title: Hepatitis C virus infection in systemic lupus erythematosus: a case-control study.
abstract: 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.
  
  
  CONCLUSIONS
  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.affiliation: Service d'Hépatologie et de Gastroentérologie, Hôpital de Bicêtre, Kremlin Bicêtre, Paris, France.
authors.forename: Gabriel
authors.initials: G
authors.lastname: Perlemuter
authors.forename: Patrice
authors.initials: P
authors.lastname: Cacoub
authors.forename: Abdallah
authors.initials: A
authors.lastname: Sbaï
authors.forename: Pierre
authors.initials: P
authors.lastname: Hausfater
authors.forename: Vincent
authors.initials: V
authors.lastname: Thibault
authors.forename: Thi Huong Du
authors.initials: TH
authors.lastname: Le
authors.forename: Bertrand
authors.initials: B
authors.lastname: Wechsler
authors.forename: Catherine
authors.initials: C
authors.lastname: Buffet
authors.forename: Jean Charles
authors.initials: JC
authors.lastname: Piette
mesh_terms: D000293:Adolescent; D000328:Adult; D017668:Age of Onset; D000368:Aged; D000974:Antibodies, Antinuclear / Q000097:blood; D000914:Antibodies, Viral / Q000032:analysis; D018501:Antirheumatic Agents / Q000627:therapeutic use; D001706:Biopsy; D003450:Cryoglobulins / Q000032:analysis / Q000276:immunology; D005260:Female; D005602:France / Q000453:epidemiology; D016174:Hepacivirus / Q000235:genetics / Q000276:immunology / Q000302:isolation & purification*; D006526:Hepatitis C / Q000150:complications* / Q000453:epidemiology / Q000473:pathology; D006801:Humans; D008103:Liver Cirrhosis / Q000473:pathology; D008180:Lupus Erythematosus, Systemic / Q000188:drug therapy / Q000209:etiology* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000032:analysis; D012189:Retrospective Studies
chemical_list: D000974:Antibodies, Antinuclear; D000914:Antibodies, Viral; D018501:Antirheumatic Agents; D003450:Cryoglobulins; D012367:RNA, Viral