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Immunopathological and Genetic Features in Slowly Progressive Insulin‐Dependent Diabetes Mellitus and Latent Autoimmune Diabetes in Adults
Author(s) -
KOBAYASHI TETSURO,
TANAKA SHOICHIRO,
HARII NORIKAZU,
AIDA KAORU,
SHIMURA HIROKI,
OHMORI MASAYUKI,
KANESIGE MASAHIRO,
SHIMADA AKIRA,
MARUYAMA TARO
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1375.009
Subject(s) - diabetes mellitus , autoantibody , medicine , islet , type 1 diabetes , insulin , type 2 diabetes , human leukocyte antigen , endocrinology , beta cell , immunology , antibody , antigen
In 1982 we proposed the presence of a subtype of type 1 diabetes [slowly progressive insulin‐dependent diabetes mellitus (SPIDDM)], which was characterized by persistently positive islet cell antibody, late age of onset, noninsulin‐dependent diabetes, and slowly progressive beta cell failure. Since then many studies demonstrated that this subtype of type 1 diabetes is prevalent in many ethnic groups and was later called the latent autoimmune diabetes in adults (LADA). Recent epidemiological studies reported that about 10% of patients with apparent type 2 diabetes have at least one autoantibodies against islet‐specific antigen with high potential to progress to insulin‐dependent state. Between SPIDDM and LADA some differences are reported in terms of some genetic predispositions including HLA class II and class I genes, vitamin D receptor gene, and CTLA4 genes. Common features in SPIDDM and LADA including preserved beta cells at the onset of diabetes and weak T cell response to residual beta cells suggest that these subtypes of type 1 diabetes are suitable candidates for prevention treatment for further progression of beta cell failure.