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Alpelisib-Induced Diabetic Ketoacidosis in a Non-diabetic Patient

Alpelisib is a phosphoinositol-3-kinase alpha catalytic subunit (PIK3CA) inhibitor used in patients with PIK3CA mutated breast cancer. The phosphatidylinositol 3-kinase (PI3K) pathway is responsible for activating protein kinase-B (AKT), and activated AKT promotes translation of glucose transporter...

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Detalles Bibliográficos
Autores principales: Fugere, Tyler, Roy, Arya Mariam, Makhoul, Issam
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cureus 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8648282/
https://www.ncbi.nlm.nih.gov/pubmed/34900474
http://dx.doi.org/10.7759/cureus.19295
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author Fugere, Tyler
Roy, Arya Mariam
Makhoul, Issam
author_facet Fugere, Tyler
Roy, Arya Mariam
Makhoul, Issam
author_sort Fugere, Tyler
collection PubMed
description Alpelisib is a phosphoinositol-3-kinase alpha catalytic subunit (PIK3CA) inhibitor used in patients with PIK3CA mutated breast cancer. The phosphatidylinositol 3-kinase (PI3K) pathway is responsible for activating protein kinase-B (AKT), and activated AKT promotes translation of glucose transporter 4 and glycogen synthesis in insulin-responsive tissues. Therefore, it is perhaps not surprising that hyperglycemia is the most common side effect of alpelisib, though diabetic ketoacidosis (DKA) appears to be a rare complication. This case describes the unique presentation of a patient with no prior history of diabetes who presented with DKA after starting alpelisib, and returned to euglycemia off of insulin just three days after stopping the drug suggesting that alpelisib can cause DKA in patients who did not previously have diabetes, and that the hyperglycemia is completely reversible upon discontinuation of the PIK3CA inhibitor and consequent restoration of the PI3K/AKT pathway.
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spelling pubmed-86482822021-12-10 Alpelisib-Induced Diabetic Ketoacidosis in a Non-diabetic Patient Fugere, Tyler Roy, Arya Mariam Makhoul, Issam Cureus Endocrinology/Diabetes/Metabolism Alpelisib is a phosphoinositol-3-kinase alpha catalytic subunit (PIK3CA) inhibitor used in patients with PIK3CA mutated breast cancer. The phosphatidylinositol 3-kinase (PI3K) pathway is responsible for activating protein kinase-B (AKT), and activated AKT promotes translation of glucose transporter 4 and glycogen synthesis in insulin-responsive tissues. Therefore, it is perhaps not surprising that hyperglycemia is the most common side effect of alpelisib, though diabetic ketoacidosis (DKA) appears to be a rare complication. This case describes the unique presentation of a patient with no prior history of diabetes who presented with DKA after starting alpelisib, and returned to euglycemia off of insulin just three days after stopping the drug suggesting that alpelisib can cause DKA in patients who did not previously have diabetes, and that the hyperglycemia is completely reversible upon discontinuation of the PIK3CA inhibitor and consequent restoration of the PI3K/AKT pathway. Cureus 2021-11-05 /pmc/articles/PMC8648282/ /pubmed/34900474 http://dx.doi.org/10.7759/cureus.19295 Text en Copyright © 2021, Fugere et al. https://creativecommons.org/licenses/by/3.0/This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Endocrinology/Diabetes/Metabolism
Fugere, Tyler
Roy, Arya Mariam
Makhoul, Issam
Alpelisib-Induced Diabetic Ketoacidosis in a Non-diabetic Patient
title Alpelisib-Induced Diabetic Ketoacidosis in a Non-diabetic Patient
title_full Alpelisib-Induced Diabetic Ketoacidosis in a Non-diabetic Patient
title_fullStr Alpelisib-Induced Diabetic Ketoacidosis in a Non-diabetic Patient
title_full_unstemmed Alpelisib-Induced Diabetic Ketoacidosis in a Non-diabetic Patient
title_short Alpelisib-Induced Diabetic Ketoacidosis in a Non-diabetic Patient
title_sort alpelisib-induced diabetic ketoacidosis in a non-diabetic patient
topic Endocrinology/Diabetes/Metabolism
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8648282/
https://www.ncbi.nlm.nih.gov/pubmed/34900474
http://dx.doi.org/10.7759/cureus.19295
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