OBJECTIVE: Viruses might be one of the elements that trigger systemic lupus erythematosus (SLE). Steroid therapy may influence the natural history of virus infections. The most frequent extrahepatic manifestations of hepatitis C virus (HCV) including arthralgia, myalgia, sicca syndrome, and antinuclear antibodies, may mimic a connective tissue disease, particularly SLE. Reports on the association between SLE and HCV infection are scarce. We investigated the association of HCV infection and SLE. METHODS: Retrospective case-control monocentric study of 19 patients with SLE and anti-HCV antibodies versus 42 randomized SLE patients without anti-HCV antibodies, matched for age and sex, coming from our cohort of 700 patients with SLE. SLE and HCV-infection features were reviewed. RESULTS: Mode of infection was blood product transfusion, drug addiction, or unknown. Prevalence of lupus clinical manifestations, antinuclear, anti-dsDNA, anti-extractable nuclear antigen antibodies, and complement levels was not different between HCV positive and negative SLE patients. Prevalence of cryoglobulin was higher in SLE patients with anti-HCV antibodies (p < 0.04), but none had a mixed cryoglobulinemia syndrome. ALT activity was increased in 11 HCV positive patients and 13 had detectable HCV RNA. Liver biopsy showed cirrhosis in 2 and mild fibrosis and activity in 5. One patient treated with interferon-alpha had a sustained virological response without SLE flare. Steroid therapy did not seem to alter HCV course. CONCLUSION: SLE in HCV positive patients shows higher prevalence of cryoglobulin without mixed cryoglobulinemia syndrome. HCV infection has moderate signs of biochemical and liver pathological severity. SLE by itself or treated with steroids does not seem to worsen HCV infection.
OBJECTIVE: Viruses might be one of the elements that trigger systemic lupus erythematosus (SLE). Steroid therapy may influence the natural history of virus infections. The most frequent extrahepatic manifestations of hepatitis C virus (HCV) including arthralgia, myalgia, sicca syndrome, and antinuclear antibodies, may mimic a connective tissue disease, particularly SLE. Reports on the association between SLE and HCV infection are scarce. We investigated the association of HCV infection and SLE. METHODS: Retrospective case-control monocentric study of 19 patients with SLE and anti-HCV antibodies versus 42 randomized SLEpatients without anti-HCV antibodies, matched for age and sex, coming from our cohort of 700 patients with SLE. SLE and HCV-infection features were reviewed. RESULTS: Mode of infection was blood product transfusion, drug addiction, or unknown. Prevalence of lupus clinical manifestations, antinuclear, anti-dsDNA, anti-extractable nuclear antigen antibodies, and complement levels was not different between HCV positive and negative SLEpatients. Prevalence of cryoglobulin was higher in SLEpatients with anti-HCV antibodies (p < 0.04), but none had a mixed cryoglobulinemia syndrome. ALT activity was increased in 11 HCV positive patients and 13 had detectable HCV RNA. Liver biopsy showed cirrhosis in 2 and mild fibrosis and activity in 5. One patient treated with interferon-alpha had a sustained virological response without SLE flare. Steroid therapy did not seem to alter HCV course. CONCLUSION:SLE in HCV positive patients shows higher prevalence of cryoglobulin without mixed cryoglobulinemia syndrome. HCV infection has moderate signs of biochemical and liver pathological severity. SLE by itself or treated with steroids does not seem to worsen HCV infection.
Authors: Jae Hee Lim; Yun Nah Lee; Young Seok Kim; Sang Gyune Kim; Seung Won Jeong; Jae Young Jang; Hong Soo Kim; Sae Hwan Lee; Tae Kwann Park Journal: Korean J Hepatol Date: 2011-03