title: Pancreatic autoantibodies in inflammatory bowel disease.
abstract: BACKGROUND
  Autoantibodies against exocrine pancreas (PABs) have been reported to be specific for Crohn's disease (CD), albeit at a low prevalence (30%). We studied PABs in patients with inflammatory bowel disease (IBD), unaffected family members, and control subjects.
  
  
  METHODS
  A Belgian study cohort of 575 subjects, including 289 IBD patients (CD, 169 patients; ulcerative colitis [UC], 120 patients), 108 unaffected first-degree relatives, 78 subjects with non-IBD gastrointestinal disorders (gastrointestinal control subjects [GIcos]), and 100 healthy control subjects (Hcos), were tested for PAB by a standardized indirect immunofluorescence method.
  
  
  RESULTS
  The prevalence of PABs in this study cohort was 32% for CD, 23.3% for UC, and 22.2% for their unaffected family members (all P < 0.001), compared with 1.3% for GIcos and 0% for Hcos. Two staining patterns could be observed: an intracellular pattern (IC); and an extracellular pattern (EC). The EC was significantly more prevalent in CD patients compared with UC patients (P = 0.014), and higher titers of this pattern were found in CD patients (P = 0.01). Both PAB patterns were negatively associated with stricturing disease behavior of CD (P = 0.021). The IC was associated with familial CD (P = 0.0009) and familial UC (P = 0.0003).
  
  
  CONCLUSIONS
  The prevalence of PAB found in CD patients in this study was similar to that cited in previous reports. In contrast to these reports, we also found an increased prevalence of PABs in patients with UC and in unaffected first-degree relatives of IBD patients. We observed two main staining patterns, both of which were present in IBD and were associated with specific phenotypes of the disease.
authors.affiliation: Department of Gastroenterology, University Hospital Gasthuisberg, Katholieke Universiteit Leuven, Leuven, Belgium.
authors.forename: Sofie
authors.initials: S
authors.lastname: Joossens
authors.forename: Severine
authors.initials: S
authors.lastname: Vermeire
authors.forename: Kristel
authors.initials: K
authors.lastname: Van Steen
authors.forename: Godelieve
authors.initials: G
authors.lastname: Godefridis
authors.forename: Greet
authors.initials: G
authors.lastname: Claessens
authors.forename: Marie
authors.initials: M
authors.lastname: Pierik
authors.forename: Robert
authors.initials: R
authors.lastname: Vlietinck
authors.forename: Raymond
authors.initials: R
authors.lastname: Aerts
authors.forename: Paul
authors.initials: P
authors.lastname: Rutgeerts
authors.forename: Xavier
authors.initials: X
authors.lastname: Bossuyt
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D019268:Antibodies, Antineutrophil Cytoplasmic / Q000097:blood*; D001530:Belgium; D016022:Case-Control Studies; D015331:Cohort Studies; D003093:Colitis, Ulcerative / Q000453:epidemiology / Q000235:genetics / Q000276:immunology*; D003424:Crohn Disease / Q000453:epidemiology / Q000235:genetics / Q000276:immunology*; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D020022:Genetic Predisposition to Disease; D006801:Humans; D007515:Islets of Langerhans / Q000276:immunology; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D012680:Sensitivity and Specificity
chemical_list: D019268:Antibodies, Antineutrophil Cytoplasmic