Sir,- Professor Meuer et al reported that in uraemic non-responders to hepatitis B vaccine, antibodies to hepatitis B surface antigen (anti-HBs) develop when interleukin-2 (IL-2) is given with plasma-derived vaccine. Haemodialysis patients are at risk of acquiring a hepatic disease of viral origin. The low (or lack of) response to hepatitis B vaccine in such patients is generally accepted to be due to their immunosuppression. Moreover, Meuer et al have reported a possible defect in monocyte function, which may account for the non-responsiveness. We have given 40 ĩg of the yeast-derived hepatitis B vaccine (Engerix-B) alone to 41 patients or in combination with 2 MU of human recombinant interferon-gamma (rIFN-gamma, Boehringer Ingelheim) to 40 patients in a three-dose schedule at 0, 1, and 6 months; the patients were having long-term haemodialysis and had several types of nephropathy, but had not been exposed to hepatitis B virus (HBV) or been vaccinated.
The rate of anti-HBs seroconversion was higher in vaccinees who received rIFN-gamma than in those who did not; after the second dose differences were significant (87,5% vs 62,5%, p<0,025). After one year of follow-up the percentage of vaccinees who were anti-HBs seropositive was much the same (over 80%) in the two groups. No special toxicity associated with rIFN-gamma administration was observed. Furthermore, the anti-HBs titre was usually higher, but not significantly so, in patients who received the vaccine plus rIFN-gamma. Imparied monocyte activity could explain the lack of response to IL-2 administration. In-vivo stimulation of the immune system seems to be essential to improve anti-HBV response: rIFN-gamma has been shown to enhance antibody synthesis. Our data are encouraging with respect to the use of rIFN-gamma as an inducer of anti-HBs seroconversion in immunocompromised non-responders.