title: Celiac disease and non-organ-specific autoantibodies in patients with chronic hepatitis C virus infection.
abstract: OBJECTIVE
  Considering that celiac disease (CD) is an autoimmune-based entity and the hepatitis C virus is suspected of being able to trigging autoimmune reactions, it has been hypothesized that hepatitis C virus infection might predispose to CD. The aim of this study was to investigate CD-related antibodies in a large series of hepatitis C virus-infected subjects that were also tested for non-organ-specific autoantibodies (NOSA) as indirect marker of autoimmune disorders.
  
  
  METHODS
  Two hundred and forty-four patients with chronic hepatitis C virus infection (HCV-patients) and 121 patients with HCV-negative liver disease (non-HCV-patients) underwent NOSA determination and celiac serology (firstly, anti-tissue transglutaminase antibodies, then the cases which tested positive were subsequently evaluated for the presence of antiendomysial antibodies). Serum samples from 42 of the HCV-patients who underwent interferon-alpha therapy after enrollment were tested for celiac antibodies and NOSA even after stopping treatment. Additionally, sera from 1,230 blood donors were assayed for celiac serology as healthy control population.
  
  
  RESULTS
  Positive anti-endomysial antibodies (AEA) were found in 5/244 (2%) HCV-patients, 1/121 (0.8%) non-HCV-patients and 2/1,230 (0.16%) blood donors, with a significant difference between HCV-patients and blood donors (P = 0.02; Odds ratio 12.8; 95% Confidence Interval 2.4-66). NOSA were found in 51 HCV-patients but only one of them had positive AEA. Eight out of 42 HCV-patients treated with interferon-alpha developed NOSA under therapy and none of them had CD antibodies.
  
  
  CONCLUSIONS
  AEA occur in 2% of HCV-patients and their presence is independent of other patterns of autoimmunity.
authors.affiliation: Cystic Fibrosis and Paediatric Gastroenterology Unit, Dipartimento di Scienze Pediatriche Mediche e Chirurgiche, Università di Messina, Messina, Italy.
authors.forename: Caterina
authors.initials: C
authors.lastname: Ruggeri
authors.forename: Agata Tiziana
authors.initials: AT
authors.lastname: La Masa
authors.forename: Stefania
authors.initials: S
authors.lastname: Rudi
authors.forename: Giovanni
authors.initials: G
authors.lastname: Squadrito
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Di Pasquale
authors.forename: Sergio
authors.initials: S
authors.lastname: Maimone
authors.forename: Gaia
authors.initials: G
authors.lastname: Caccamo
authors.forename: Salvatore
authors.initials: S
authors.lastname: Pellegrino
authors.forename: Giovanni
authors.initials: G
authors.lastname: Raimondo
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Magazzù
mesh_terms: D000328:Adult; D000368:Aged; D000998:Antiviral Agents / Q000627:therapeutic use; D001323:Autoantibodies / Q000097:blood*; D015551:Autoimmunity; D002446:Celiac Disease / Q000201:enzymology / Q000276:immunology*; D005260:Female; D019204:GTP-Binding Proteins; D019698:Hepatitis C, Chronic / Q000188:drug therapy / Q000201:enzymology / Q000276:immunology*; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D000091345:Protein Glutamine gamma Glutamyltransferase 2; D012802:Sicily; D011503:Transglutaminases / Q000276:immunology*
chemical_list: D000998:Antiviral Agents; D001323:Autoantibodies; D016898:Interferon-alpha; D000091345:Protein Glutamine gamma Glutamyltransferase 2; D011503:Transglutaminases; D019204:GTP-Binding Proteins