The frequency and clinical features of acute hepatitis B virus (HBV) infection with and without a hepatitis D virus (HDV) co-infection was investigated retrospectively in the Stockholm region during two different time periods, September 1977-October 1978 and November 1984-October 1986. Totally, 31/229 (14%) patients with acute HBV infection had a HDV co-infection. No change in the frequency of co-infections, 12% and 15%, respectively, was observed between the 1970s and 1980s. Among the 31 HDV co-infected patients 74% were intravenous drug addicts. Totally 23/66 (35%) intravenous drug addicts with acute HBV infection had HDV co-infection. Clinically a biphasic rise of the serum levels of alanine aminotransferase and bilirubin was noted among 63% of the HDV co-infected patients but only among 8% of the solely HBV infected patients (p less than 0.001). A clinically more severe hepatitis was seen significantly more often among the HDV co-infected patients than among the solely HBV infected.
In 1979-1980, a distinct outbreak of hepatitis A occurred among homosexual men in Stockholm, Sweden, city and county area. The epidemic comprised 145 known cases. It began in December 1979 and progressed in waves during the following 10 months, with three distinct peaks separated by about six-week intervals. Actually, the incidence of hepatitis A in the Stockholm area showed a fivefold increase during 1980 as compared to the previous year. Clinical serologic, and social characteristics were studied more closely in 98 of the 145 homosexual men. Verification of hepatitis A was made by a solid-phase radioimmunoassay technique for detection of antibody to hepatitis A virus of the immunoglobulin M class. In addition, 64% of the men showed findings consistent with a prior hepatitis B (antibody to hepatitis B core antigen and/or antibody to hepatitis B surface antigen) and 34% were Treponema pallidum immobilization-positive from a prior or concomitant syphilis. Employment in risk professionals was common; thus, 19% worked in restaurants or otherwise handled food and 20% were engaged in medical care as compared to the 1% occupied in either branch of work among the general population in Sweden. Sexual habits with multiple partners and oral-anal sexual contacts were judged to be of major importance in the spread of this epidemic. Some spread of hepatitis A to the general population probably occurred due to the risk occupations of many homosexual men.
An epidemiologic study covering about 1/3 of the adult Swedish population showed an annual incidence of chronic active hepatitis (CAH) of 1.6 per 100,000. At least 45% had a viral cause of their CAH, the proportion being distinctly higher in large cities than in rural ones. Drugs, alcohol, and metabolic disorders were rarely identified as etiologic factors. The prevalence of ulcerative colitis and gluten enteropathy was remarkably high in idiopathic CAH. Compared with antibody-negative patients with idiopathic CAH, antibody-positive patients showed higher rates of the female sex, IgG increase, anti-HBs negativity, compliance with the Mayo criteria for treatment, and absence of previous episode of jaundice. Furthermore, in autoantibody-negative idiopathic CAH the prevalence of anti-HBs antibodies was at least three times greater than in the Swedish population, suggesting a viral cause of some forms of idiopathic CAH, a suggestion supported by the clinical pattern of the disease.
This study was performed to investigate the efficiency of 5 ml of 16.5% immunoglobulin (Ig) with an antibody titer against hepatitis A (anti-HAV) of 1:4000, using the HAVAB RIA technique, as pre-infection prophylaxis in 610 Swedish UN soldiers stationed in Sinai for 6 months. Sera were collected from 553 of these soldiers before, during, and after their service and were tested by the HAVAB technique for anti-HAV. Only 13 of 553 (2.4%) were immune before their service. During the first 5 months in Sinai, only one subclinical case of hepatitis A occurred among the men. Thereafter, two subclinical and four clinical cases occurred, although one of the subclinical cases and the four clinical ones did not occur until after the 6-month period. Thus, the Ig prophylaxis scheme used seems to offer almost complete passive protection for 5 months.
BACKGROUND: Only 10-20% of patients treated with interferon alfa alone attain long-term benefits. More effective regimens are needed. METHODS: Twenty Swedish patients with chronic hepatitis C virus infection, ten with a prior non-response and ten with a non-sustained response to interferon alfa treatment alone, were treated with interferon alfa-2b and ribavirin in combination for 24 weeks, then followed up for another 24 weeks. Patients received interferon alfa-2b subcutaneously 3 MU thrice weekly and oral ribavirin 1000-1200 mg/day. RESULTS: All ten patients with a prior non-sustained response to interferon alone had a sustained biochemical response with normal aminotransferase levels at follow-up; nine also had a sustained viral response with a negative HCV-RNA test in serum. Among the ten patients with a prior biochemical non-response to interferon alone, five had normal aminotransferase levels at the end of therapy; four were negative for HCV RNA in serum. At follow-up, three had normal aminotransferase levels and a negative HCV-RNA test in serum. No major adverse effect was seen, apart from fatigue and an expected fall in hemoglobin levels from a mean of 155 g/l to 124 g/l at the end of therapy. All patients completed the treatment schedule, but the ribavirin dose was reduced in one patient because of a fall in hemoglobin to 99 g/l. CONCLUSIONS: These results indicate that combination treatment with interferon alfa-2b and ribavirin offers a chance of sustained biochemical response and virus eradication in a subset of patients who fail to achieve sustained response with interferon alfa alone.
The prevalence, epidemiology and consequences of delta infection were analysed in 60 patients attending the Roslagstull Hospital for Infectious Diseases, Stockholm, Sweden, between 1972 and 1982. All of the patients had biopsy-documented chronic hepatitis B. Using radioimmunoassay techniques, sera from all patients were tested for antibodies to hepatitis A virus, for hepatitis B surface antigen and the corresponding antibody, for antibodies to hepatitis B core antigen, for hepatitis B e antigen and the corresponding antibody and for antibodies to delta antigen. All 60 patients underwent a liver biopsy which was repeated in 28 patients. 32% of the patients (19/60) were found to be anti-delta positive. The majority of the anti-delta positive patients were either immigrants from non-European countries or addicts (both 9/19 or 47%). Infections with delta agent were found to have already occurred in the Stockholm region in the early 1970s. During the study period, four of the patients developed clinical and laboratory signs of acute hepatitis in association with a delta infection. Among the anti-delta positive patients, 63% (12/19) were classified as having chronic active hepatitis, with or without cirrhosis, as against 39% (16/41) of the anti-delta negative patients. Histological progression to cirrhosis was observed in two of the four anti-delta positive patients with initial chronic active or chronic persistent hepatitis.