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

Sera from children with various clinical categories of hepatitis were examined for hepatitis B surface (HBs) antigen (Ag) by radiommunoassay and for antibody to HBsAg (anti-HBs) by the passive hemagglutination test. It was found that frequencies of HBsAg and anti-HBs in 56 cases of acute hepatitis were 55% (31/56) and 11% (6/56), respectively. All of 4 patients with chronic hepatitis were found to have persistent HBs antigenemia. As for hepatitis in infant under the age of 6 months HBs Ag was detected in 2 each of 31 cases of neonatal hepatitis and of 15 cases of anicteric hepatitis. The data suggest the importance of HB virus as an etiologic agent of acute and chronic hepatitis in children in this country, however, other agents were supposed to be responsible for hepatitis in early infancy. Anti-HBs Ab was first detected in 15% of a group of children age from 3 to 5 years in Rishiri Island and in 12% of children aged from 6 to 9 years in Sapporo City. Frequency increased gradually through school age in both areas. Thus, HB virus infection seems to be common in the childhood population in urban as well as rural area of Hokkaido district.
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PMID:Clincial and edidemiological studies on hepatitis B in children. 85 41

Twenty-three infants born to asymptomatic hepatitis B surface antigen (HBSAg) carrier mothers were followed up to determine the vertical transmission of hepatitis B virus. Four infants became positive for HBSAg within four months after birth. Three showed hepatic dysfunction; liver biopsy specimens demonstrated mild chronic hepatitis in one and persistent hepatitis in another. In six infants followed up for more than six months after birth, antibody to HBSAg (anti-HBS) without antigenemia could be detected. Antigenemia of cord blood strongly suggested that hepatitis B viral infection of the infant would occur. HBSAg was also demonstrated in breast milk by radioimmunoassay in three cases. These findings indicate that vertical transmission of hepatitis B virus occurs in many infants born to asymptomatic HBSAg carrier mothers, and that some of them become persistent carriers or develop chronic hepatitis without showing any signs suggesting hepatic involvement.
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PMID:Hepatitis B surface antigen and chronic hepatitis in infants born to asymptomatic carrier mothers. 86 15

The apparent well-being of some children who as neonates were believed to have obstructive jaundice prompted us to study the clinical course, histologic features and possible etiologic factors in 17 children with cholestasis in the neonatal period. During a follow-up period of five months to 22 years, all had signs of chronic cholestasis, but only four died (two from nonhepatic causes); the others live remarkably normal lives. Serial hepatic biopsies in 11 showed a variety of initial lesions, which progressed to hypoplasia of the intrahepatic bile ducts, increasing portal fibrosis and eventual cirrhosis. Although evidence of possible viral infection was found in only 10 cases, a hepatitis, beginning either before or after birth, appears to be a likely original cause. The histologic changes seen may represent different stages of one process, starting as cholestasis with or without evidence of hepatitis and progressing to obliteration or failure of normal growth of the intrahepatic bile ducts.
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PMID:Intrahepatic cholestasis in childhood. 95 76

Cell-mediated immunity (CMI) to hepatitis B surface antigen (HBsAg) was investigated in patients who recovered from acute hepatitis B and in chronic carriers of the antigen, either with or without liver disease. The study was performed using leucocyte migration inhibition test and purified HBsAg. In antigen-negative post-hepatitis patients the frequency of cellular immunity to HBsAg (63.6%) showed a significant difference to controls. On the other hand, only one out of 5 antigen-positive post-hepatitis patients showed sensitisation to HBsAg; four out of these cases had chronic hepatitis at liver biopsy. In HBsAg-chronic carriers, with or without liver disease, the frequency of CMI to HBsAg was not significant to controls. A significant correlation was noted between inflammatory activity and inhibition of migration. Our results suggest that a normal cellular immune response to HBsAg is necessary for the recovery from acute hepatitis B and for the clearance of the virus. In HBsAg-chronic carriers this response seems to be absent or inadequate, leading to the state of healthy chronic carriers or to the evolution to HBsAg-chronic hepatitis, respectively. The high frequency of CMI in HBsAg-negative chronic active hepatitis, suggests that hepatitis B virus infection may play a role in the ethiology of the disease.
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PMID:[Infection due to hepatitis B virus and host immune response]. 101 86

Cell-mediated immunity to a liver specific membrane protein (LP1) has been studied in patients with different types of liver diseases, using the leucocyte migration inhibition test. A high frequency of cellular sensitization to LP1 was detected in untreated chronic active hepatitis, with no significant differences between HBsAg-positive and negative cases. Inhibition of migration is a long-lasting reaction in the spontaneous evolution of the disease, while immunosuppressive treatment normalizes the test only in cases with complete remission. In viral hepatitis B cell-mediated immunity to the liver specific membrane protein can be detected in the acute phase of the disease as a time-limited reaction, exhausted with the clearance of the virus from the liver. An inhibition of migration with LP1 was found also in some cases of HBsAg-positive post-hepatitis patients, in chronic persistant hepatitis, mainly HBsAg-positive, and in asymptomatic chronic carriers of the antigen B. Most of these cases showed a progression to chronic active hepatitis, in clinical and histopathological prospective studies. Our results suggest that cell-mediated immune response to liver specific antigens plays a major role in the pathogenesis of chronic active hepatitis. Moreover the evaluation of these reactions in chronic liver diseases may help in the diagnosis and in the control of the immunosuppressive therapy. Hepatitis B virus infection must be considered one of the possible cause responsible for the rising of autoimmunity to the liver.
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PMID:[Liver-specific proteins and autoimmunity in inflammatory liver diseases]. 101 92

Hepatitis B antigen of subtype ay is prevalent in Australian Aboriginal populations, but only subtype ad was found in Torres Strait Islanders. Both subtypes were found in Caucasion hepatitis patients and blood donors from Brisbane. Antigenaemia in Aborigines was more prevalent in Northern Territory than in Queensland, and in males in all areas, but different age distributions were found in Queensland (maximal over 30 years) and Northern Territory (maximal under 30 years). Family clustering was striking in all populations where genealogies were known. In a limited survey antibody was found to be more common than antigen in all Aboriginal groups, the prevalence increasing with age with a peak at 11 to 30 years. Hepatitis B virus infection was equally common in some areas of high and low arbovirus activity providing some evidence against arthropod transmission of hepatitis B virus in these areas.
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PMID:Hepatitis B in Australian Aborigines and Torres Strait Islanders: georgraphical, age and familial distribution of antigen subtypes and antibody. 106 8

A series of 67 liver biopsies (20 kidney transplant recipients and 47 outpatients with hepatitis) was investigated for the presence of hepatitis B antigen core (HBc) and surface (HBs) components by immunofluorescence and electron microscopy. The variable appearance of the core in liver cell nuclei and of the surface in the cytoplasm allowed the recognition of expression patterns which, together with histologic parameters, could be integrated into four reaction types of diagnostic and prognostic implications: Type I (Elimination Type). No components or only occasional expression of HBc; histologically, classic lobular hepatitis; clinically, acute, self-limited viral hepatitis. Type II (HBc Predominance, or Immunosuppression Type). Abundant core expression in each liver cell nucleus and moderate appearance of HBs; histologically, nonaggressive inflammation (nonspecific reactive or portal hepatitis); clinically, mild, chronic, persistent hepatitis in transplant patients. Type III (HBs Predominance, or Nonaggressive Type). Prominent HBs expression largely in the absence of HBc; histologically, nonaggressive inflammation (nonspecific reactive and portal hepatitis) or normal liver tissue, together with ground-glass hepatocytes in light microscopy, as a correlate of HBs-containing hepatocytes; clinically, hepatitis B antigen carrier, or chronic persistent hepatitis. Type IV (HBc+s Equivalence, or Aggressive Type). Spotty expression of both components, especially of core; histologically, periportal hepatitis; clinically, mainly corresponds to chronic aggressive hepatitis and to acute hepatitis with possible transition to chronicity. As a unifying concept for these types, it is suggested that immune responsiveness determines the reaction pattern, the key mechanism being immune elimination of affected cells. Between efficient elimination (type I) and effective immunosuppression (type II), a graded elimination insufficiency is found in chronic forms (types III and IV), explaining the persistence and probably also the aggressiveness of hepatitis B virus infection.
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PMID:Pattern of core and surface expression in liver tissue reflects state of specific immune response in hepatitis B. 108 35

The role of antibodies to the surface antigen of hepatitis B virus (HBsAg) and to the hepatitis B core antigen (HBcAg) and of cell-mediated immunity in hepatitis B virus infections and in resistance to challenge was studied in six chimpanzees. Two chimpanzees were studied during primary hepatitis B virus infection while being treated with cyclophosphamide (5-15 mg/kg im three times per week). Cyclophosphamide treatment may have predisposed these chimpanzees to chronic hepatitis B virus infections. Four other chimpanzees convalescent from primary hepatitis B virus infection (subtype ayw) were challanged with hepatitis Bvirus; two were callenged with heterologous virus (subtype adw) without immunosuppression, and two were challenged with homologous virus (subtype syw)while being treated with cyclophosphamide. Chimpanzees with residual humoral immunity, demonstrable by serum antibodies against the group determinant a and subdeterminant y of HBsAg, resisted challenge with either heterologous or homologous hepatitis B virus despite cyclophosphamide immunosuppression in the latter case. Antibodies to the hepatitis B virus core did not appear necessary for protection against hepatitis B virus infection in these chimps.
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PMID:Effects of cyclophosphamide on hepatitis B virus infection and challenge in chimpanzees. 111 92

The hepatic lesion in Reye's syndrome (acute encephalopathy with fatty degeneration of viscera) was studied by light microscopy of sequential biopsy specimens obtained in 49 children. The hepatic lesion is a morphologically characteristic, rapidly evolving, and reversible toxic hepatitis. In specimens obtained with 48 hr of onset of neurological deterioration, the severity of the diffuse microvesicular steatosis is best appreciated in frozen sections stained for lipid content. Variation in severity of hepatocyte glycogen depletion in early biopsies correlates with other histological measures of severity, and with the occurrence of hypoglycemia, severity of the encephalopathy at the time of admission, and mortality rate. Histochemical studies suggest that the hepatic lesion is attributable to mitochondrial injury and other evidence that supports this hypothesis is briefly reviewed. The etiology of the syndrome and its relationship to the viral disease which usually precedes it are unknown.
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PMID:The hepatic lesion in Reye's syndrome. 115 86

The diagnosis of chronic active (aggressive) hepatitis is based mainly on characteristic morphological changes. During a 7-year period, 85 cases were diagnosed in three medical departments in Copenhagen. This material is presented by clinical, biochemical, and serological variables at the time of diagnosis. None of the patients had simultaneously occurring Australia antigen and circulating autoantibodies. A comparison between two serologically homogeneous groups revealed significant differences in sex and age distribution onset of disease, and biochemical activity. The investigation suggests the existence of aetiologically different forms of chronic active hepatitis. Some cases are apparently caused by a persistent viral infection, while others may be due to a primary autoimmune mechanism. A considerable number of the patients stated that they had had prolonged intake of the potentially hepatotoxic laxative, oxyphenisatin. Nineteen patients were challenged with the drug and eight reacted with an increased biochemical activity in the liver disease. All these patients belonged to the group with circulating autoantibodies. It is possible that oxyphenisatin may be the primary cause of the chronic liver damage in some cases.
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PMID:Chronic active hepatitis. Aetiological considerations based on clinical and serological studies. 117 55


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