Herpes zoster and hepatitis B: detection of Hepatitis B surface antigen in vesicle fluid.
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Biomedical subjects
Publications and source records attributed to G Norkrans.
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Radioimmunoassays for detection of hepatitis B surface antigen (HBsAg), antibody to HBsAg (anti-HBs), antibody to hepatitis B core antigen (anti-HBc), antibody to hepatitis A virus (anti-HAV), and anti-HAV of IgM class were used to verify hepatitis A and hepatitis B infection in 33 drug addicts with multiple attacks of hepatitis. Hepatitis A was confirmed serologically in 23 (32%) of 71 total hepatitis episodes, while hepatitis B was confirmed in 30 episodes (42%). The remaining 18 hepatitis episodes (25%) were, by serological exclusion, also of Epstein-Barr virus and cytomegalovirus infection, classified as hepatitis non-A, non-B. However, while as many as 13 (39%) of the 33 primary attacks of hepatitis were of the type non-A, non-B, this type was never observed as a third attack. In no case were two attacks of hepatitis A or hepatitis B demonstrated in the same individual, but two different episodes of hepatitis non-A, non-B were observed in one patient. The maximal serum levels of alanine aminotransferase and bilirubin were significantly lower in patients with hepatitis non-A, non-B as compared with those with hepatitis B. Development of chronic liver disease occurred in only two (7%) of the 28 addicts who continued to be followed up.
The serum levels of IgA, IgG and IgM were determined by the single radial immunodiffusion method in 86 patients with acute viral hepatitis serologically differentiated by radioimmunoassays. The levels of IgA and IgG were similar in patients with hepatitis A, B and non-A, non-B, while differences in IgM levels were observed between the three groups. The hepatitis non-A, non-B group had significantly lower levels of IgM than both the hepatitis A and hepatitis B group, a finding which may be diagnostically useful if hepatitis A serology fails.
In spite of routine screening for HBsAg by a sensitive radioimmunoassay, some cases of posttransfusion hepatitis B still occur. The frequency in the Gothenburg Blood Center is 1 clinical case per 10,000 bloods units transfused. About the same incidence has been noted for clinically overt cases of hepatitis non-A, non-B. In contrast to findings reported by others, the latter incidence has been rather stable over the last 5 years.
Nine patients with chronic HBsAg-positive hepatitis and persistence of HBeAg and/or core-associated DNA polymerase activity in serum for at least 1 year were followed up regularly with liver function tests for 2--7 years after onset of illness. HBsAg was present in all patients during an average follow-up period of 5 years. Seven of the 9 patients had persistently abnormal liver function tests. Persistence of HBeAg and/or Dane particle associated DNA polymerase in serum for more than 1 year after onset of illness thus seems to indicate a further long period of HBsAg present in serum and impaired liver function.
Interferon treatment (3.0 x 10(6) units of human leucocyte interferon) was initiated in a 64-year-old woman with acute hepatitis B infection showing a prolonged course. A decline in serum bilirubin, HBsAg and DNA polymerase activity started during the 10-day period of interferon treatment, and 4 weeks after start of treatment the liver function tests were quite normal. It is possible that the interferon treatment had a beneficial influence on the clinical course of the illness and may be worth trying also in acute fulminant cases of viral hepatitis.
A radioimmunoassay was used to determine the presence of the hepatitis B e antigen (HBeAg) and anti-HBe in the serum of 12 hepatitis B patients, who were follofed from an early phase of the illness into convalescence. The duration of detectable HBeAg in serum from these patients, in all ow whom the disease ran a normal course, was compared with the persistence of HBeAg in serum of nine patients with a protracted course and persistence of HBsAg in serum for more than 1 year. None of the hepatitis B patients with a normal course of the disease had HBeAg demonstrable for more than 9 weeks after the onset of illness (mean 5.4 weeks), whereas all patients developing chronic hepatitis had HBeAg in serum for more than 1 year after the onset of illness. These findings indicate that the detection of HBeAg in serum by radioimmunoassay for 10 weeks or more after the onset of illness implies a great risk of progression of the hepatitis B infection to chronic liver disease.
A newborn infant, born to a HBsAg-positive drug addict with HBeAg and DNA-polymerase activity in serum, was treated with repeated very high doses of hepatitis B immune globulin (HBIg). The mother turned HBsAg-negative about 8 months after deliver and the HBIg prophylaxis was then discontinued. A check-up of the infant about a year later revealed normal liver function tests but significantly increased levels of antibodies against HBcAg and HBsAg indicating a post subclinical hepatitis B infection, apparently without harm to the infant.
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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Immune serum globulin prophylaxis for foreign travellers should be reserved for those at high risk having no immunity against hepatitis A. In this study from Sweden the incidence of tourist hepatitis in different age groups was correlated to the prevalence of antibodies to hepatitis A virus (anti-HAV) in the population. 58% of individuals over 50 years had anti-HAV and travellers in these ages seldom experienced "tourist hepatitis". In younger age groups a low prevalence of anti-HAV (11%) was combined with a higher incidence of tourist hepatitis.
In a clinical series of 148 patients with acute hepatitis, serological analysis of hepatitis A and hepatitis B markers revealed 16% of the cases as hepatitis type non-A, non-b. Hepatitis A was diagnosed in 27% of the patients with drug addicts as the predominating category, while serological evidence of hepatitis B infection was found in 57%, again with drug addicts in the majority. Drug addicts also predominated among the non-A, non-B cases, and possibly this category of patients is today the main reservoir not only of hepatitis B but also of hepatitis A and non-A, non-B.
The prevalence of antibodies against hepatitis A virus (anti-HAV) was studied in a Swedish city population. A great difference was observed in different age groups. Anti-HAV was not found in the serum of young individuals while the prevalence was high in older ages (87% in individuals 60 years or older). This pattern of hepatitis A exposure is quite different from that reported for instance from the Mediterranean area and may indicate a very low frequency of hepatitis A exposure in Scandinavia today. The high prevalence of anti-HAV in older Swedes possibly reflects hepatitis A exposure in childhood during World War I and II when hepatitis A was more common.
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To examine the association between e antigen and hepatitis-B surface antigen (HBs Ag) we studied 90 inpatients with acute viral hepatitis type B. e Antigen was present in 24 of the patients; these patients had detectable levels of HBs Ag for significantly longer than the 66 with no e antigen in their serum. The HBs Ag subtypes D (adw) and Y (ayw) were similarly distributed among patients with e antigen and among those without, and no differences in the results of biochemical liver function tests were observed between the two groups during the acute phase of illness. Three of the five patients who developed clinical and histological signs of chronic liver disease were positive for e antigen, a finding which supports the hypothesis that e antigen has a prognostic value in hepatitis B.