title: Disappearance of anti-Saccharomyces cerevisiae antibodies in coeliac disease during a gluten-free diet.
abstract: BACKGROUND
  Anti-Saccharomyces cerevisiae antibodies (ASCAs) are known to be positive in about 65% of Crohn's disease patients, in up to 43% of coeliac disease patients and in 0-5% of healthy controls. Coeliac disease might be an in-vivo model for unravelling the role of mucosal integrity in the formation of ASCAs since mucosal abnormalities normalize during a gluten-free diet (GFD).
  
  
  OBJECTIVE
  Firstly, to evaluate, retrospectively, the frequency of ASCA positivity in coeliac patients both at diagnosis and during follow-up on a GFD. Secondly, to study the correlation between ASCA positivity and mucosal damage.
  
  
  METHODS
  One hundred and eleven patients with histologically proven coeliac disease, positive endomysium antibodies on diagnosis and normalization of trans-glutaminase antibodies (t-TGAs) after successful adherence to a GFD were included. ASCAs, IgA and IgG were tested by enzyme-linked immunosorbent assays both at diagnosis and after the GFD.
  
  
  RESULTS
  Eighty-three children and 28 adults were included in this study. The mean age at diagnosis was 4.6 years for children and 48 years for adults. At diagnosis 15/83 (18%) of children were ASCA positive (either IgG or IgA), compared to 17/28 (61%) of adults. After successful adherence to a GFD and normalization of t-TGAs only one child remained ASCA positive (1%) compared to eight adults (29%). Two out of 28 (7%) adults remained positive for both IgA and IgG ASCAs.
  
  
  CONCLUSIONS
  In the majority of patients ASCAs disappeared during a GFD. In children this disappearance of ASCA positivity was more pronounced. This can be explained by the well-known fact that gut permeability normalizes much better in children than in adults. Also, the adults had higher levels of ASCAs at diagnosis. This was probably because they had been exposed to gluten for longer and therefore had more long-lasting damage.
authors.affiliation: Department of Gastroenterology, VU University Medical Center, Amsterdam and Gastroenterology, Rijnstate Hospital, Arnhem, The Netherlands.
authors.forename: Rosalie Ch
authors.initials: RCh
authors.lastname: Mallant-Hent
authors.forename: B
authors.initials: B
authors.lastname: Mary
authors.forename: E
authors.initials: E
authors.lastname: von Blomberg
authors.forename: Zhere
authors.initials: Z
authors.lastname: Yüksel
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Wahab
authors.forename: Chad
authors.initials: C
authors.lastname: Gundy
authors.forename: Gerrit A
authors.initials: GA
authors.lastname: Meyer
authors.forename: Chris J J
authors.initials: CJ
authors.lastname: Mulder
mesh_terms: D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000368:Aged; D000908:Antibodies, Fungal / Q000097:blood*; D001323:Autoantibodies / Q000097:blood; D002446:Celiac Disease / Q000178:diet therapy* / Q000276:immunology* / Q000382:microbiology / Q000503:physiopathology; D002648:Child; D002675:Child, Preschool; D005260:Female; D005983:Glutens / Q000008:administration & dosage*; D006801:Humans; D018928:Immunity, Mucosal; D007070:Immunoglobulin A / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D007223:Infant; D007413:Intestinal Mucosa / Q000276:immunology / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D012441:Saccharomyces cerevisiae / Q000276:immunology*
chemical_list: D000908:Antibodies, Fungal; D001323:Autoantibodies; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D005983:Glutens