BACKGROUND/AIM: We investigated the pathogenic role of chronic hepatitis B virus (HBV) and C virus (HCV) in some connective tissue diseases including systemic lupus erythematosus (SLE), overlap syndrome, rheumatoid arthritis (RA), seronegative spondylarthritis (SS) and the association with chronic liver disease. METHODOLOGY: There were studied 155 patients, aged among 18 to 64 years old: 57 with SLE, 22 with overlap, 26 with RA, 30 with SS. The diagnoses were established using modified ARA criteria. There were performed complex immunology tests, percutaneous liver biopsy, HLA, Elisa tests with Riba confirmation for detecting HCV and HBV. RESULTS: 17% of SLE patients were infected with hepatitis viruses, predominantly B (70%). Half of them had a hepatic involvement due to the hepatitis viruses. 23% of RA patients were equally B\C infected with only one case of hepatic involvement secondary to hepatitis viruses. All the HCV infected patients had rheumatoid factor (RF) IgG-IgM type, with low serum levels of haemolytic complement (CH50), increases serum levels of circulating immune complexes (CIC) and evidence of HLA DR4 In the group of SS 40% of patients were infected mostly with HBV. In HLA B27 (+) anchylosing spondylitis (AS) the incidence of HBV was 100%. CONCLUSIONS: There is no high prevalence of HCV infection in SLE, overlap syndrome or RA, compared to the control group. In SS the prevalence is increased (40%), especially HLA B27 (+) AS group (33%), in which HBV is noticed at a rate of 100%. The association SLE-HCV favours the visceral involvement especially renal ones, while the presence of HBV is associated with decrease of lupus activity. In RA, HCV induces IgG-IgM RF with complement activation, being considered as a trigger of the disease in HLA DR4 patients. In HLA B27 (+) AS. HBV may trigger the development of disease in genetically susceptible individuals.
BACKGROUND/AIM: We investigated the pathogenic role of chronic hepatitis B virus (HBV) and C virus (HCV) in some connective tissue diseases including systemic lupus erythematosus (SLE), overlap syndrome, rheumatoid arthritis (RA), seronegative spondylarthritis (SS) and the association with chronic liver disease. METHODOLOGY: There were studied 155 patients, aged among 18 to 64 years old: 57 with SLE, 22 with overlap, 26 with RA, 30 with SS. The diagnoses were established using modified ARA criteria. There were performed complex immunology tests, percutaneous liver biopsy, HLA, Elisa tests with Riba confirmation for detecting HCV and HBV. RESULTS: 17% of SLEpatients were infected with hepatitis viruses, predominantly B (70%). Half of them had a hepatic involvement due to the hepatitis viruses. 23% of RApatients were equally B\C infected with only one case of hepatic involvement secondary to hepatitis viruses. All the HCV infectedpatients had rheumatoid factor (RF) IgG-IgM type, with low serum levels of haemolytic complement (CH50), increases serum levels of circulating immune complexes (CIC) and evidence of HLA DR4 In the group of SS 40% of patients were infected mostly with HBV. In HLA B27 (+) anchylosing spondylitis (AS) the incidence of HBV was 100%. CONCLUSIONS: There is no high prevalence of HCV infection in SLE, overlap syndrome or RA, compared to the control group. In SS the prevalence is increased (40%), especially HLA B27 (+) AS group (33%), in which HBV is noticed at a rate of 100%. The association SLE-HCV favours the visceral involvement especially renal ones, while the presence of HBV is associated with decrease of lupus activity. In RA, HCV induces IgG-IgM RF with complement activation, being considered as a trigger of the disease in HLA DR4patients. In HLA B27 (+) AS. HBV may trigger the development of disease in genetically susceptible individuals.