| Titre : | Timing of initial cereal exposure in infancy and risk of islet autoimmunity. (2003) |
| Auteurs : | Jill-M NORRIS ; Katherine BARRIGA ; George-S EISENBARTH ; ERLICH (Henry-A) : USA. Department of Human Genetics Roche Molecular Systems Inc. Alameda. CA. ; Michelle HOFFMAN ; Georgeanna KLINGENSMITH ; Marian REWERS ; Barbara Davis Center for Childhood Diabetes. University of Colorado Health Sciences Center. Denver. USA |
| Type de document : | Article |
| Dans : | JAMA - Journal of the american medical association (vol. 290, n° 13, 2003) |
| Pagination : | 1713-1720 |
| Langues: | Anglais |
| Mots-clés : | Céréale ; Régime alimentaire ; Enfant ; Homme ; Facteur risque ; Etiologie ; Epidémiologie ; Glande endocrine [pathologie] ; Immunopathologie ; Maladie autoimmune |
| Résumé : | [BDSP. Notice produite par INIST-CNRS R0xP5hIE. Diffusion soumise à autorisation]. Context : Dietary exposures in infancy have been implicated, albeit inconsistently, in the etiology of type 1 diabetes mellitus (DM). Objective : To examine the association between cereal exposures in the infant diet and appearance of islet autoimmunity (IA). Design : Birth cohort study conducted from 1994 to 2002 with a mean follow-up of 4 years. Setting Newborn screening for HLA was done at St Joseph's Hospital in Denver, Colo. First-degree relatives of type 1 DM individuals were recruited from the Denver metropolitan area. Participants We enrolled 1183 children at increased type 1 DM risk, defined as either HLA genotype or having a first-degree relative with type 1 DM, at birth and followed them prospectively. We obtained exposure and outcome measures for 76% of enrolled children. Participants had variable lengths of follow-up (9 months to 9 years). Main Outcome Measures : Blood draws for the detection of insulin autoantibody, glutamic acid decarboxylase autoantibody, or IA-2 autoantibody were performed at 9,15, and 24 months and annually thereafter. Children with IA (n=34) were defined as those testing positive for at least 1 of the autoantibodies on 2 or more consecutive visits and who tested positive or had diabetes on their most recent visit. Results : Children initially exposed to cereals between ages 0 and 3 months (hazard ratio [HR], 4.32 ; 95% confidence interval [Cl], 2.0-9.35) and those who were exposed at 7 months or older (HR, 5.36 ; 95% Cl, 2.08-13.8) had increased hazard of IA compared with those who were exposed during the fourth through sixth month, after adjustment for HLA genotype, family history of type 1 DM, ethnicity, and maternal age. In children who were positive for the HLA-DRB1 *03/04, DQB8 genotype, adjusted HRs were 5.55 (95% Cl, 1.92-16.03) and 12.53 (95% Cl, 3.19-49.23) for initial cereal exposure between ages 0 to 3 months and at 7 months or older, respectively. Conclusion : There may be a window of exposure to cereals in infancy outside which initial exposure increases IA risk in susceptible children. |
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