Autoimmune (type 1) diabetes
Lindbladh, Ida ; Svärd, Agnes Andersson LU
and Lernmark, Åke
LU
(2019)
p.769-787
- Abstract
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... (More)
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.
(Less)
- author
- Lindbladh, Ida
; Svärd, Agnes Andersson
LU
and Lernmark, Åke
LU
- organization
- publishing date
- 2019-10-18
- type
- Chapter in Book/Report/Conference proceeding
- publication status
- published
- subject
- keywords
- Autoimmune diabetes, Environmental factors, Genetic susceptibility, HLA, Insulitis, Islet autoantibodies, Islet autoimmunity, Type 1 diabetes
- host publication
- The Autoimmune Diseases
- editor
- Rose, Noel R. and Mackay, Ian R.
- edition
- 6
- pages
- 769 - 787
- publisher
- Academic Press
- external identifiers
-
- scopus:85081297887
- ISBN
- 9780128121023
- 9780128122426
- DOI
- 10.1016/B978-0-12-812102-3.00041-5
- language
- English
- LU publication?
- yes
- id
- 22cfccdc-0eb0-4428-9b8d-2fc4cbcbebfe
- date added to LUP
- 2020-03-23 23:16:17
- date last changed
- 2024-05-15 08:19:56
@inbook{22cfccdc-0eb0-4428-9b8d-2fc4cbcbebfe,
abstract = {{<p>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.</p>}},
author = {{Lindbladh, Ida and Svärd, Agnes Andersson and Lernmark, Åke}},
booktitle = {{The Autoimmune Diseases}},
editor = {{Rose, Noel R. and Mackay, Ian R.}},
isbn = {{9780128121023}},
keywords = {{Autoimmune diabetes; Environmental factors; Genetic susceptibility; HLA; Insulitis; Islet autoantibodies; Islet autoimmunity; Type 1 diabetes}},
language = {{eng}},
month = {{10}},
pages = {{769--787}},
publisher = {{Academic Press}},
title = {{Autoimmune (type 1) diabetes}},
url = {{http://dx.doi.org/10.1016/B978-0-12-812102-3.00041-5}},
doi = {{10.1016/B978-0-12-812102-3.00041-5}},
year = {{2019}},
}