title: Anti-Saccharomyces cerevisiae antibodies status is associated with oral involvement and disease severity in Crohn disease.
abstract: OBJECTIVE
  To determine anti-Saccharomyces cerevisiae antibodies (ASCA) status and its relation to disease phenotype in patients with inflammatory bowel disease (IBD).
  
  
  METHODS
  A total of 301 Scottish patients with early-onset IBD-197 Crohn disease (CD), 76 ulcerative colitis (UC), 28 indeterminate colitis (IC)-and 78 healthy control individuals were studied. ASCA status (IgA, IgG) was determined by enzyme-linked immunosorbent assay. ASCA status was then analyzed in relation to CD phenotype.
  
  
  RESULTS
  Patients with CD had a higher prevalence of ASCA than patients with UC and healthy controls: 82/197 versus 12/76, odds ratio (OR) 3.80 (1.93-7.50) and 82/197 versus 6/78, OR 8.56 (3.55-20.62), respectively. Univariate analysis showed that positive ASCA status was associated with oral CD (17/25 vs 59/153, OR 3.39 [1.38-8.34]), perianal CD (39/77 vs 38/108, OR 1.89 [1.04-3.44]) and the presence of granulomata (63/132 vs 15/52, OR 2.25 [1.13-4.48]) and also with markers of disease severity: raised C-reactive protein (44/90 vs 12/49, OR 2.95[1.36-6.37]), hypoalbuminemia (44/85 vs 20/74, OR 2.28[1.19-4.37]), and surgery (27/49 vs 54/147, OR 2.11 [1.10-4.06]). From multivariate analysis, the presence of oral disease (adjusted P = 0.001, OR 22.22 [3.41-142.86]) and hypoalbuminemia (adjusted P = 0.01, OR 4.78 [1.40-16.39]) was found to be independently associated with ASCA status. No association was demonstrated between ASCA and IBD candidate genes.
  
  
  CONCLUSIONS
  Patients with CD had a higher prevalence of ASCA than did other patients with IBD. ASCA status described patients with CD who had a specific phenotype, showing an association with markers of disease severity and oral CD involvement.
authors.affiliation: Department of Paediatric Gastroenterology, Yorkhill Hospital, UK. richardrussell@nhs.net
authors.forename: R K
authors.initials: RK
authors.lastname: Russell
authors.forename: B
authors.initials: B
authors.lastname: Ip
authors.forename: M C
authors.initials: MC
authors.lastname: Aldhous
authors.forename: M
authors.initials: M
authors.lastname: MacDougall
authors.forename: H E
authors.initials: HE
authors.lastname: Drummond
authors.forename: I D R
authors.initials: ID
authors.lastname: Arnott
authors.forename: P M
authors.initials: PM
authors.lastname: Gillett
authors.forename: P
authors.initials: P
authors.lastname: McGrogan
authors.forename: L T
authors.initials: LT
authors.lastname: Weaver
authors.forename: W M
authors.initials: WM
authors.lastname: Bisset
authors.forename: G
authors.initials: G
authors.lastname: Mahdi
authors.forename: D C
authors.initials: DC
authors.lastname: Wilson
authors.forename: J
authors.initials: J
authors.lastname: Satsangi
mesh_terms: D000293:Adolescent; D000908:Antibodies, Fungal / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D002648:Child; D003093:Colitis, Ulcerative / Q000097:blood / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D003424:Crohn Disease / Q000097:blood / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005838:Genotype; D006304:Health Status; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D008297:Male; D015999:Multivariate Analysis; D016017:Odds Ratio; D012441:Saccharomyces cerevisiae / Q000276:immunology*; D016036:Seroepidemiologic Studies; D012720:Severity of Illness Index
chemical_list: D000908:Antibodies, Fungal; D015415:Biomarkers; D007070:Immunoglobulin A; D007074:Immunoglobulin G