Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

Thyroid autoantibodies in cord blood sera from children and adolescents with autoimmune thyroiditis.

Svensson, Johan LU ; Lindberg, Bengt LU ; Ericsson, Ulla-Britt ; Olofsson, Per LU ; Jonsson, Bjorn and Ivarsson, Sten LU (2006) In Thyroid 16(1). p.79-83
Abstract
Autoimmune thyroid disease is common among women of childbearing age. Thyroid autoantibodies are predominantly of the immunoglobulin G (IgG)-type and pass the placental barrier from mother to child. Recent studies have suggested a pathogenetic role for transplacentally transmitted autoantibodies in the development of autoimmune disease. The aim of the present study was to investigate if children and adolescents with autoimmune thyroiditis (AIT) have been exposed to thyroid autoantibodies already in utero. Cord blood sera taken at delivery from 34 newborns who had developed AIT during childhood and adolescence, and sera from 31 of their mothers, were analyzed for the presence of autoantibodies against thyroid peroxidase (TPOAb) and... (More)
Autoimmune thyroid disease is common among women of childbearing age. Thyroid autoantibodies are predominantly of the immunoglobulin G (IgG)-type and pass the placental barrier from mother to child. Recent studies have suggested a pathogenetic role for transplacentally transmitted autoantibodies in the development of autoimmune disease. The aim of the present study was to investigate if children and adolescents with autoimmune thyroiditis (AIT) have been exposed to thyroid autoantibodies already in utero. Cord blood sera taken at delivery from 34 newborns who had developed AIT during childhood and adolescence, and sera from 31 of their mothers, were analyzed for the presence of autoantibodies against thyroid peroxidase (TPOAb) and thyroglobulin (TgAb), and compared to 233 randomly selected control children and their mothers. The prevalence of TPOAb in cord blood sera was elevated among the children and adolescents with AIT compared to controls (38% versus 14%; odds ratio [OR] 4.12, p < 0.001). An increased prevalence of TPOAb was also found among their mothers (29% versus 15%; OR 2.17, p < 0.048). No significant difference in the prevalence of TgAb was found either between children with AIT and the control children (18% versus 9%; OR 2.16, p < 0.15), or between their mothers and the control mothers (23% versus 12%; OR 2.17, p < 0.16). Most of the TPOAb-positive children had TPOAb-positive mothers, indicating the maternal origin of their TPOAb. In conclusion, a large proportion of children who later developed AIT had already been exposed to transplacentally transmitted TPOAb in utero. Whether these autoantibodies have any pathogenetic role in the development of AIT in offspring or if they simply mirror the inheritance of AIT, remains to be investigated. (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
Thyroid
volume
16
issue
1
pages
79 - 83
publisher
Mary Ann Liebert, Inc.
external identifiers
  • pmid:16487018
  • wos:000235907200012
  • scopus:33644772143
  • pmid:16487018
ISSN
1557-9077
DOI
10.1089/thy.2006.16.79
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Pediatrics/Urology/Gynecology/Endocrinology (013240400), Paediatric Endocrinology Research Group (013243010), Research Unit for Urogynaecology and Reproductive Pharmacology (013242710), Diabetes and Celiac Unit (013241540)
id
71ec3c2b-f068-4af5-8766-052e868fd053 (old id 153452)
date added to LUP
2016-04-01 15:51:08
date last changed
2022-03-14 20:26:28
@article{71ec3c2b-f068-4af5-8766-052e868fd053,
  abstract     = {{Autoimmune thyroid disease is common among women of childbearing age. Thyroid autoantibodies are predominantly of the immunoglobulin G (IgG)-type and pass the placental barrier from mother to child. Recent studies have suggested a pathogenetic role for transplacentally transmitted autoantibodies in the development of autoimmune disease. The aim of the present study was to investigate if children and adolescents with autoimmune thyroiditis (AIT) have been exposed to thyroid autoantibodies already in utero. Cord blood sera taken at delivery from 34 newborns who had developed AIT during childhood and adolescence, and sera from 31 of their mothers, were analyzed for the presence of autoantibodies against thyroid peroxidase (TPOAb) and thyroglobulin (TgAb), and compared to 233 randomly selected control children and their mothers. The prevalence of TPOAb in cord blood sera was elevated among the children and adolescents with AIT compared to controls (38% versus 14%; odds ratio [OR] 4.12, p &lt; 0.001). An increased prevalence of TPOAb was also found among their mothers (29% versus 15%; OR 2.17, p &lt; 0.048). No significant difference in the prevalence of TgAb was found either between children with AIT and the control children (18% versus 9%; OR 2.16, p &lt; 0.15), or between their mothers and the control mothers (23% versus 12%; OR 2.17, p &lt; 0.16). Most of the TPOAb-positive children had TPOAb-positive mothers, indicating the maternal origin of their TPOAb. In conclusion, a large proportion of children who later developed AIT had already been exposed to transplacentally transmitted TPOAb in utero. Whether these autoantibodies have any pathogenetic role in the development of AIT in offspring or if they simply mirror the inheritance of AIT, remains to be investigated.}},
  author       = {{Svensson, Johan and Lindberg, Bengt and Ericsson, Ulla-Britt and Olofsson, Per and Jonsson, Bjorn and Ivarsson, Sten}},
  issn         = {{1557-9077}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{79--83}},
  publisher    = {{Mary Ann Liebert, Inc.}},
  series       = {{Thyroid}},
  title        = {{Thyroid autoantibodies in cord blood sera from children and adolescents with autoimmune thyroiditis.}},
  url          = {{http://dx.doi.org/10.1089/thy.2006.16.79}},
  doi          = {{10.1089/thy.2006.16.79}},
  volume       = {{16}},
  year         = {{2006}},
}