ODP056 The Treatment of Opioid Addiction Leading to Secondary Adrenal Insufficiency

Abstract

Abstract Background As we continue to learn about the opioid crisis in America, more patients are seeking treatment for their opioid addictions. This treatment includes buprenorphine/naloxone, a partial opioid agonist and opioid antagonist. Though there is known evidence of opioid-induced secondary adrenal insufficiency, there is scarce data regarding the effect of buprenorphine/naloxone on the hypothalamic-pituitary-adrenal (HPA) axis. Here we describe a case of secondary adrenal insufficiency in a patient who is on long-term treatment for her opioid addiction with buprenorphine/naloxone. Clinical Case A 30 year old female with a past medical history of ADHD, OCD, PTSD, and menorrhagia presented with extreme fatigue, 100-pound weight gain, hair loss, and intermittent red flushing on hands and face over the past year. Labs showed low androstenedione (21 ng/dL, n 41 - 262 ng/dL), low testosterone (6.5 ng/dL, n 10. 0 - 55. 0 ng/dL) and low DHEA-S levels (55.6 ug/dL, n 84.8 - 378. 0 ug/dL). Further history revealed that the patient had been on Buprenorphine/Naloxone for 4 years for opioid addiction. Testing revealed a low morning cortisol level (5.6 ug/dL, n 6.2 - 19.4 ug/dL). The patient was started on hydrocortisone 10mg in the morning and 5mg in the afternoon with improvement of symptoms. Repeat testing after holding hydrocortisone revealed a cortisol level (6.6 n 6.2 - 19.4 ug/dL) and an inappropriately low-normal ACTH level (16 pg/mL, n 6 - 50 pg/mL). Cosyntropin stimulation test did not show an adequate response with a baseline cortisol level of 3.4 ug/dL, (n 5. 0 - 23. 0 ug/dL), 30 minute cortisol level of 6.9 ug/dL and 60 minute cortisol level of 8.2 ug/dL (n >18. 0 ug/dL). ACTH drawn at that time was low (<5 pg/mL n 6 - 50 pg/mL). Pituitary MRI was completed and findings were insignificant. Due to continued fatigue, the hydrocortisone dose was increased to 15mg in the morning and 5mg in the afternoon with improvement in symptoms with a plan to retest the adrenal axis as she continues to wean off the Buprenorphine/Naloxone. Conclusion This case calls attention to secondary adrenal insufficiency caused by the treatment of opioid addiction with buprenorphine/naloxone. Further investigation of adrenal insufficiency secondary to buprenorphine/naloxone use is warranted given the frequency of use of this combination to treat the ongoing opiate addiction crisis in America. Presentation: No date and time listed