Hepatitis B infection and changes in interferon‐α and ‐γ production in patients with systemic lupus erythematosus in Taiwan

According to previous reports, the prevalence of hepatitis B virus (HBV) infection in patients with systemic lupus erythematosus (SLE) is varied. There has been no report on Taiwan, a hyperendemic area for HBV infection. Furthermore, impaired production of interferon (IFN) in peripheral blood mononuclear cells (PBMC) has been reported to be potentially pathogenic to both chronic HBV infection and SLE. However, the production of IFN in patients with both diseases coexisting is unknown. The aims of this study were to evaluate the prevalence of HBV infection in lupus patients in Taiwan and to measure the production of IFN in patients with both diseases coexisting. One hundred and seventy-three consecutive lupus patients and a control group of 692 age- and sex-matched healthy subjects were included for evaluation of the prevalence of HBsAg. Four groups of subjects (patients with SLE and HbsAg, SLE, chronic hepatitis B and normal controls) were selected for evaluation of the in vitro production of IFN-α and -γ. Six (3.5%) of the 173 SLE patients were positive for HBsAg, which was significantly lower than that of controls (14.7%; P<0.0001). Patients with coexistent SLE and chronic HBV infection had less lupus activity, including less proteinuria (P= 0.02) and a lower serum titre of anti-double stranded DNA antibodies (anti-dsDNA; P=0.04), than HBsAg-negative lupus patients. The in vitro production of IFN-α in patients with chronic hepatitis B was significantly lower than in those patients with SLE or in the normal control group (P< 0.01). The yields of IFN-α and -γ in patients with coexistent SLE and chronic HBV infection were significantly different from those patients with SLE alone (P< 0.05), but close to those of patients with chronic HBV infection. In conclusion, the prevalence of HBsAg carriers is significantly lower in lupus patients in Taiwan. Patients with coexistent SLE and chronic HBV infection had less lupus activity. Interferon-α and -γ may play a role in the above phenomenon.