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Diabetes-Related Autoantibodies and Gestational Diabetes

¹ Servei d'Endocrinologia i Nutrició, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain
² Departament de Medicina, Universitat Autònoma de Barcelona, Barcelona, Spain
³ Centro de Investigación Biomédica del Área de Bioingeniería, Biomateriales y Nanotecnología, Instituto de Salud Carlos III, Barcelona, Spain

Address correspondence and reprint requests to Prof. Dr. Alberto de Leiva, Servei d'Endocrinologia i Nutrició, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Avinguda Sant Antoni M. Claret, 167, 08025, Barcelona, Spain. E-mail: aleiva@santpau.es

Abbreviations: AA, autoantibody • DRA, diabetes-related autoantibody • GADA, autoantibodies to GAD • IA, insulin antibody • IAA, insulin autoantibody • ICA, islet cell autoantibody • LADA, latent autoimmune diabetes in adults

The first 300 words of the full text of this article appear below.

	INTRODUCTION

 
Gestational diabetes mellitus (GDM) has long been recognized as a heterogeneous disorder (1,2), with autoimmunity against the ß-cell contributing in a small subset of patients (3).

	HETEROGENEITY OF AUTOIMMUNE DIABETES: AN OVERVIEW—

 
Autoimmune diabetes is caused by the destruction of ß-cells of pancreatic islets by an immune-mediated process, promoted by the interaction of genetic and environmental factors (4). Autoantibodies (AAs) against pancreatic ß-cell antigens precede the clinical onset of type 1 diabetes (4). Circulating islet cell antibodies, originally described by indirect immunofluorescence in 1974 (5), have been demonstrated in the great majority of individuals with type 1 diabetes, both at the preclinical state and at the onset of clinically overt diabetes, and they persist in the circulation for a long time. Islet cell AAs include autoantibodies to islet cell cytoplasm (islet cell autoantibodies [ICAs]), to native insulin (insulin autoantibodies [IAAs]), to GAD (GADA) (6–8), and to tyrosine phosphatases (insulinoma-associated antigens IA-2A and IA-2ß) (9,10).

Age not only modifies the risk of autoimmune diabetes, but also the presence of AAs, the intensity of ß-cell destruction, the rate of progression to overt diabetes, and the degree of residual insulin secretion. Approximately 30% of subjects with classic autoimmune diabetes (type 1A diabetes) present after age 35 years (11). Childhood autoimmune diabetes is associated with an increased prevalence of alleles DR3, DQB1*0201 and DR4, and DQB1*0302, with the proportion of heterozygotes declining with age at diagnosis (12). Children with the allele HLA DR2, DQB1*0602, almost never develop diabetes, whereas this allele confers a much lower protection for adult-onset autoimmune diabetes (13).

Since the discovery of AAs against islet cell antigens, it has been recognized that a fraction of adults considered to have type 2 . . . [Full Text of this Article]

	DRAs AND DIABETIC PREGNANCY

 
Prevalence and titers
ICAs.
IAAs.
GADAs and IA-2As.
Transplacental passage of DRAs and related effects

	DRAs AND THE RISK OF MATERNAL GLUCOSE INTOLERANCE/DIABETES—

 

	AUTOIMMUNE GDM: A DISTINCT PRE-DIABETIC STAGE—

 

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