Toce Michael S, Stefater Margaret A, Breault David T, Burns Michele M
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.
Clin Toxicol (Phila). 2018 Jan;56(1):74-76. doi: 10.1080/15563650.2017.1338347. Epub 2017 Jun 26.
Methadone is a synthetic μ-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.
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.
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.
美沙酮是一种合成的μ-阿片受体激动剂，用于治疗疼痛、新生儿戒断综合征和阿片类药物依赖。过量使用可导致瞳孔缩小、呼吸抑制和中枢神经系统抑制。低血糖的报道较为罕见。我们报告一例11个月大的男性，在急性意外接触美沙酮后发生了低酮性、高胰岛素性低血糖。
该患者为一名此前健康的11个月大男性，出现呼吸衰竭。他被插管并转至一家大型三级医疗中心，其体格检查发现瞳孔缩小。实验室检查结果显示血糖为17mg/dL、胰岛素水平升高且血清β-羟基丁酸水平降低。给予患者葡萄糖推注后血糖有所改善。静脉注射纳洛酮改善了他的瞳孔缩小和精神状态。到达时检测的美沙酮定量水平为123ng/mL。乙醇、水杨酸盐、磺脲类药物以及低血糖的代谢原因检测均为阴性。一项禁食研究显示血糖正常，胰岛素受到抑制且酮体生成正常。病例讨论：我们报告一例11个月大的男性，在急性意外接触美沙酮后发生了低酮性、高胰岛素性低血糖。排除了低酮性低血糖的其他解释。在接受美沙酮治疗疼痛的癌症患者中曾有美沙酮诱发低血糖的报道，但尚未确定其机制。基于该病例，我们认为患者的低血糖是美沙酮诱导胰岛素分泌的结果。
本病例提示高胰岛素血症是美沙酮相关性低血糖的发病机制。新发低血糖的鉴别诊断应考虑美沙酮暴露情况。
