Linked Life Data

10330299

Source:http://linkedlifedata.com/resource/pubmed/id/10330299

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1999-6-29
pubmed:abstractText
We report here our prospective study of 15,224 non-diabetic, first-degree relatives of probands with immune-mediated (type 1) diabetes (IMD), of which 135 were found to eventually develop diabetes. We determined islet cell, insulin, GAD65, insulinoma-associated antigen-2 and 2beta autoantibodies (ICA, IAA, GAD65A, IA-2A and IA-2betaA), on the first available serum samples. The latter three autoantibodies were however assayed on subsets of the relatives with and without ICA, IAA and/or GAD65A, plus most of the relatives who developed diabetes. Of the relatives who progressed to diabetes, 94% had at least one of these autoantibodies on the first screening, while ICA proved to be the most sensitive single marker (sensitivity 74%). Risk of diabetes was however negligible when ICA was found in the absence of the others (5-year risk=5.3%), but increased dramatically whenever two or more autoantibodies were present (5-year risk=28.2% and 66.2%, respectively). The most predictive combination of markers was ICA plus IA-2A and/or IA-2beta A. Loss of first phase insulin release to IVGTT also occurred only in those ICA-positive relatives who had one or more of the other autoantibodies. The data suggests that significant beta-cell damage is seen only when the underlying autoimmunity has spread to multiple antigenic islet cell determinants. Combinations of the autoantibodies occurred most often in relatives with the highest risk HLA-DR/DQ phenotypes. These data document that only relatives positive for at least two or more of these five autoantibodies are at significant risk of diabetes themselves. Intervention trials for the prevention of type 1 diabetes could be designed based on testing for these autoantibodies alone, without the need for HLA typing and IVGTT testing.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0896-8411
pubmed:author
pubmed:copyrightInfo
Copyright 1999 Academic Press.
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
279-87
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:10330299-Adolescent, pubmed-meshheading:10330299-Adult, pubmed-meshheading:10330299-Aged, pubmed-meshheading:10330299-Aged, 80 and over, pubmed-meshheading:10330299-Autoantibodies, pubmed-meshheading:10330299-Child, pubmed-meshheading:10330299-Child, Preschool, pubmed-meshheading:10330299-Diabetes Mellitus, Type 1, pubmed-meshheading:10330299-Female, pubmed-meshheading:10330299-Glutamate Decarboxylase, pubmed-meshheading:10330299-HLA-DQ Antigens, pubmed-meshheading:10330299-HLA-DQ beta-Chains, pubmed-meshheading:10330299-Humans, pubmed-meshheading:10330299-Infant, pubmed-meshheading:10330299-Infant, Newborn, pubmed-meshheading:10330299-Insulin, pubmed-meshheading:10330299-Male, pubmed-meshheading:10330299-Middle Aged, pubmed-meshheading:10330299-Protein Tyrosine Phosphatase, Non-Receptor Type 1, pubmed-meshheading:10330299-Protein Tyrosine Phosphatases
pubmed:year
1999
pubmed:articleTitle
Only multiple autoantibodies to islet cells (ICA), insulin, GAD65, IA-2 and IA-2beta predict immune-mediated (Type 1) diabetes in relatives.
pubmed:affiliation
Departments of Pediatrics and Biometry and Genetics, Louisiana State University Medical School at the Research Institute for Children, New Orleans, LA, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't