OBJECTIVE: To establish whether children with type 1 diabetes mellitus (T1D) with signs of pronounced beta-cell-specific autoimmunity as reflected by high autoantibody titers or positivity for several beta-cell-specific autoantibodies show a different pattern of month of birth (MOB) compared with children with T1D and low beta-cell autoimmunity and that of the general population. RESEARCH DESIGN AND METHODS: Cosinor analysis was used to analyze MOB rhythmicity in Swedish children with new onset T1D (n = 572), in whom the glutamate decarboxylase autoantibody (GAD65Ab) titer was determined and compared with that in 833 healthy children, and in 505 children with T1D in Berlin, in whom the titers of autoantibodies to insulin, GAD65, and islet antigen-2 were compared with the MOB pattern in the general population (n = 446 571). RESULTS: In both cohorts of children with T1D, we found that children with either a high GAD65Ab titer (above the 80th percentile) or positivity for three beta-cell-specific autoantibodies differed in their pattern of MOB from the healthy population. CONCLUSIONS: Our past and present observations support the hypothesis that the autoimmune process leading to childhood T1D is in part triggered in the perinatal period by viral infections in genetically susceptible individuals. The present study suggests that the process is linked to titer levels of autoantibodies.
OBJECTIVE: To establish whether children with type 1 diabetes mellitus (T1D) with signs of pronounced beta-cell-specific autoimmunity as reflected by high autoantibody titers or positivity for several beta-cell-specific autoantibodies show a different pattern of month of birth (MOB) compared with children with T1D and low beta-cell autoimmunity and that of the general population. RESEARCH DESIGN AND METHODS: Cosinor analysis was used to analyze MOB rhythmicity in Swedish children with new onset T1D (n = 572), in whom the glutamate decarboxylase autoantibody (GAD65Ab) titer was determined and compared with that in 833 healthy children, and in 505 children with T1D in Berlin, in whom the titers of autoantibodies to insulin, GAD65, and islet antigen-2 were compared with the MOB pattern in the general population (n = 446 571). RESULTS: In both cohorts of children with T1D, we found that children with either a high GAD65Ab titer (above the 80th percentile) or positivity for three beta-cell-specific autoantibodies differed in their pattern of MOB from the healthy population. CONCLUSIONS: Our past and present observations support the hypothesis that the autoimmune process leading to childhood T1D is in part triggered in the perinatal period by viral infections in genetically susceptible individuals. The present study suggests that the process is linked to titer levels of autoantibodies.
Authors: L M Shulman; C S Hampe; A Ben-Haroush; Y Perepliotchikov; F Vaziri-Sani; S Israel; K Miller; H Bin; B Kaplan; Z Laron Journal: Diabet Med Date: 2014-02-25 Impact factor: 4.359