Seroconversion to islet autoantibodies between early pregnancy and delivery in non-diabetic mothers
Lindehammer, Sabina LU ; Jönsson, Ida LU ; Midberg, Bo LU ; Ivarsson, Sten LU ; Lynch, Kristian LU ; Dillner, Joakim LU and Lernmark, Åke LU
(2011)
In Journal of Reproductive Immunology
88(1).
p.72-79
- Abstract
- Islet autoantibodies are currently used to classify type 1 diabetes at diagnosis as they reflect the autoimmune pathogenesis of the disease. The presence of maternal autoantibodies reactive with pancreatic islet antigens is thought to increase the risk for type 1 diabetes in the offspring. The objective of this study was to determine seroconversion to islet autoantibodies in non-diabetic mothers during pregnancy. Screening of 33,682 mothers between September 2000 and August 2004 in the Diabetes Prediction in Skane (DiPiS) study showed that at delivery, 242 non-diabetic mothers had increased titers of islet autoantibodies reactive with glutamic acid decarboxylase (GADA), islet antigen-2 (IA-2A) or insulin (IAA), alone or in combination.... (More)
- Islet autoantibodies are currently used to classify type 1 diabetes at diagnosis as they reflect the autoimmune pathogenesis of the disease. The presence of maternal autoantibodies reactive with pancreatic islet antigens is thought to increase the risk for type 1 diabetes in the offspring. The objective of this study was to determine seroconversion to islet autoantibodies in non-diabetic mothers during pregnancy. Screening of 33,682 mothers between September 2000 and August 2004 in the Diabetes Prediction in Skane (DiPiS) study showed that at delivery, 242 non-diabetic mothers had increased titers of islet autoantibodies reactive with glutamic acid decarboxylase (GADA), islet antigen-2 (IA-2A) or insulin (IAA), alone or in combination. Control mothers (n = 1419), who were islet autoantibody negative at delivery, were randomly selected and matched by age, parity and pregnancy sampling date. Mothers positive for GADA (92%), IA-2A (84%) or IAA (65%) at delivery had increased titers already evident in early pregnancy. Titers declined for GADA (p<0.0001). IA-2A (p<0.0001) and IAA (p<0.0001). Seroconversion during pregnancy was observed for GADA in 10 (8%), IA-2A in 3 (16%) and IAA in 37 (35%) mothers. It is concluded that non-diabetic mothers with islet autoantibodies at delivery had significantly higher titers during early pregnancy than at delivery. As the statistical power in the seroconverting mothers was insufficient, further studies are needed to determine if the risk for type 1 diabetes in the offspring differs between mothers who already had increased titers of islet autoantibodies during early pregnancy or acquired them during pregnancy. (C) 2010 Elsevier Ireland Ltd. All rights reserved. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1882436
- author
- Lindehammer, Sabina
LU
; Jönsson, Ida
LU
; Midberg, Bo
LU
; Ivarsson, Sten
LU
; Lynch, Kristian
LU
; Dillner, Joakim
LU
and Lernmark, Åke
LU
- organization
- publishing date
- 2011
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Autoimmunity, Pregnancy, Seroconversion, Glutamic acid decarboxylase, autoantibody, Islet antigen-2 autoantibody, Insulin autoantibody
- in
- Journal of Reproductive Immunology
- volume
- 88
- issue
- 1
- pages
- 72 - 79
- publisher
- Elsevier
- external identifiers
-
- wos:000286540100011
- scopus:78650228451
- pmid:21111487
- ISSN
- 1872-7603
- DOI
- 10.1016/j.jri.2010.10.002
- language
- English
- LU publication?
- yes
- id
- b8509d47-4996-4e1b-ba34-8e9f748935b0 (old id 1882436)
- date added to LUP
- 2016-04-01 10:40:52
- date last changed
- 2022-01-26 01:30:10
@article{b8509d47-4996-4e1b-ba34-8e9f748935b0,
abstract = {{Islet autoantibodies are currently used to classify type 1 diabetes at diagnosis as they reflect the autoimmune pathogenesis of the disease. The presence of maternal autoantibodies reactive with pancreatic islet antigens is thought to increase the risk for type 1 diabetes in the offspring. The objective of this study was to determine seroconversion to islet autoantibodies in non-diabetic mothers during pregnancy. Screening of 33,682 mothers between September 2000 and August 2004 in the Diabetes Prediction in Skane (DiPiS) study showed that at delivery, 242 non-diabetic mothers had increased titers of islet autoantibodies reactive with glutamic acid decarboxylase (GADA), islet antigen-2 (IA-2A) or insulin (IAA), alone or in combination. Control mothers (n = 1419), who were islet autoantibody negative at delivery, were randomly selected and matched by age, parity and pregnancy sampling date. Mothers positive for GADA (92%), IA-2A (84%) or IAA (65%) at delivery had increased titers already evident in early pregnancy. Titers declined for GADA (p<0.0001). IA-2A (p<0.0001) and IAA (p<0.0001). Seroconversion during pregnancy was observed for GADA in 10 (8%), IA-2A in 3 (16%) and IAA in 37 (35%) mothers. It is concluded that non-diabetic mothers with islet autoantibodies at delivery had significantly higher titers during early pregnancy than at delivery. As the statistical power in the seroconverting mothers was insufficient, further studies are needed to determine if the risk for type 1 diabetes in the offspring differs between mothers who already had increased titers of islet autoantibodies during early pregnancy or acquired them during pregnancy. (C) 2010 Elsevier Ireland Ltd. All rights reserved.}},
author = {{Lindehammer, Sabina and Jönsson, Ida and Midberg, Bo and Ivarsson, Sten and Lynch, Kristian and Dillner, Joakim and Lernmark, Åke}},
issn = {{1872-7603}},
keywords = {{Autoimmunity; Pregnancy; Seroconversion; Glutamic acid decarboxylase; autoantibody; Islet antigen-2 autoantibody; Insulin autoantibody}},
language = {{eng}},
number = {{1}},
pages = {{72--79}},
publisher = {{Elsevier}},
series = {{Journal of Reproductive Immunology}},
title = {{Seroconversion to islet autoantibodies between early pregnancy and delivery in non-diabetic mothers}},
url = {{https://lup.lub.lu.se/search/files/2047813/1894385.pdf}},
doi = {{10.1016/j.jri.2010.10.002}},
volume = {{88}},
year = {{2011}},
}