12221 Chronic Opioid Use Causing Secondary Adrenal Insufficiency: A Case Report

Abstract Disclosure: M.S. Hossain: None. B. Tiwari: None. B. Gautam: None. S. Hossain: None. S.C. Kumar: None. D.S. Rosenthal: None. H. Liao: None. Introduction: Opioid-induced adrenal insufficiency (OIAI) is a growing concern affecting 9% to 29% of chronic opioid users[1]. Many clinicians, particul...

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Veröffentlicht in:Journal of the Endocrine Society 2024-10, Vol.8 (Supplement_1)
Hauptverfasser: Hossain, Md Shajjad, Tiwari, Bishal, Gautam, Bharat, Hossain, Sadaf, Kumar, Salini Chellappan, Rosenthal, David S, Liao, Huijuan
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Sprache:eng
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Zusammenfassung:Abstract Disclosure: M.S. Hossain: None. B. Tiwari: None. B. Gautam: None. S. Hossain: None. S.C. Kumar: None. D.S. Rosenthal: None. H. Liao: None. Introduction: Opioid-induced adrenal insufficiency (OIAI) is a growing concern affecting 9% to 29% of chronic opioid users[1]. Many clinicians, particularly those lacking specialized training in endocrinology, may have limited understanding of this complication, leading to delays in diagnosis and effective treatment which result in poor clinical outcome[1]. We present a case of a 37 year old female on high dose chronic methadone, who presented with hypotension and was diagnosed with OIAI. Case Presentation: A 37 year old female with a history of polysubstance abuse, depression and chronic methadone use was admitted to the hospital with hypotension and dizziness as well as weight loss, poor appetite, generalized weakness and amenorrhea. Patient reported having low blood pressure for many years, leading to multiple hospital admissions and primary care visits but managed conservatively without definitive diagnosis. She was using methadone 80 mg daily for the past 11 years. Patient denied history of autoimmune disease, tuberculosis, fungal infection, coagulopathy or other endocrinopathies. Vital signs were normal except BP of 89/52 mmHg with a normal heart rate. The patient appeared pale and malnourished on physical examination, with no hyperpigmentation and all other physical findings were normal. Blood tests showed normal blood sugar, and kidney and liver function. Additionally, her electrolytes were normal with no acid-base disturbance. Hypotension persisted despite adequate fluid resuscitation and other potential causes for hypotension were ruled out. Further investigation showed a morning serum cortisol of 1.89 ug/dL (5.27-22.45 ug/dL) which was consistent on repeat morning serum cortisol 1.95 ug/dL (5.27-22.45 ug/dl), plasma ACTH below 5 pg/ml (6-50 pg/ml). Her prolactin, LH and FSH were normal and had abnormal thyroid function panel due to low T3 syndrome. Patient was treated with hydrocortisone of 100 mg every 8 hours, resulting in rapid improvement of blood pressure and resolution of her symptoms. Hydrocortisone tapered to physiological dose for maintenance therapy on discharge. Outpatient 1 mcg ACTH stimulation test showed baseline cortisol
ISSN:2472-1972
2472-1972
DOI:10.1210/jendso/bvae163.1167