详细记录  
题名:Insulin secretion and sensitivity in the prediction of type 1 diabetes in children with advanced beta-cell autoimmunity.
作者:SILJANDER HT; HERMANN R; HEKKALA A; LAHDE J; TANNER L; KESKINEN P; JORMA I; SIMELL OG; VEIJOLA R; KNIP M;
来源:Eur J Endocrinol. 2013 Jul 31. [ IF= 0.00 ] ]
URL :10.1530/EJE-13-0206
日期:20130830
摘要:OBJECTIVE - Reduced early insulin response has been shown to predict type 1
diabetes (T1D) in first-degree relatives of diabetic patients, while its role, as
well as that of insulin resistance, has remained poorly defined in young children
representing the general population. Predictive values of these markers and their
relation to other risk factors of T1D were assessed in children with advanced
beta-cell autoimmunity, i.e. persistent positivity for two or more
autoantibodies.DESIGN AND METHODS - Intravenous glucose tolerance tests (IVGTTs)
were performed in 218 children with HLA-DQB1-conferred disease susceptibility and
advanced beta-cell autoimmunity. Baseline, metabolic, and growth data were
compared between children progressing to diabetes and those remaining unaffected.
Hazard ratios (HR) for disease predictors and progression rate to T1D were
assessed.RESULTS - Children developing T1D were younger at seroconversion,
progressed more rapidly to advanced beta-cell autoimmunity, and had lower
first-phase insulin response (FPIR) and homeostasis model assessment index for
insulin resistance (HOMA-IR) than those remaining non-diabetic. Levels of
HOMA-IR/FPIR, islet cell antibodies, insulin autoantibodies (IAA), and islet
antigen 2 antibodies (IA-2A) were higher in progressors. Body mass index standard
deviation scores (BMI SDS), FPIR, age at IVGTT, and levels of IAA and IA-2A were
predictive for T1D.CONCLUSIONS -Young age, higher BMI SDS, reduced FPIR, and
higher levels of IAA and IA-2A predicted T1D in young children with HLA-conferred
disease susceptibility and advanced beta-cell autoimmunity. Disease risk
estimates were successfully stratified by the assessment of metabolic status and
BMI. The role of insulin resistance as an accelerator of the disease process was
minor.

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