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Slowly Progressive Insulin-Dependent Diabetes Mellitus or Latent Autoimmune Diabetes of Adult
a Institute of Cell and Molecular Science, Queen Mary College, University of London, London E1 2AT, UK
Key Words: autoimmune diabetes • glutamic acid decarboxylase antibodies • islet cell antibodies • insulinoma-associated antigen-2 • ketoacidosis
Address for correspondence: Prof. David Leslie, Institute of Cell and Molecular Science, Centre for Diabetes & Metabolic Medicine, Bart's and The London, Queen Mary's School of Medicine & Dentistry, 4 Newark Street, Nondon, E1 2AT. Voice: +44 (0)20 7882 2482 or +44 (0)20 7601 7446; fax: +44 (0) 20 7882 2186 or +44 (0) 20 7601 7449. e-mail: r.d.g.leslie{at}qmul.ac.uk
Autoimmune diabetes is due to destruction of insulin-secreting beta islet cells by an immune-mediated process, which is induced and promoted by the interaction of genetic and environmental factors. This form of diabetes is one of a group of autoimmune diseases that affect about 10% of the population in the developed world. The detection of diabetes-associated autoantibodies, including glutamic acid decarboxylase antibodies (GADA), islet cell antibodies (ICA), and insulinoma-associated (IA-2) autoantibodies is widely held to reflect an underlying autoimmune pathology but the clinical features associated with the presence of these diabetes-associated autoantibodies is highly variable ranging from lack of symptoms with normal glucose tolerance to catastrophic and potentially fatal diabetic ketoacidosis. It is the purpose of this article to establish the range of metabolic features associated with diabetes-associated autoimmune changes and discuss how this metabolic spectrum itself reflects a spectrum of immune and clinical changes that cast light on the nature of autoimmune diabetes.
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