Non-Fasting Hypoglycemia Secondary to Opioid Induced Adrenal Insufficiency: A Case Report

Background: A patient on chronic methadone therapy presented following a suicide attempt, was noted to have recurrent episodes of non-fasting symptomatic hypoglycemia and was diagnosed with opioid induced adrenal insufficiency (OIAI). Opioid induced endocrinopathies are underappreciated, particularly in the midst of a growing opioid epidemic in the United States. We believe this is the first reported clinical case of OIAI associated with non-fasting hypoglycemia. Clinical Case: A 33-year-old female with history of depression and heroine abuse on methadone therapy presented after a suicide attempt by methadone overdose. Home medications included 170mg of methadone daily for the past 5 years. She was afebrile, heart rate of 68, blood pressure 102/72, respiratory rate of 10, oxygen saturation 92%. On exam she was lethargic with altered mental status and had pinpoint pupils. Labs showed a normal complete blood count and metabolic panel. Urine toxicology was positive for methadone. Clinical picture improved temporarily after Narcan administration however 1 hour later she was confused again, with a fingerstick glucose of 50mg/dL and she was admitted to ICU for monitoring. In the ICU she continued to be lethargic with dizziness, nausea and headaches. She continued to have approximately 4 spontaneous episodes of hypoglycemia per day, despite having a good appetite and increased parenteral glucose administration. Blood pressure continued to be marginal, ranging from 85–100/50–60. There was no obvious source of infection. Urine sulfonylurea screen was negative. Investigations showed a morning cortisol of 2.23 ug/dL. A 250 µg ACTH stimulation test showed an inadequate response. The am basal plasma cortisol was 2.25 ug/dL with 15.28 ug/dL and 15.13 ug/dL at 30 and 60 minutes respectively (6.20–19.40ug/dL). She was diagnosed with hypoglycemia secondary to OIAI. Given the patient’s critical condition she was initially started on stress dose of hydrocortisone 80mg every 8 hours. Attempts to down titrate the methadone dose were unsuccessful. Patient’s symptoms improved and hypoglycemia subsided. She was discharged home on hydrocortisone 10mg qam & 5 mg qpm and she was continued on Methadone 170mg daily. Conclusion: OIAI is an under-recognized clinical entity with potentially serious adverse outcomes. Currently, 3% to 4% of US adults receive long-term opioid treatment. OIAI is present in 9—29% of individuals on chronic opioids. Opioids act through suppression of the HPA axis, primarily at the level of the hypothalamus, mediated through either delta or kappa receptors leading to a decrease in ACTH and cortisol secretion. Management should include decreasing and ideally discontinue opioids, along with glucocorticoid replacement until documented recovery of the HPA axis. Reference: Reference: (1)Donegan, Diane et al. Opioid-Induced Adrenal Insufficiency. Mayo Clin. Proc. 2018 93(7), 937–944.