[Exposure to hepatitis B of health personnel, policemen and healthy blood donors in Gothenburg].
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Biomedical subjects
Publications and source records attributed to S Hermodsson.
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The occurrence of the delta (delta) agent was analyzed in 89 patients with acute hepatitis B infection during 1976-1979 in Gothenburg, Sweden, and in 46 patients (16 drug addicts) with chronic HBsAg-positive liver disease. Four of the patients with acute hepatitis B had transiently detectable anti-delta antibodies in serum. At least three of these four cases were associated with intravenous drug abuse. Eleven of the HBsAg carriers (24%) were anti-delta-positive, and all of them were drug addicts. One of the drug addicts transmitted hepatitis B infection without detectable anti-delta in serum to two other non-addicts via parenteral routes. Apparently, in Sweden today delta-infection is mostly restricted to drug addicts and seldom found in other groups of hepatitis B patients.
Epidural malignant tumour often causes weakness of the legs as well as pain. A series of 37 consecutive cases treated with surgery for these symptoms is presented. Considerable pain reduction was achieved in half of the cases, and 6 months after surgery one fourth could walk. The authors have found bone cement (polymethyl methacrylate) to be quite suitable for stabilizing the spinal column. Surgery is regarded as complementary to the use of cytostatics, hormones and radiotherapy.
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Hepatitis B Immunoglobulin with an antibody content of 2 300 IU was injected i.m. into five healthy female volunteers without Hepatitis B markers in serum (HBsAg, anti-HBs, anti-HBc). The uptake of anti-HBs after i.m. injection was calculated by measuring the concentration of antibody in plasma. An international standard (WHO) containing 100 IU/ml was used as reference. The serum concentration of anti-HBs was analysed on day 1, 3, 5, 7, 9, 11, 13, 28 and 56 after the single i.m. injection. The peak serum concentrations after one single injection were observed between day 5 and 11. The mean recovery rate was calculated according to a compartment model where the plasma volume was estimated to be 45 ml/kg body weight. The mean recovery rate expressed as percentage of injected dose was 19.2% with a range of 14.2-28.2%. The mean biological half life of anti-HBs was 21.7 days. The recovery rate of Hepatitis B Immunoglobulin injected i.m. seems to be somewhat lower than expected but is within the same range as i.e. Ig anti-D (Eklund et al, BMJ 1982, 284: 854-855). The peak serum concentration of anti-HBs was reached comparatively late after the injection. This finding may in part explain the discouraging protection of Hepatitis B Immunoglobulin in the post-exposure situation. Intravenous administration of anti-HBs with an immediate peak concentration followed by vaccination will possibly be a better alternative for post-exposure prophylaxis against Hepatitis B.
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HBeAg and anti-HBe were determined by radioimmunoassay (Abbott HBe) in serial serum samples from 22 patients who had been HBsAg-positive for more than 1 year. Seventeen patients (77%) were HBeAg-positive at onset of illness. Eight of these patients were persistently HBeAg-positive during 2.5-8.5 years' follow-up study (mean, 5.4 years). Chronic persistent hepatitis (CPH) developed in one of these patients and chronic active hepatitis (CAH) in seven patients. Nine persistently HBsAg-positive patients were transiently HBeAg-positive. Seven of these patients developed CPH, and they all lost HBeAg within 2 years of onset of illness. One patient, who was HBeAg-positive for 4 years, developed CAH with cirrhosis after loss of HBeAg. In five patients, HBeAg could not be detected. They were anti-HBe-positive at onset of illness; four developed CAH and/or cirrhosis, and one developed CPH. Progression from CPH or nonspecific reactive hepatitis to CAH was observed in two persistently HBeAg-positive patients. Prolonged detection of HBeAg in CPH is a reason for repeated liver biopsy to reevaluate the diagnosis. The behaviour of the e-antigen system in CAH seems to be more complex than in CPH, perhaps indicating a different pathogenetic mechanism of chronicity in CAH.
Natural killer (NK) cell activity against several types of target cells was found to be subnormal in patients with systemic lupus erythematosus (SLE). Interferon (IFN) boosted the NK activity of cells from SLE patients to a significantly lesser degree than cells from normal controls. The production of IFN after stimulation of blood cells with Sendai virus was significantly decreased in SLE patients with active disease, and in a substantial proportion of the patients the production of phytohaemagglutinin (PHA)-induced IFN was below normal limits. Although the production of virus-induced IFN was clearly inversely correlated to disease activity no such correlation was observed for PHA-induced IFN. Serum levels of both pH2 stable and pH2 labile IFN were significantly higher in SLE patients than in controls. The findings clearly show that SLE is associated with abnormalities in the NK cell-IFN system but it cannot be stated whether these abnormalities are causally related to the development of disease or are secondary to pathological changes in SLE.
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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.
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.
43 patients with chronic active hepatitis (CAH) exhibited significantly higher levels of antibodies against measles and polio type 2 und 3 when compared to 43 age- and sex-matched healthy controls. No significant differences were found for antibodies against polio type 1, rubella, herpes simplex, mumps virus, and tetanus. There was no correlation between antibody levels and the presence of HLA-B8 and/or HLA-B12. The antibody response to vaccination with polio vaccine (killed) and tetanus toxoid was not higher in CAH patients carrying HLA-B8 and/or HLA-B12 than in patients without these antigens. The results indicate that CAH is associated with an increased immunoreactivity, which is, however, not linked to HLA-B8 and/or HLA-B12.
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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Sera from 44 patients with a well-documented diagnosis of chronic active hepatitis (CAH) were analysed for antibodies to hepatitis A virus (anti-HAV), hepatitis B surface antigen (HBsAg) and anti-HBs, e-antigen (HBeAg) and anti-HBe, as well as antibodies to hepatitis B core antigen (anti-HBc). Twenty-two patients had serologic evidence of hepatitis A infection. The frequency of anti-HAV was low in patients under 50 years of age (21%) but high among older patients (72%). There was, however, no significant difference between patients and age-matched controls regarding the prevalence of anti-HAV in serum. Markers for hepatitis B virus were found in 10 patients or 23% as compared with about 10% in Swedish blood donors. The results indicate that hepatitis A virus is of little importance in the pathogenesis of CAH and confirm the association between hepatitis B virus and development of chronic active hepatitis.