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Slowly Progressive Type 1 Diabetes Mellitus: Current Knowledge And Future Perspectives

Slowly progressive type 1 insulin-dependent diabetes mellitus (SPIDDM), sometimes referred to as latent autoimmune diabetes in adults (LADA), is a heterogeneous disease that is often confused with type 1 and type 2 diabetes. As a result, there were few diagnostic criteria for this disorder until 201...

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Autores principales: Nishimura, Akihiro, Matsumura, Kimio, Kikuno, Shota, Nagasawa, Kaoru, Okubo, Minoru, Mori, Yasumichi, Kobayashi, Tetsuro
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6886592/
https://www.ncbi.nlm.nih.gov/pubmed/31819572
http://dx.doi.org/10.2147/DMSO.S191007
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author Nishimura, Akihiro
Matsumura, Kimio
Kikuno, Shota
Nagasawa, Kaoru
Okubo, Minoru
Mori, Yasumichi
Kobayashi, Tetsuro
author_facet Nishimura, Akihiro
Matsumura, Kimio
Kikuno, Shota
Nagasawa, Kaoru
Okubo, Minoru
Mori, Yasumichi
Kobayashi, Tetsuro
author_sort Nishimura, Akihiro
collection PubMed
description Slowly progressive type 1 insulin-dependent diabetes mellitus (SPIDDM), sometimes referred to as latent autoimmune diabetes in adults (LADA), is a heterogeneous disease that is often confused with type 1 and type 2 diabetes. As a result, there were few diagnostic criteria for this disorder until 2012, when the Japan Diabetes Society established criteria that could be used in clinical practice. A primary question is whether pathologic markers for type 1 or type 2 diabetes are present in the pancreas of patients with SPIDDM, because the phenotype of SPIDDM is similar to both type 1 and type 2 diabetes. Recent studies clarified pathologic findings in the pancreas of patients with SPIDDM, which included T-cell-mediated insulitis, a marker of type 1 diabetes; pseudoatrophic islets (islets specifically devoid of beta cells), another hallmark of type 1 diabetes; and a lack of amylin (ie, islet amyloid polypeptide) deposition to the islet cells, a pathologic marker of type 2 diabetes. In terms of preventing the loss of beta-cell function in patients with SPIDDM, several studies have shown that some drugs, including dipeptidyl peptidase-4 inhibitors, are effective. There is an increased need for early diagnosis of SPIDDM to preserve beta-cell function. This review presents updated findings on the pathogenesis and immunologic findings of the affected pancreas, diagnostic markers, risk factors for progression of beta-cell dysfunction, epidemiology, clinical features, diagnostic strategies, prevention strategies, and clinical options for patients with SPIDDM.
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spelling pubmed-68865922019-12-09 Slowly Progressive Type 1 Diabetes Mellitus: Current Knowledge And Future Perspectives Nishimura, Akihiro Matsumura, Kimio Kikuno, Shota Nagasawa, Kaoru Okubo, Minoru Mori, Yasumichi Kobayashi, Tetsuro Diabetes Metab Syndr Obes Review Slowly progressive type 1 insulin-dependent diabetes mellitus (SPIDDM), sometimes referred to as latent autoimmune diabetes in adults (LADA), is a heterogeneous disease that is often confused with type 1 and type 2 diabetes. As a result, there were few diagnostic criteria for this disorder until 2012, when the Japan Diabetes Society established criteria that could be used in clinical practice. A primary question is whether pathologic markers for type 1 or type 2 diabetes are present in the pancreas of patients with SPIDDM, because the phenotype of SPIDDM is similar to both type 1 and type 2 diabetes. Recent studies clarified pathologic findings in the pancreas of patients with SPIDDM, which included T-cell-mediated insulitis, a marker of type 1 diabetes; pseudoatrophic islets (islets specifically devoid of beta cells), another hallmark of type 1 diabetes; and a lack of amylin (ie, islet amyloid polypeptide) deposition to the islet cells, a pathologic marker of type 2 diabetes. In terms of preventing the loss of beta-cell function in patients with SPIDDM, several studies have shown that some drugs, including dipeptidyl peptidase-4 inhibitors, are effective. There is an increased need for early diagnosis of SPIDDM to preserve beta-cell function. This review presents updated findings on the pathogenesis and immunologic findings of the affected pancreas, diagnostic markers, risk factors for progression of beta-cell dysfunction, epidemiology, clinical features, diagnostic strategies, prevention strategies, and clinical options for patients with SPIDDM. Dove 2019-11-28 /pmc/articles/PMC6886592/ /pubmed/31819572 http://dx.doi.org/10.2147/DMSO.S191007 Text en © 2019 Nishimura et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Review
Nishimura, Akihiro
Matsumura, Kimio
Kikuno, Shota
Nagasawa, Kaoru
Okubo, Minoru
Mori, Yasumichi
Kobayashi, Tetsuro
Slowly Progressive Type 1 Diabetes Mellitus: Current Knowledge And Future Perspectives
title Slowly Progressive Type 1 Diabetes Mellitus: Current Knowledge And Future Perspectives
title_full Slowly Progressive Type 1 Diabetes Mellitus: Current Knowledge And Future Perspectives
title_fullStr Slowly Progressive Type 1 Diabetes Mellitus: Current Knowledge And Future Perspectives
title_full_unstemmed Slowly Progressive Type 1 Diabetes Mellitus: Current Knowledge And Future Perspectives
title_short Slowly Progressive Type 1 Diabetes Mellitus: Current Knowledge And Future Perspectives
title_sort slowly progressive type 1 diabetes mellitus: current knowledge and future perspectives
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6886592/
https://www.ncbi.nlm.nih.gov/pubmed/31819572
http://dx.doi.org/10.2147/DMSO.S191007
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