title: Age at development of type 1 diabetes- and celiac disease-associated antibodies and clinical disease in genetically susceptible children observed from birth.
abstract: OBJECTIVE
  To compare the ages and sequence in which antibodies associated with type 1 diabetes and celiac disease appear and overt diseases develop in children with an HLA-conferred susceptibility to both diseases.
  
  
  METHODS
  We observed 2,052 children carrying genetic risks for both type 1 diabetes and celiac disease from birth until the median age of 5.7 years and analyzed diabetes- and celiac disease-associated antibodies in serum samples collected at 3- to 12-month intervals. Diabetes was confirmed by World Health Organization criteria and celiac disease by duodenal biopsies.
  
  
  RESULTS
  Altogether 342 children seroconverted to positivity for at least one diabetes-associated autoantibody and 88 to positivity for at least one celiac disease-associated antibody at the median ages of 3.0 and 1.5 years, respectively (P < 0.001). If only children with biochemically defined diabetes-associated autoantibodies against insulin, GAD, or IA-2A protein (n = 146) and children with tissue transglutaminase autoantibodies were compared (n = 86), the median seroconversion ages were 2.5 and 3.0 years (P = 0.011). Fifty-one children progressed to overt diabetes at 4.5 years and 44 children to celiac disease at 4.3 years (P = 0.257). Of the 19 children who developed both diabetes- and celiac disease-associated antibodies, 3 progressed to both diabetes and celiac disease.
  
  
  CONCLUSIONS
  Children with HLA-conferred susceptibility to type 1 diabetes and celiac disease develop celiac disease-associated antibodies mostly at a younger age or the same age at which they develop diabetes-associated autoantibodies. Clinical diabetes and celiac disease are commonly diagnosed at the same median age.
authors.affiliation: Juvenile Diabetes Research Foundation Center for Prevention of Type 1 Diabetes in Finland. satu.simell@tyks.fi
authors.forename: Satu
authors.initials: S
authors.lastname: Simell
authors.forename: Sanna
authors.initials: S
authors.lastname: Hoppu
authors.forename: Tuu
authors.initials: T
authors.lastname: Simell
authors.forename: Marja-Riitta
authors.initials: MR
authors.lastname: Ståhlberg
authors.forename: Markku
authors.initials: M
authors.lastname: Viander
authors.forename: Taina
authors.initials: T
authors.lastname: Routi
authors.forename: Ville
authors.initials: V
authors.lastname: Simell
authors.forename: Riitta
authors.initials: R
authors.lastname: Veijola
authors.forename: Jorma
authors.initials: J
authors.lastname: Ilonen
authors.forename: Heikki
authors.initials: H
authors.lastname: Hyöty
authors.forename: Mikael
authors.initials: M
authors.lastname: Knip
authors.forename: Olli
authors.initials: O
authors.lastname: Simell
mesh_terms: D017668:Age of Onset; D001323:Autoantibodies / Q000032:analysis* / Q000276:immunology; D002446:Celiac Disease / Q000175:diagnosis / Q000453:epidemiology* / Q000235:genetics / Q000276:immunology; D002648:Child; D002675:Child, Preschool; D003922:Diabetes Mellitus, Type 1 / Q000175:diagnosis / Q000453:epidemiology* / Q000235:genetics / Q000276:immunology; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D007223:Infant; D008297:Male
chemical_list: D001323:Autoantibodies