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Diabetic ketoacidosis: a challenging diabetes phenotype
SUMMARY: We describe three patients presenting with diabetic ketoacidosis secondary to ketosis prone type 2, rather than type 1 diabetes. All patients were treated according to a standard DKA protocol, but were subsequently able to come off insulin therapy while maintaining good glycaemic control. K...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Bioscientifica Ltd
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5404460/ https://www.ncbi.nlm.nih.gov/pubmed/28458888 http://dx.doi.org/10.1530/EDM-16-0109 |
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author | Small, Cliona Egan, Aoife M Elhadi, El Muntasir O’Reilly, Michael W Cunningham, Aine Finucane, Francis M |
author_facet | Small, Cliona Egan, Aoife M Elhadi, El Muntasir O’Reilly, Michael W Cunningham, Aine Finucane, Francis M |
author_sort | Small, Cliona |
collection | PubMed |
description | SUMMARY: We describe three patients presenting with diabetic ketoacidosis secondary to ketosis prone type 2, rather than type 1 diabetes. All patients were treated according to a standard DKA protocol, but were subsequently able to come off insulin therapy while maintaining good glycaemic control. Ketosis-prone type 2 diabetes (KPD) presenting with DKA has not been described previously in Irish patients. The absence of islet autoimmunity and evidence of endogenous beta cell function after resolution of DKA are well-established markers of KPD, but are not readily available in the acute setting. Although not emphasised in any current guidelines, we have found that a strong family history of type 2 diabetes and the presence of cutaneous markers of insulin resistance are strongly suggestive of KPD. These could be emphasised in future clinical practice guidelines. LEARNING POINTS: Even in white patients, DKA is not synonymous with type 1 diabetes and autoimmune beta cell failure. KPD needs to be considered in all patients presenting with DKA, even though it will not influence their initial treatment. Aside from markers of endogenous beta cell function and islet autoimmunity, which in any case are unlikely to be immediately available to clinicians, consideration of family history of type 2 diabetes and cutaneous markers of insulin resistance might help to identify those with KPD and are more readily apparent in the acute setting, though not emphasised in guidelines. Consideration of KPD should never alter the management of the acute severe metabolic derangement of DKA, and phasing out of insulin therapy requires frequent attendance and meticulous and cautious surveillance by a team of experienced diabetes care providers. |
format | Online Article Text |
id | pubmed-5404460 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Bioscientifica Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-54044602017-04-28 Diabetic ketoacidosis: a challenging diabetes phenotype Small, Cliona Egan, Aoife M Elhadi, El Muntasir O’Reilly, Michael W Cunningham, Aine Finucane, Francis M Endocrinol Diabetes Metab Case Rep Unique/Unexpected Symptoms or Presentations of a Disease SUMMARY: We describe three patients presenting with diabetic ketoacidosis secondary to ketosis prone type 2, rather than type 1 diabetes. All patients were treated according to a standard DKA protocol, but were subsequently able to come off insulin therapy while maintaining good glycaemic control. Ketosis-prone type 2 diabetes (KPD) presenting with DKA has not been described previously in Irish patients. The absence of islet autoimmunity and evidence of endogenous beta cell function after resolution of DKA are well-established markers of KPD, but are not readily available in the acute setting. Although not emphasised in any current guidelines, we have found that a strong family history of type 2 diabetes and the presence of cutaneous markers of insulin resistance are strongly suggestive of KPD. These could be emphasised in future clinical practice guidelines. LEARNING POINTS: Even in white patients, DKA is not synonymous with type 1 diabetes and autoimmune beta cell failure. KPD needs to be considered in all patients presenting with DKA, even though it will not influence their initial treatment. Aside from markers of endogenous beta cell function and islet autoimmunity, which in any case are unlikely to be immediately available to clinicians, consideration of family history of type 2 diabetes and cutaneous markers of insulin resistance might help to identify those with KPD and are more readily apparent in the acute setting, though not emphasised in guidelines. Consideration of KPD should never alter the management of the acute severe metabolic derangement of DKA, and phasing out of insulin therapy requires frequent attendance and meticulous and cautious surveillance by a team of experienced diabetes care providers. Bioscientifica Ltd 2017-02-28 /pmc/articles/PMC5404460/ /pubmed/28458888 http://dx.doi.org/10.1530/EDM-16-0109 Text en © 2017 The authors http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en_GB This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en_GB) . |
spellingShingle | Unique/Unexpected Symptoms or Presentations of a Disease Small, Cliona Egan, Aoife M Elhadi, El Muntasir O’Reilly, Michael W Cunningham, Aine Finucane, Francis M Diabetic ketoacidosis: a challenging diabetes phenotype |
title | Diabetic ketoacidosis: a challenging diabetes phenotype |
title_full | Diabetic ketoacidosis: a challenging diabetes phenotype |
title_fullStr | Diabetic ketoacidosis: a challenging diabetes phenotype |
title_full_unstemmed | Diabetic ketoacidosis: a challenging diabetes phenotype |
title_short | Diabetic ketoacidosis: a challenging diabetes phenotype |
title_sort | diabetic ketoacidosis: a challenging diabetes phenotype |
topic | Unique/Unexpected Symptoms or Presentations of a Disease |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5404460/ https://www.ncbi.nlm.nih.gov/pubmed/28458888 http://dx.doi.org/10.1530/EDM-16-0109 |
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