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Predictors of associated autoimmune diseases in families with type 1 diabetes: results from the Type 1 Diabetes Genetics Consortium.
MedLine Citation:
PMID:  21744463     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
BACKGROUND: Type 1 diabetes (T1D) is a clinically heterogeneous disease. The presence of associated autoimmune diseases (AAIDs) may represent a distinct form of autoimmune diabetes, with involvement of specific mechanisms. The aim of this study was to find predictors of AAIDs in the Type 1 Diabetes Genetics Consortium data set. METHODS: Three thousand two hundred and sixty-three families with at least two siblings with T1D were included. Clinical information was obtained using questionnaires, anti-GAD (glutamic acid decarboxylase) and anti-protein tyrosine phosphatase (IA-2) were measured and human leukocyte antigen (HLA) genotyping was performed. Siblings with T1D with and without AAIDs were compared and a multivariate regression analysis was performed to find predictors of AAIDs. T1D-associated HLA haplotypes were defined as the four most susceptible and protective, respectively. RESULTS: One or more AAIDs were present in 14.4% of the T1D affected siblings. Age of diabetes onset, current age and time since diagnosis were higher, there was a female predominance and more family history of AAIDs in the group with AAIDs, as well as more frequent anti-GAD and less frequent anti-IA-2 antibodies. Risk and protective HLA haplotype distributions were similar, though DRB1*0301-DQA1*0501-DQB1*0201 was more frequent in the group with AAIDs. In the multivariate analysis, female gender, age of onset, family history of AAID, time since diagnosis and anti-GAD positivity were significantly associated with AAIDs. CONCLUSIONS: In patients with T1D, the presence of AAIDs is associated with female predominance, more frequent family history of AAIDs, later onset of T1D and more anti-GAD antibodies, despite longer duration of the disease. The predominance of certain HLA haplotypes suggests that specific mechanisms of disease may be involved. Copyright © 2011 John Wiley & Sons, Ltd.
Authors:
Ana M Wägner; Angelo Santana; Marta Herńndez; Julia C Wiebe; Javier Nóvoa; Dídac Mauricio;
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Publication Detail:
Type:  JOURNAL ARTICLE    
Journal Detail:
Title:  Diabetes/metabolism research and reviews     Volume:  27     ISSN:  1520-7560     ISO Abbreviation:  -     Publication Date:  2011 Jul 
Date Detail:
Created Date:  2011-7-11     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100883450     Medline TA:  Diabetes Metab Res Rev     Country:  -    
Other Details:
Languages:  ENG     Pagination:  493-498     Citation Subset:  -    
Copyright Information:
Copyright © 2011 John Wiley & Sons, Ltd.
Affiliation:
Endocrinology Department, Complejo Hospitalario Universitario Insular-Materno Infantil, de Gran Canaria, Spain; Departamento de Ciencias Médicas y Quirúrgicas, Universidad de Las Palmas de Gran Canaria, Spain. awagner@dcmq.ulpgc.es.
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