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SUN-276 Acute Pancreatitis and Diabetic Ketoacidosis in an 8-Year-Old Following Induction Therapy for Pre-B Acute Lymphocytic Leukemia

Introduction Peg-Asparaginase and Dexamethasone are both used in the induction therapy for pre-B Acute Lymphocytic Leukemia (ALL) and have overlapping adverse effects. Peg-Asparaginase is an enzyme that causes depletion of asparagine which is an essential amino acid for leukemia cells. Dexamethasone...

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Autores principales: Schissler, Kathryn, Diaz, Nicolle, Sarmiento, Adriana, Abdella, Haneen, Diaz, Alejandro
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Endocrine Society 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6553267/
http://dx.doi.org/10.1210/js.2019-SUN-276
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author Schissler, Kathryn
Diaz, Nicolle
Sarmiento, Adriana
Abdella, Haneen
Diaz, Alejandro
author_facet Schissler, Kathryn
Diaz, Nicolle
Sarmiento, Adriana
Abdella, Haneen
Diaz, Alejandro
author_sort Schissler, Kathryn
collection PubMed
description Introduction Peg-Asparaginase and Dexamethasone are both used in the induction therapy for pre-B Acute Lymphocytic Leukemia (ALL) and have overlapping adverse effects. Peg-Asparaginase is an enzyme that causes depletion of asparagine which is an essential amino acid for leukemia cells. Dexamethasone is a long-acting glucocorticoid with a 30-fold increase in anti-inflammatory activity relative to Hydrocortisone. Hyperglycemia and acute pancreatitis are both adverse reactions of Peg-asparaginase and glucocorticoids. Clinical case An 8-year-old male with obesity presented with acute pancreatitis and diabetic ketoacidosis (DKA) following induction therapy for pre-B ALL. The patient was euglycemic at the time of diagnosis. On day 1 induction chemotherapy was administered which included IV vincristine, IT cytarabine and PO dexamethasone (4 mg BID daily). On day 2, patient developed hyperglycemia (167 mg/dL). On day 4 he received IV Peg-Asparaginase (3,800 IU). On day 8 patient returned with back pain, fatigue, polydipsia, polyuria, and Kussmaul breathing. Labs revealed hyperglycemia (1,118 mg/dL), metabolic acidosis with an elevated anion gap (pH 7.14, pCO2 < 17 mmHg, HCO3 4.6 mmol/L, anion gap 36), elevated lipase (2,256 IU/L), mild transaminitis, and elevated creatinine and BUN. Pancreatic ultrasound was consistent with pancreatitis. The patient was admitted to the pediatric ICU for insulin drip and management of pancreatitis. On day 10 he was transitioned to SQ glargine insulin. Chemotherapy was restarted with dexamethasone and vincristine. Patient had persistent hyperglycemia requiring lispro insulin to cover meals and to correct hyperglycemia. His glucose normalized on this treatment and insulin was tapered down to be discontinued 9 days after initially started. His HbA1c was 7.5% (normal <5.6%) and he had negative T1DM-related antibodies. A CT of the abdomen showed pancreatic inflammation but no fluid collection or necrosis. At the time of discharge, patient was euglycemic. In the following months, in the absence of glucocorticoids and asparaginase, the patient had multiple admissions for recurrent pancreatitis with development of a pseudocyst. No further episodes of hyperglycemia were documented. Conclusion DKA can develop as side effect of treatment with Peg-Asparaginase and glucocorticoids. Patients treated with these medications need to be closely monitored to identify and treat hyperglycemia and pancreatitis as early as it develops.
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spelling pubmed-65532672019-06-13 SUN-276 Acute Pancreatitis and Diabetic Ketoacidosis in an 8-Year-Old Following Induction Therapy for Pre-B Acute Lymphocytic Leukemia Schissler, Kathryn Diaz, Nicolle Sarmiento, Adriana Abdella, Haneen Diaz, Alejandro J Endocr Soc Pediatric Endocrinology Introduction Peg-Asparaginase and Dexamethasone are both used in the induction therapy for pre-B Acute Lymphocytic Leukemia (ALL) and have overlapping adverse effects. Peg-Asparaginase is an enzyme that causes depletion of asparagine which is an essential amino acid for leukemia cells. Dexamethasone is a long-acting glucocorticoid with a 30-fold increase in anti-inflammatory activity relative to Hydrocortisone. Hyperglycemia and acute pancreatitis are both adverse reactions of Peg-asparaginase and glucocorticoids. Clinical case An 8-year-old male with obesity presented with acute pancreatitis and diabetic ketoacidosis (DKA) following induction therapy for pre-B ALL. The patient was euglycemic at the time of diagnosis. On day 1 induction chemotherapy was administered which included IV vincristine, IT cytarabine and PO dexamethasone (4 mg BID daily). On day 2, patient developed hyperglycemia (167 mg/dL). On day 4 he received IV Peg-Asparaginase (3,800 IU). On day 8 patient returned with back pain, fatigue, polydipsia, polyuria, and Kussmaul breathing. Labs revealed hyperglycemia (1,118 mg/dL), metabolic acidosis with an elevated anion gap (pH 7.14, pCO2 < 17 mmHg, HCO3 4.6 mmol/L, anion gap 36), elevated lipase (2,256 IU/L), mild transaminitis, and elevated creatinine and BUN. Pancreatic ultrasound was consistent with pancreatitis. The patient was admitted to the pediatric ICU for insulin drip and management of pancreatitis. On day 10 he was transitioned to SQ glargine insulin. Chemotherapy was restarted with dexamethasone and vincristine. Patient had persistent hyperglycemia requiring lispro insulin to cover meals and to correct hyperglycemia. His glucose normalized on this treatment and insulin was tapered down to be discontinued 9 days after initially started. His HbA1c was 7.5% (normal <5.6%) and he had negative T1DM-related antibodies. A CT of the abdomen showed pancreatic inflammation but no fluid collection or necrosis. At the time of discharge, patient was euglycemic. In the following months, in the absence of glucocorticoids and asparaginase, the patient had multiple admissions for recurrent pancreatitis with development of a pseudocyst. No further episodes of hyperglycemia were documented. Conclusion DKA can develop as side effect of treatment with Peg-Asparaginase and glucocorticoids. Patients treated with these medications need to be closely monitored to identify and treat hyperglycemia and pancreatitis as early as it develops. Endocrine Society 2019-04-30 /pmc/articles/PMC6553267/ http://dx.doi.org/10.1210/js.2019-SUN-276 Text en Copyright © 2019 Endocrine Society https://creativecommons.org/licenses/by-nc-nd/4.0/ This article has been published under the terms of the Creative Commons Attribution Non-Commercial, No-Derivatives License (CC BY-NC-ND; https://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Pediatric Endocrinology
Schissler, Kathryn
Diaz, Nicolle
Sarmiento, Adriana
Abdella, Haneen
Diaz, Alejandro
SUN-276 Acute Pancreatitis and Diabetic Ketoacidosis in an 8-Year-Old Following Induction Therapy for Pre-B Acute Lymphocytic Leukemia
title SUN-276 Acute Pancreatitis and Diabetic Ketoacidosis in an 8-Year-Old Following Induction Therapy for Pre-B Acute Lymphocytic Leukemia
title_full SUN-276 Acute Pancreatitis and Diabetic Ketoacidosis in an 8-Year-Old Following Induction Therapy for Pre-B Acute Lymphocytic Leukemia
title_fullStr SUN-276 Acute Pancreatitis and Diabetic Ketoacidosis in an 8-Year-Old Following Induction Therapy for Pre-B Acute Lymphocytic Leukemia
title_full_unstemmed SUN-276 Acute Pancreatitis and Diabetic Ketoacidosis in an 8-Year-Old Following Induction Therapy for Pre-B Acute Lymphocytic Leukemia
title_short SUN-276 Acute Pancreatitis and Diabetic Ketoacidosis in an 8-Year-Old Following Induction Therapy for Pre-B Acute Lymphocytic Leukemia
title_sort sun-276 acute pancreatitis and diabetic ketoacidosis in an 8-year-old following induction therapy for pre-b acute lymphocytic leukemia
topic Pediatric Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6553267/
http://dx.doi.org/10.1210/js.2019-SUN-276
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