PMID:[Morphological diagnostic criteria of nonspecific reactive hepatitis]. 652 67

Over a 3-year period, 149 Yucpa Indians in Venezuela developed hepatitis; 34 persons died and at least 22 developed chronic hepatitis. Children and young adults were primarily affected, especially males. Serologic testing showed that hepatitis B virus infection was highly endemic in this population, but also that 65% of patients had hepatitis B virus surface antigen (HBsAg) during or after illness. Most patients had evidence of delta-agent superinfection; 86% of HBsAg-positive patients had delta antibody, and delta antigen was found in specimens taken during autopsies on 7 of 9 patients. Serologic data suggested that most infections were due to delta superinfection of hepatitis B carriers, and that more than 60% of these infections progressed to chronic disease. Delta agent infection, and particularly delta superinfection of hepatitis B carriers, appears to be an ominous occurrence that may develop in populations among whom hepatitis B virus infection is endemic, and who have no other risk factor for delta infection.
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PMID:Delta virus infection and severe hepatitis. An epidemic in the Yucpa Indians of Venezuela. 669 55

Patients with non-A, non-B post-transfusion hepatitis were followed from the onset of their disease until their blood tests normalized, until they died, or until the present time. Of 66 patients, 30 had a spontaneous resolution of their biochemical disease. Ten patients died or were begun on immunosuppressive therapy with transaminases still abnormal. The remaining 26 patients had abnormal transaminase levels when last seen. By actuarial analysis, only 54% of hepatitis patients are predicted to develop s spontaneous biochemical remission within 3 yr. No further resolutions have occurred after that time, Icteric and anicteric acute disease may be equally likely to progress to chronic disease. Initial and follow-up liver biopsy specimens have revealed both chronic persistent and chronic active hepatitis. Two patients showed histologic evidence of cirrhosis, and a third developed a hepatic coagulopathy and sphenomegaly. No other patient to date, however, has veveloped overt evidence of hepatocellular failure or portal hypertension. Thus, non-A, non-B post-transfusion hepatitis frequently results in biochemical evidence of chronic liver disease, and in a few patients cirrhosis may develop slowly and in a clinically inapparent fashion.
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PMID:The long-term course of non-A, non-B post-transfusion hepatitis. 677 6

The progression of acute viral hepatitis non-A, non-B in a group of young female patients with well defined disease was evaluated retrospectively over a period of 21/2 years. The histologically proved chronification rate was 39 per cent. It was looked for a correlation between some parameters in the acute phase of the disease, the distribution of HLA antigens, and the progression to chronicity. There were no statistically ensured differences of HLA antigens between patients with chronic hepatitis non-A, non-B, patients with healed acute one, patients with chronic hepatitis type B, and the normal population. The level of transaminases within the acute phase of the illness did not allow to draw any conclusion for the further progression of the disease. But icteric patients seemed to develop chronic disease more seldom. In this time, the reason of the high chronification rate after infection by hepatitis virus(es) non-A, non-B is not yet clear.
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PMID:[Chronicity of non-A, non-B hepatitis. Evaluation of the clinical course with special reference to the types of distribution of HLA antigens and clinical criteria]. 681 4

Serological parameters were compared in 15 cases of Coxiella burnetii infection comprising 5 cases each of primary Q fever, chronic granulomatous hepatitis, and endocarditis. The diagnosis was made on the basis of clinical history and serology and on the isolation of C. burnetii phase I from biopsy specimens of liver and bone marrow from two patients with granulomatous hepatitis and from the aortic valve vegetations of five patients with endocarditis. The temporal sequences of immunoglobulin levels, rheumatoid factor, and specific antibody responses to phase II and phase I antigens of C. burnetii were evaluated as predictive correlates of the three Q fever entities. Serum levels of immunoglobulin classes G, M, and A were variable in all the entities of Q fever. Increased mean levels (in milligrams per deciliter) of immunoglobulin G (IgG) and IgA were noted with chronic disease in the sera of some patients, whereas IgM levels were not significantly different from normal values. Rheumatoid factor was significantly elevated in chronic disease but not in primary Q fever. The temporal sequence of C. burnetii phase II and phase I antibodies were compared by microagglutination, complement fixation, and indirect microimmunofluorescence tests. All of these serological tests were useful in distinguishing primary from chronic disease. Thus, the ratio of anti-phase II to anti-phase I antibodies was greater than 1, greater than or equal to 1, and less than or equal to 1 for primary Q fever, granulomatous hepatitis, and Q fever endocarditis, respectively. Moreover, the high phase-specific IgA antibody titers in the indirect microimmunofluorescence test were diagnostic for endocarditis.
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PMID:Serological evaluation of O fever in humans: enhanced phase I titers of immunoglobulins G and A are diagnostic for Q fever endocarditis. 688 55

Formerly the diagnosis of acute and chronic non-A, non-B hepatitis was made by the exclusion of other causes. However, in 1989 cloning of an antigenic component of the hepatitis C virus (HCV) was reported. This led to first- and second-generation tests for antibody to HCV (anti-HCV) in serum. HCV has been associated with acute and chronic posttransfusion and sporadic non-A, non-B hepatitis, and with hepatocellular carcinoma. Viral HCV RNA can be estimated with the polymerase chain reaction test, but this technically difficult test is not generally available. The entire viral genome has been sequenced. The envelope region shows considerable variation, and mutant HCV infections are being described already. There are geographic variations in the prevalence of anti-HCV, but usually about 0.5% to 1% of healthy blood donors test positive. Parenteral exposure to blood, especially by transfusion or drug abuse, remains a certain means of acquiring HCV infection. The method by which millions without parenteral risk factors acquire HCV remains uncertain. Vertical transmission and sexual and family spread occur only rarely. Body secretions are free of the virus. The mode of transmission may become clarified when tests for viral HCV as opposed to anti-HCV become generally available. Acute HCV infection usually is mild, and the chronic disease is also indolent. Carriers of hepatitis B virus or alcoholics who also test positive for HCV have more serious disease. Chronic HCV infection must be distinguished from autoimmune chronic active hepatitis. The most important difference is the response to corticosteroid therapy, which is good in autoimmune hepatitis and poor in HCV-related disease. Hepatocellular carcinoma can complicate HCV-related cirrhosis, usually about 20 years after infection with HCV. Recombinant interferon-alpha is used to treat chronic HCV disease, but selection of patients, dose, and duration of therapy are uncertain. In general, 50% of patients respond to the treatment, but 50% of these will have a relapse, with an overall response rate of 25%. Liver transplantation in patients with end-stage HCV disease usually is followed by infection of the graft.
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PMID:Chronic hepatitis C. 751 76

Aplastic anemia (AA) is a rare complication of viral hepatitis affecting mainly children or young adults. Most reported cases have been associated with community-acquired non-A, non-B hepatitis, but hepatitis A and B have also been implicated in a few patients. We report on a 43-year-old woman with severe AA, in association with acute hepatitis C virus (HCV) infection, diagnosed by detection of HCV RNA by the polymerase chain reaction technique. Her AA was successfully treated with anti-thymocyte globulin and cyclosporin A. The hepatitis C progressed to chronic disease but, despite a follow-up time of 2 years, the patient still has no detectable anti-HCV antibodies, as evaluated with a second-generation anti-HCV assay.
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PMID:Severe aplastic anemia associated with seronegative community-acquired hepatitis C virus infection. 768 49


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