Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

Seasonality of month of birth differs between type 1 diabetes patients with pronounced beta-cell autoimmunity and individuals with lesser or no beta-cell autoimmunity

Lewy, H ; Hampe, CS ; Kordonouri, O ; Haberland, H ; Landin-Olsson, Mona LU ; Törn, Carina LU and Laron, Z (2008) In Pediatric Diabetes 9(1). p.46-52
Abstract
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... (More)
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. (Less)
Please use this url to cite or link to this publication:
author
; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Pediatric Diabetes
volume
9
issue
1
pages
46 - 52
publisher
Wiley-Blackwell
external identifiers
  • pmid:18036133
  • wos:000255130200008
  • scopus:38349102512
  • pmid:18036133
ISSN
1399-543X
DOI
10.1111/j.1399-5448.2007.00265.x
language
English
LU publication?
yes
id
fc31a4c8-da0b-4a4b-b7ed-7f72c4a97cf3 (old id 1143097)
date added to LUP
2016-04-01 11:56:39
date last changed
2024-10-08 15:45:39
@article{fc31a4c8-da0b-4a4b-b7ed-7f72c4a97cf3,
  abstract     = {{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.}},
  author       = {{Lewy, H and Hampe, CS and Kordonouri, O and Haberland, H and Landin-Olsson, Mona and Törn, Carina and Laron, Z}},
  issn         = {{1399-543X}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{46--52}},
  publisher    = {{Wiley-Blackwell}},
  series       = {{Pediatric Diabetes}},
  title        = {{Seasonality of month of birth differs between type 1 diabetes patients with pronounced beta-cell autoimmunity and individuals with lesser or no beta-cell autoimmunity}},
  url          = {{http://dx.doi.org/10.1111/j.1399-5448.2007.00265.x}},
  doi          = {{10.1111/j.1399-5448.2007.00265.x}},
  volume       = {{9}},
  year         = {{2008}},
}