title: Prevalence of Celiac disease among children in Finland.
abstract: BACKGROUND
  Wheat, rye, and barley proteins induce celiac disease, an autoimmune type of gastrointestinal disorder, in genetically susceptible persons. Because the disease may be underdiagnosed, we estimated the prevalence of the disease and tested the hypothesis that assays for serum autoantibodies can be used to detect untreated celiac disease and that positive findings correlate with specific HLA haplotypes.
  
  
  METHODS
  Serum samples were collected from 3654 students (age range, 7 to 16 years) in 1994 and screened in 2001 for endomysial and tissue transglutaminase antibodies. HLA typing was also performed on stored blood samples. All antibody-positive subjects were asked to undergo small-bowel biopsy in 2001.
  
  
  RESULTS
  Of the 3654 subjects, 56 (1.5 percent) had positive antibody tests, as determined in 2001. Results of the two antibody tests were highly concordant. As of 1994, none of the subjects had received a clinical diagnosis of celiac disease, but 10 who had positive tests for both antibodies in serum obtained in 1994 received the diagnosis between 1994 and 2001. Of the 36 other subjects with positive antibody assays who agreed to undergo biopsy in 2001, 27 had evidence of celiac disease on biopsy. Thus, the estimated biopsy-proved prevalence was 1 case in 99 children. All but two of the antibody-positive subjects had either the HLA-DQ2 or the HLA-DQ8 haplotype. The prevalence of the combination of antibody positivity and an HLA haplotype associated with celiac disease was 1 in 67.
  
  
  CONCLUSIONS
  The presence of serum tissue transglutaminase and endomysial autoantibodies is predictive of small-bowel abnormalities indicative of celiac disease. There is a good correlation between autoantibody positivity and specific HLA haplotypes. We estimate that the prevalence of celiac disease among Finnish schoolchildren is at least 1 case in 99 children.
authors.affiliation: Pediatric Research Center, Medical School, University of Tampere, Tampere, Finland. markku.maki@uta.fi
authors.forename: Markku
authors.initials: M
authors.lastname: Mäki
authors.forename: Kirsi
authors.initials: K
authors.lastname: Mustalahti
authors.forename: Jorma
authors.initials: J
authors.lastname: Kokkonen
authors.forename: Petri
authors.initials: P
authors.lastname: Kulmala
authors.forename: Mila
authors.initials: M
authors.lastname: Haapalahti
authors.forename: Tuomo
authors.initials: T
authors.lastname: Karttunen
authors.forename: Jorma
authors.initials: J
authors.lastname: Ilonen
authors.forename: Kaija
authors.initials: K
authors.lastname: Laurila
authors.forename: Ingrid
authors.initials: I
authors.lastname: Dahlbom
authors.forename: Tony
authors.initials: T
authors.lastname: Hansson
authors.forename: Peter
authors.initials: P
authors.lastname: Höpfl
authors.forename: Mikael
authors.initials: M
authors.lastname: Knip
mesh_terms: D000293:Adolescent; D001323:Autoantibodies / Q000097:blood*; D001706:Biopsy; D002446:Celiac Disease / Q000175:diagnosis / Q000453:epidemiology* / Q000276:immunology; D002648:Child; D015331:Cohort Studies; D005260:Female; D005387:Finland / Q000453:epidemiology; D006650:Histocompatibility Testing; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D007421:Intestine, Small / Q000473:pathology; D008297:Male; D018485:Muscle Fibers, Skeletal / Q000276:immunology*; D009297:Nasal Mucosa / Q000033:anatomy & histology; D015995:Prevalence; D011503:Transglutaminases / Q000276:immunology*
chemical_list: D001323:Autoantibodies; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D011503:Transglutaminases