Immunopathological and genetic features in slowly progressive insulin-dependent diabetes mellitus and latent autoimmune diabetes in adults

Ann N Y Acad Sci. 2006 Oct:1079:60-6. doi: 10.1196/annals.1375.009.

Abstract

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.

Publication types

  • Review

MeSH terms

  • Adult
  • Age of Onset
  • Autoantibodies / immunology
  • Autoimmune Diseases / genetics*
  • Autoimmune Diseases / immunology*
  • Autoimmune Diseases / pathology
  • Diabetes Mellitus, Type 1 / classification
  • Diabetes Mellitus, Type 1 / genetics*
  • Diabetes Mellitus, Type 1 / immunology*
  • Diabetes Mellitus, Type 1 / pathology
  • Disease Progression
  • Epitopes
  • Genetic Predisposition to Disease
  • Glutamate Decarboxylase / immunology
  • Histocompatibility Antigens Class I / genetics
  • Histocompatibility Antigens Class II / genetics
  • Humans
  • Islets of Langerhans / immunology
  • Receptors, Calcitriol / genetics
  • Risk Factors

Substances

  • Autoantibodies
  • Epitopes
  • Histocompatibility Antigens Class I
  • Histocompatibility Antigens Class II
  • Receptors, Calcitriol
  • islet cell antibody
  • Glutamate Decarboxylase