TY - JOUR
KW - Humans
KW - Hypoglycemia/chemically induced
KW - Infant
KW - Male
KW - Methadone/adverse effects
KW - Naloxone/therapeutic use
KW - pediatric
KW - hyperinsulinism
KW - Opioid
KW - Overdose
AU - Michael S. Toce
AU - Margaret A. Stefater
AU - David T. Breault
AU - Michele M. Burns
A1 - 
AB - BACKGROUND: Methadone is a synthetic mu-opioid receptor agonist that is used in the management of pain, neonatal abstinence withdrawal syndrome, and opioid dependence. Overdose can cause miosis, respiratory depression, and central nervous system depression. Rarely, hypoglycemia has been reported. We present the case of an 11-month-old male who developed hypoketotic, hyperinsulinemic, hypoglycemia after an acute, unintentional methadone exposure. CASE DETAILS: The patient was a previously healthy 11-month-old male who presented in respiratory failure. He was intubated and transferred to a large tertiary care center where his physical exam was notable for miosis. His labs were notable for a blood glucose of 17 mg/dL, an elevated insulin level, and suppressed serum beta-hydroxybutyrate. The patient was given a dextrose bolus with improvement in blood glucose. Administration of IV naloxone improved his miosis and mental status. A quantitative methadone level was sent upon arrival and was 123 ng/mL. Testing for ethanol, salicylates, sulfonylureas, and metabolic causes of hypoglycemia was negative. A fasting study showed euglycemia with suppression of insulin and appropriate ketosis. Case discussion: We present the case of an 11-month-old male who developed hypoketotic, hyperinsulinemic, hypoglycemia after an acute, unintentional methadone exposure. Alternative explanations for hypoketotic hypoglycemia were rule out. Methadone-induced hypoglycemia has been reported in cancer patients receiving methadone for pain, but a mechanism has not been identified. Based on this case, we believe that the patient's hypoglycemia was the result of methadone-induced insulin secretion. CONCLUSIONS: This case proposes that hyperinsulinism is the mechanism responsible for methadone-associated hypoglycemia. Methadone exposure should be included in the differential diagnosis of new onset hypoglycemia.
AD - a Harvard Medical Toxicology Program , Boston Children's Hospital , Boston , MA , USA.; b Division of Endocrinology, Department of Medicine , Boston Children's Hospital , Boston , MA , USA.; b Division of Endocrinology, Department of Medicine , Boston Children's Hospital , Boston , MA , USA.; a Harvard Medical Toxicology Program , Boston Children's Hospital , Boston , MA , USA.; c Division of Emergency Medicine, Department of Medicine , Boston Children's Hospital , Boston , MA , USA.
BT - Clinical toxicology (Philadelphia, Pa.)
C5 - Healthcare Disparities; Opioids & Substance Use
CP - 1
CY - England
DO - 10.1080/15563650.2017.1338347
IS - 1
JF - Clinical toxicology (Philadelphia, Pa.)
LA - eng
M1 - Journal Article
N2 - BACKGROUND: Methadone is a synthetic mu-opioid receptor agonist that is used in the management of pain, neonatal abstinence withdrawal syndrome, and opioid dependence. Overdose can cause miosis, respiratory depression, and central nervous system depression. Rarely, hypoglycemia has been reported. We present the case of an 11-month-old male who developed hypoketotic, hyperinsulinemic, hypoglycemia after an acute, unintentional methadone exposure. CASE DETAILS: The patient was a previously healthy 11-month-old male who presented in respiratory failure. He was intubated and transferred to a large tertiary care center where his physical exam was notable for miosis. His labs were notable for a blood glucose of 17 mg/dL, an elevated insulin level, and suppressed serum beta-hydroxybutyrate. The patient was given a dextrose bolus with improvement in blood glucose. Administration of IV naloxone improved his miosis and mental status. A quantitative methadone level was sent upon arrival and was 123 ng/mL. Testing for ethanol, salicylates, sulfonylureas, and metabolic causes of hypoglycemia was negative. A fasting study showed euglycemia with suppression of insulin and appropriate ketosis. Case discussion: We present the case of an 11-month-old male who developed hypoketotic, hyperinsulinemic, hypoglycemia after an acute, unintentional methadone exposure. Alternative explanations for hypoketotic hypoglycemia were rule out. Methadone-induced hypoglycemia has been reported in cancer patients receiving methadone for pain, but a mechanism has not been identified. Based on this case, we believe that the patient's hypoglycemia was the result of methadone-induced insulin secretion. CONCLUSIONS: This case proposes that hyperinsulinism is the mechanism responsible for methadone-associated hypoglycemia. Methadone exposure should be included in the differential diagnosis of new onset hypoglycemia.
PP - England
PY - 2018
SN - 1556-9519; 1556-3650
SP - 74
EP - 76
EP - 
T1 - A case report of methadone-associated hypoglycemia in an 11-month-old male
T2 - Clinical toxicology (Philadelphia, Pa.)
TI - A case report of methadone-associated hypoglycemia in an 11-month-old male
U1 - Healthcare Disparities; Opioids & Substance Use
U2 - 28650702
U3 - 10.1080/15563650.2017.1338347
VL - 56
VO - 1556-9519; 1556-3650
Y1 - 2018
Y2 - Jan
ER -