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

A modified trichrome stain is described for the intrahepatic localization of the hepatitis B surface antigen; HBsAg containing cells exhibit specific green metachromasia contrasting with the granular brown colour of non infected hepatocytes and with the deep eosinophilic colour of ground glass cells of HBsAg-negative alcoholic or drug hepatitis. The technique is simple and reliable for routine screening of HBsAg positive material; its sensitivity is greater than H & E, similar orcein and inferior to immunohistochemistry as performed on frozen sections. Histological diagnosis can be made on the same slide, since several other morphological details are provided in the trichrome stained preparations. With this technique 387 biopsies from HBsAg seronegative individuals were negative; full cytoplasms metachromasia was mostly seen in asymptomatic HBsAg carriers, focal or partial staining in patients with histological evidence of liver cell necrosis. The presence and the staining pattern of HBsAg were of no help in predicting transition to chronicity or a transition from chronic persistent to chronic active hepatitis.
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PMID:A trichrome stain for the intrahepatic localization of the hepatitis B surface antigen (HBsAg). 7 38

A solid phase micro-immunoradiometric assay (micro-SPIRA) for the detection of hepatitis e antigen (HBeAg) and antibody has been developed. Chimpanzee anti-HBe/2 was developed by repeated immunizations with purified antigen containing HBeAg/1 and HBeAg/2. An anti-HBe/2 titer of 1:4 was determined by immunodiffusion (ID) analysis. Anti-HBe/1 was not detected. The anti-HBe IgG used in the assay was purified from plasma by a combination of DEAE-cellulose and affinity chromatography. The sensitivity of the micro-SPIRA for antigen and antibody was 193 ng/ml and 65 ng/ml, respectively. By comparing relative endpoint titers obtained by ID to micro-SPIRA, it was determined that micro-SPIRA for antigen and antibody is 320 and greater than 1300 times more sensitive, respectively, than ID. The specificity of the assay was ascertained by the examination of various non-B specimens. The application of the assay to a panel of 50 hepatitis B surface antigen (HBsAg)-positive specimens resulted in an increase in positivity of 18% for antigen and 22% for antibody.
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PMID:Radioimmunoassay for the detection of hepatitis e antigen (HBeAG) and antibody (anti-HBe). 8 Apr 34

Renal histology in 163 Japanese children, aged 3 to 15, with proteinuria and/or haematuria showed that 11 had membranous nephropathy (M.N) and the rest had various other renal diseases. Hepatitis-B-virus surface antigen (HBsAg) was identified, by a reversed passive haemagglutination method, in the serum of all the patients with M.N. but in only 4.6% of the patients with other renal diseases. 6 of the 11 mothers of the children with M.N. were positive for HBsAg, and 1 was positive for antibody to HBsAg (anti-HBs). These findings suggest that M.N. in Japanese children is mainly, if not exclusively, caused by hepatitis-B virus and that in most instances the virus is transmitted from mother to child.
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PMID:Strong association between membranous nephropathy and hepatitis-B surface antigenaemia in Japanese children. 8 85

The prevalence of serological markers of active of past hepatitis-B virus (H.B.V.) infection was determined in 80 Greek patients with primary hepatocellular carcinoma (P.H.C.), 160 age and sex matched controls and 40 patients with metastatic liver cancer (M.L.C.). The relative risk of the various patterns of H.B.V. serological markers for P.H.C. was calculated. Active H.B.V. infection, as indicated by positive tests for hepatitis-B surface antigen (HBsAg), or antibody to hepatitis-B core antigen (anti-HBc) without antibody to HBsAg) (anti-HBs), was associated with P.H.C. (relative risk 10.4) but not with M.L.C. (relative risk 1.2). Patients without markers and those who had recovered from hepatitis B (anti-HBs-positive) had approximately the same low risk for P.H.C. (relative risk 0.8). Active infection was more common in P.H.C. patients with co-existing cirrhosis than in those without cirrhosis (67% versus 26%). Thus the relationship between active hepatitis B and P.H.C. seen in African and Asian populations is now seen in a European Caucasian population with different racial, environmental, and dietary circumstances.
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PMID:Hepatitis B and primary hepatocellular carcinoma in a European population. 8 32

Emergency endoscopy was performed on two patients subsequently found to be hepatitis B surface antigen carriers. Before their carrier state was determined, nine other patients underwent endoscopy using the same instruments, which had been routinely cleaned between procedures. These patients were all notified within five days of the incident, given standard gamma globulin, and prospectively followed for the development of hepatitis. After one of the endoscopes was gas sterilized, the next three patients undergoing endoscopy were also followed. One of the hepatitis B surface antigen carriers was positive for antibody to e antigen; the other carrier had neither e antigen nor antibody. None of these individuals developed signs or symptoms of hepatitis, abnormal serum glutamic pyruvate transaminase elevations, or serologic evidence of hepatitis B exposure. From these data, and other recorded experiences, it appears that routine cleansing of endoscopy equipment is sufficient in preventing the transmission of hepatitis B.
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PMID:Failure of endoscopic transmission of hepatitis B. 8 14

Twelve infants, born to mothers with hepatitis B virus infection, were inoculated within 7 days of birth with immune serum globulin containing antibody to hepatitis B surface antigen (HBsAg) titers of 1:32 to 1:64 as measured by passive hemagglutination. Six of nine infants (66.7%) born to HBsAg-positive carrier mothers became HBsAg-positive within 3 mo of age. In addition, two of three treated infants born to mothers with acute hepatitis B during the delivery period also developed HBsAg. The hepatitis e antigen was detected in four of five carrier mothers and in two mothers with acute hepatitis, whose infants subsequently became HBsAg positive. In addition, hepatitis B-specific DNA polymerase activity was detected in the seven HBsAg-positive mothers who transmitted the virus to their infants. All eight infants have remained persistently HBsAg positive. Thus, the immune serum globulin containing low-titer antibody to HBsAg is not protective when given to infants born to HBsAg carrier mothers or to mothers with acute hepatitis B during the delivery period.
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PMID:Failure of immune serum globulin to prevent hepatitis B virus infection in infants born to HBsAg-positive mothers. 8 62

An epidemic of acute hepatitis B followed the administration of human immunoglobulin to members of the staff of a mission hospital in India and their families. Jaundice developed in 123 (38%) of 325 persons inoculated. Hepatitis-B surface antigen was detected in three of the batches of immunoglobulin which were available for testing.
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PMID:Epidemic hepatitis B caused by commercial human immunoglobulin. 8 88

A receptor for polymerized human serum albumin was demonstrated on Dane particles as well as on 20-nm hepatitis B surface antigen particles, isolated from asymptomatic carriers of hepatitis B virus who were positive for HBeAg. In contrast, such receptor was not born by 20-nm hepatitis B surface antigen particles obtained from carriers positive for antibody to HBeAg. Hepatitis B surface antigen particles with the receptor were heavier than those without, and when treated with pronase, they became lighter and lost the receptor. The receptor is responsible for the agglutination of erythrocytes coated with polymerized human serum albumin by the serum of patients with Type B hepatitis and asymptomatic carriers, which have been attributed to autoantibodies directed to denatured albumin molecules. When albumin fractions of chimpanzees were polymerized with glutaraldehyde, they also bound with the receptor on hepatitis B surface antigen. Polymerized albumin fractions of all the other experimental animals without susceptibility to hepatitis B virus, however, failed to bind with the receptor. These results seem to suggest a possible role of the receptor on Dane particles (presently accepted hepatitis B virions) for polymerized albumin molecules in infecting hepatocytes both in humans and chimpanzees.
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PMID:A receptor for polymerized human and chimpanzee albumins on hepatitis B virus particles co-occurring with HBeAg. 10 74

Sera of 480 hospitalized hepatitis patients were tested for hepatitis B surface antigen (HBsAg), antibody to HBsAg (anti-HBs) and to hepatitis B core antigen (anti-HBc), antibody to hepatitis A virus (anti-HAV) and anti-HAV of IgM-class. Serological markers indicating hepatitis A infection were found in 107 (22.3%) and markers indicating hepatitis B in 297 patients (61.9%), while 63 patients (13.1%) were classified as hepatitis type "non-A, non-B". The latter group mainly comprised drug addicts (50.8%), cases of post-transfusion hepatitis (11.1%) and patients without obvious hepatitis exposure (28.6%). In spite of these epidemiological similarities to hepatitis B, the maximum levels of serum alanine aminotransferase and bilirubin were comparable to those in patients with hepatitis A and significantly lower than in hepatitis B infection. Chronic hepatitis developed in 7.1% of the "non-A, non-B" patients, a figure close to that reported for hepatitis B.
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PMID:Clinical, epidemiological and prognostic aspects of hepatitis "non-A, non-B"--a comparison with hepatitis A and B. 11 11

Hepatitis B virus-like particles (including DANE particles) with DNA polymerase activity but negative for HBs Ag have been identified in NON-A, NON-B hepatitis sera positive for HC Ag. Although specifically associated with the particles, HC Ag is not a surface antigen of the hepatitis C virus identified here for the first time. The relationship of this agent with HBV seems obvious, and deserves further study.
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PMID:[Identification of a virus similar to hepatitis B virus in non-A non-B hepatitis]. 12 Jul 82


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