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Islet autoantibodies in cord blood from children who developed type I (insulin-dependent) diabetes mellitus before 15 years of age

Lindberg, B. LU ; Ivarsson, S. A. ; Landin-Olsson, M. LU ; Sundkvist, G. LU ; Svanberg, L. and Lernmark, Å LU orcid (1999) In Diabetologia 42(2). p.181-187
Abstract

Islet autoantibodies are early markers for Type I (insulin-dependent) diabetes mellitus. The aim of this study was to establish whether islet autoantibodies were present at birth in children who developed Type I diabetes before 15 years of age. Cord blood sera from 81 children who developed Type I diabetes between 10 months and 14.9 years of age were tested for glutamic acid decarboxylase autoantibodies (GAD65Ab), islet cell antigen 512 autoantibodies (ICA512Ab), insulin autoantibodies (IAA) all by quantitative radioligand binding assays and islet cell autoantibodies (ICA) by indirect immunofluorescence. Cord blood sera from 320 randomly selected matched children were controls. The children who developed Type I diabetes had an increased... (More)

Islet autoantibodies are early markers for Type I (insulin-dependent) diabetes mellitus. The aim of this study was to establish whether islet autoantibodies were present at birth in children who developed Type I diabetes before 15 years of age. Cord blood sera from 81 children who developed Type I diabetes between 10 months and 14.9 years of age were tested for glutamic acid decarboxylase autoantibodies (GAD65Ab), islet cell antigen 512 autoantibodies (ICA512Ab), insulin autoantibodies (IAA) all by quantitative radioligand binding assays and islet cell autoantibodies (ICA) by indirect immunofluorescence. Cord blood sera from 320 randomly selected matched children were controls. The children who developed Type I diabetes had an increased frequency of cord blood islet autoantibodies compared with control subjects: Glutamic acid decarboxylase autoantibodies were detected in 6% (5/81) patients and 2% (5/320) control subjects (p = 0.03); islet cell antigen 512 autoantibodies in 5% (4/73) patients and 1% (4/288) control subjects (p = 0.06); insulin autoantibodies (IAA) in 0% (0/79) patients and 0.3% (1/320) control subjects (p = 0.36); and islet cell autoantibodies in 10 % (8/81) patients compared with 0.6 % (2/320) control subjects (p = 0.0001). Taken together, 17 % (14/81) patients had one or more islet autoantibody compared with 4 % (12/320) control subjects (p = 0.0001). Whereas none of the control children had more than one antibody, 4 % (3/81) children who later developed Type I diabetes were double positive (p = 0.002). Although glutamic acid decarboxylase autoantibodies' concentrations in cord-blood correlated to those in the mothers' blood at the time of delivery, no corresponding correlation was found for the other two types of autoantibodies. The increased frequency of cord blood islet autoantibodies suggests that the Type I diabetes process could already be initiated in utero.

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author
; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Autoimmunity, GAD65 antibodies, ICA512 antibodies, Insulin autoantibodies, Islet cell antibodies
in
Diabetologia
volume
42
issue
2
pages
7 pages
publisher
Springer
external identifiers
  • scopus:0032925805
  • pmid:10064098
ISSN
0012-186X
DOI
10.1007/s001250051137
language
English
LU publication?
yes
id
67eb0f49-cb26-46aa-8f4d-c2f8046145e9
date added to LUP
2019-06-30 23:32:28
date last changed
2024-03-13 08:22:15
@article{67eb0f49-cb26-46aa-8f4d-c2f8046145e9,
  abstract     = {{<p>Islet autoantibodies are early markers for Type I (insulin-dependent) diabetes mellitus. The aim of this study was to establish whether islet autoantibodies were present at birth in children who developed Type I diabetes before 15 years of age. Cord blood sera from 81 children who developed Type I diabetes between 10 months and 14.9 years of age were tested for glutamic acid decarboxylase autoantibodies (GAD65Ab), islet cell antigen 512 autoantibodies (ICA512Ab), insulin autoantibodies (IAA) all by quantitative radioligand binding assays and islet cell autoantibodies (ICA) by indirect immunofluorescence. Cord blood sera from 320 randomly selected matched children were controls. The children who developed Type I diabetes had an increased frequency of cord blood islet autoantibodies compared with control subjects: Glutamic acid decarboxylase autoantibodies were detected in 6% (5/81) patients and 2% (5/320) control subjects (p = 0.03); islet cell antigen 512 autoantibodies in 5% (4/73) patients and 1% (4/288) control subjects (p = 0.06); insulin autoantibodies (IAA) in 0% (0/79) patients and 0.3% (1/320) control subjects (p = 0.36); and islet cell autoantibodies in 10 % (8/81) patients compared with 0.6 % (2/320) control subjects (p = 0.0001). Taken together, 17 % (14/81) patients had one or more islet autoantibody compared with 4 % (12/320) control subjects (p = 0.0001). Whereas none of the control children had more than one antibody, 4 % (3/81) children who later developed Type I diabetes were double positive (p = 0.002). Although glutamic acid decarboxylase autoantibodies' concentrations in cord-blood correlated to those in the mothers' blood at the time of delivery, no corresponding correlation was found for the other two types of autoantibodies. The increased frequency of cord blood islet autoantibodies suggests that the Type I diabetes process could already be initiated in utero.</p>}},
  author       = {{Lindberg, B. and Ivarsson, S. A. and Landin-Olsson, M. and Sundkvist, G. and Svanberg, L. and Lernmark, Å}},
  issn         = {{0012-186X}},
  keywords     = {{Autoimmunity; GAD65 antibodies; ICA512 antibodies; Insulin autoantibodies; Islet cell antibodies}},
  language     = {{eng}},
  month        = {{02}},
  number       = {{2}},
  pages        = {{181--187}},
  publisher    = {{Springer}},
  series       = {{Diabetologia}},
  title        = {{Islet autoantibodies in cord blood from children who developed type I (insulin-dependent) diabetes mellitus before 15 years of age}},
  url          = {{http://dx.doi.org/10.1007/s001250051137}},
  doi          = {{10.1007/s001250051137}},
  volume       = {{42}},
  year         = {{1999}},
}