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MON-909 Diabetic Ketoacidosis Following Treatment of Endogenous Hyperinsulinism
Background: There has been only one case of Diabetic Ketoacidosis (DKA) reported following treatment of endogenous hyperinsulinism in a 16 month old.[1] This has not yet been described in adults. Clinical Case: An 85 Y/O M with a PMH of metastatic gastric adenocarcinoma complicated by gastric outlet...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7207784/ http://dx.doi.org/10.1210/jendso/bvaa046.1541 |
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author | Murari, Keerti De Aguiar, Renata Da Silva Belfort |
author_facet | Murari, Keerti De Aguiar, Renata Da Silva Belfort |
author_sort | Murari, Keerti |
collection | PubMed |
description | Background: There has been only one case of Diabetic Ketoacidosis (DKA) reported following treatment of endogenous hyperinsulinism in a 16 month old.[1] This has not yet been described in adults. Clinical Case: An 85 Y/O M with a PMH of metastatic gastric adenocarcinoma complicated by gastric outlet obstruction requiring TPN was admitted for symptomatic hypoglycemia. On the day of admission, his wife noted that he appeared confused and checked his capillary blood glucose, which was 35, prompting her to call EMS who gave him IV dextrose 50% (D50). In the ED, he was placed on continuous dextrose 10% (D10) due to persistent hypoglycemia. To investigate the cause of hypoglycemia, D10 was stopped and a fast test was initiated. The patient developed symptomatic hypoglycemia 9 hours after stopping the D10. Laboratory results showed: plasma glucose 43 mg/dL, c-peptide 3.1 nmol/L, pro-insulin 18.7 pmol/L, insulin 10.7 uU/mL, beta-hydroxybutyrate (BHOB) 0.08 mmol/L. Insulin antibody and screen for oral hypoglycemic drugs were negative. Glucagon administration raised his blood glucose from 43 mg/dL to 50 mg/dL, 84 mg/dL, and 106 mg/dL after 10, 20, and 30 minutes, respectively. A diagnosis of endogeneous hyperinsulinism was made and the patient was started on Diazoxide 50 mg TID which was increased to 150 mg TID 2 days later. On day 3, Prednisone 20 mg daily was started due to inability to come off the D10 drip completely. On day 4 he was taken off D10. Due to plasma glucose >150 mg/dL, prednisone dose was reduced to 10 mg and then 5 mg on day 5 and 6, respectively. On day 8, he was found to be in DKA with a plasma glucose of 250 mg/dL, metabolic acidosis with an anion gap of 20, HCO3 of 15 mg/dL, undetectable insulin levels and BHOB of 5.49 mmol/L. Prednisone and Diazoxide were discontinued and he was started on an intravenous insulin infusion. Within 24 hours he became persistently hypoglycemic requiring D50 and prednisone was restarted. DKA developed once again and the patient was subsequently made comfort measures only. Further investigation of his endogenous hyperinsulinism was not pursued. The patient was transferred to inpatient hospice, where he passed away several days later. Conclusion: This is the first reported case of an adult patient with documented endogenous hyperinsulinism developing DKA following treatment with diazoxide and prednisone. Reference: (1) Mangla et al. J Ped End Met. 2018; 31(8): 943-945. |
format | Online Article Text |
id | pubmed-7207784 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-72077842020-05-13 MON-909 Diabetic Ketoacidosis Following Treatment of Endogenous Hyperinsulinism Murari, Keerti De Aguiar, Renata Da Silva Belfort J Endocr Soc Tumor Biology Background: There has been only one case of Diabetic Ketoacidosis (DKA) reported following treatment of endogenous hyperinsulinism in a 16 month old.[1] This has not yet been described in adults. Clinical Case: An 85 Y/O M with a PMH of metastatic gastric adenocarcinoma complicated by gastric outlet obstruction requiring TPN was admitted for symptomatic hypoglycemia. On the day of admission, his wife noted that he appeared confused and checked his capillary blood glucose, which was 35, prompting her to call EMS who gave him IV dextrose 50% (D50). In the ED, he was placed on continuous dextrose 10% (D10) due to persistent hypoglycemia. To investigate the cause of hypoglycemia, D10 was stopped and a fast test was initiated. The patient developed symptomatic hypoglycemia 9 hours after stopping the D10. Laboratory results showed: plasma glucose 43 mg/dL, c-peptide 3.1 nmol/L, pro-insulin 18.7 pmol/L, insulin 10.7 uU/mL, beta-hydroxybutyrate (BHOB) 0.08 mmol/L. Insulin antibody and screen for oral hypoglycemic drugs were negative. Glucagon administration raised his blood glucose from 43 mg/dL to 50 mg/dL, 84 mg/dL, and 106 mg/dL after 10, 20, and 30 minutes, respectively. A diagnosis of endogeneous hyperinsulinism was made and the patient was started on Diazoxide 50 mg TID which was increased to 150 mg TID 2 days later. On day 3, Prednisone 20 mg daily was started due to inability to come off the D10 drip completely. On day 4 he was taken off D10. Due to plasma glucose >150 mg/dL, prednisone dose was reduced to 10 mg and then 5 mg on day 5 and 6, respectively. On day 8, he was found to be in DKA with a plasma glucose of 250 mg/dL, metabolic acidosis with an anion gap of 20, HCO3 of 15 mg/dL, undetectable insulin levels and BHOB of 5.49 mmol/L. Prednisone and Diazoxide were discontinued and he was started on an intravenous insulin infusion. Within 24 hours he became persistently hypoglycemic requiring D50 and prednisone was restarted. DKA developed once again and the patient was subsequently made comfort measures only. Further investigation of his endogenous hyperinsulinism was not pursued. The patient was transferred to inpatient hospice, where he passed away several days later. Conclusion: This is the first reported case of an adult patient with documented endogenous hyperinsulinism developing DKA following treatment with diazoxide and prednisone. Reference: (1) Mangla et al. J Ped End Met. 2018; 31(8): 943-945. Oxford University Press 2020-05-08 /pmc/articles/PMC7207784/ http://dx.doi.org/10.1210/jendso/bvaa046.1541 Text en © Endocrine Society 2020. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com |
spellingShingle | Tumor Biology Murari, Keerti De Aguiar, Renata Da Silva Belfort MON-909 Diabetic Ketoacidosis Following Treatment of Endogenous Hyperinsulinism |
title | MON-909 Diabetic Ketoacidosis Following Treatment of Endogenous Hyperinsulinism |
title_full | MON-909 Diabetic Ketoacidosis Following Treatment of Endogenous Hyperinsulinism |
title_fullStr | MON-909 Diabetic Ketoacidosis Following Treatment of Endogenous Hyperinsulinism |
title_full_unstemmed | MON-909 Diabetic Ketoacidosis Following Treatment of Endogenous Hyperinsulinism |
title_short | MON-909 Diabetic Ketoacidosis Following Treatment of Endogenous Hyperinsulinism |
title_sort | mon-909 diabetic ketoacidosis following treatment of endogenous hyperinsulinism |
topic | Tumor Biology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7207784/ http://dx.doi.org/10.1210/jendso/bvaa046.1541 |
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