Your browser has javascript turned off or blocked. This will lead to some parts of our website to not work properly or at all. Turn on javascript for best performance.

The browser you are using is not supported by this website. All versions of Internet Explorer are no longer supported, either by us or Microsoft (read more here: https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Please use a modern browser to fully experience our website, such as the newest versions of Edge, Chrome, Firefox or Safari etc.

Default user image.

Åke Lernmark

Principal investigator

Default user image.

Autoimmune (type 1) diabetes

Author

  • Ida Lindbladh
  • Agnes Andersson Svärd
  • Åke Lernmark

Editor

  • Noel R. Rose
  • Ian R. Mackay

Summary, in English

Autoimmune (type 1) diabetes mellitus is a chronic disease without a cure. It affects primarily young people but may be diagnosed at any age. Strong genetic susceptibility characterizes the most common form of autoimmune diabetes in children younger than 18 years of age. Autoimmune diabetes is generally assumed to be hereditary, although the majority of patients do not have a family history of autoimmune diabetes. The etiology is not fully understood. However, the genetic susceptibility is strongly associated with genetic factors within the human leukocyte antigen (HLA) complex on chromosome 6. The role of HLA is associated with the development of islet autoimmunity, a stage marked by the appearance of autoantibodies against islet beta-cell proteins. Non-HLA genetic factors contribute to the risk for a first appearing islet autoantibody. Environmental etiological factors include candidate virus, but how a virus infection may yield islet autoimmunity remains to be clarified. The pathogenesis of autoimmune diabetes is characterized by a complex and prolonged autoimmune prodrome (prediabetic) phase which may last for months to years. The asymptomatic phases, Stage I (two or more autoantibodies and normoglycemia) and Stage II (two or more autoantibodies and dysglycemia), are marked by autoantibodies against either insulin (IAA), glutamic acid decarboxylase (GADA), islet antigen-2 (IA-2A), zinc transporter 8 alone, or in combination. In the third and symptomatic stage (Stage III) of disease, mononuclear cell infiltration has been detected in many but not in all patients, a beta-cell loss is significant and dysglycemia and classic symptoms of hyperglycemia develop. Lifelong insulin replacement therapy is still the only treatment. The identification of environmental determinants that trigger either IAA first or GADA first remains a major challenge to the understanding of the etiology and pathogenesis of autoimmune diabetes.

Department/s

  • Paediatric Endocrinology
  • EXODIAB: Excellence in Diabetes Research in Sweden
  • Diabetes and Celiac Unit
  • LUBIN Lab- Lund Brain Injury laboratory for Neurosurgical research

Publishing year

2019-10-18

Language

English

Pages

769-787

Publication/Series

The Autoimmune Diseases

Document type

Book chapter

Publisher

Academic Press

Topic

  • Endocrinology and Diabetes

Keywords

  • Autoimmune diabetes
  • Environmental factors
  • Genetic susceptibility
  • HLA
  • Insulitis
  • Islet autoantibodies
  • Islet autoimmunity
  • Type 1 diabetes

Status

Published

Research group

  • Paediatric Endocrinology
  • Diabetes and Celiac Unit
  • LUBIN Lab- Lund Brain Injury laboratory for Neurosurgical research

ISBN/ISSN/Other

  • ISBN: 9780128122426
  • ISBN: 9780128121023