MON-469 From Fatigue to Crisis: A Case of Primary Adrenal Insufficiency Triggered by Levothyroxine

Abstract Disclosure: H.C. Davuluri: None. A. Thomas: None. Introduction: Adrenal insufficiency can present in a dramatic manner with a myriad of initiating events. Case: A 20-year-old woman with history of Arnold-Chiari type I malformation presented to her physician’s office with complaints of shortness of breath, palpitations, lightheadedness, and fatigue. She had abnormal T-wave changes on EKG, prompting a referral to the ED. Workup revealed: Sodium 134 mEq/L [range: 135-145], potassium 5.4 mEq/L [3.5-5], D-dimer 0.37 (negative), Troponin normal x 2, FT4 0.977 ng/dl [0.8-1.9], TSH 6.260 mIU/L [0.4-5]. After ondansetron and IV fluid administration, she was markedly improved and discharged with a plan for close follow-up. A week later, repeat labs showed: sodium 131 mEq/dl, K 3.7 mEq/dl, TSH 5.500 mIU/L, fT4 1.09 ng/dl, fT3 5 ng/dl. TPO antibody was negative. She started on levothyroxine 25 mcg daily. Four days later, she presented again to the ED with confusion, generalized weakness, altered mental status, and symptoms concerning for stroke. On exam, she was hypotensive, lethargic, not oriented to time, place or person, with incoherent speech and generalized skin hyperpigmentation. Labs were remarkable for sodium 119 mEq/dl, Cr 0.77 [<1.2], glucose 117, urine tox negative. Initial head CT showed diffuse brain swelling with loss of dilation and descent of the cerebellar tonsils, which was attributed to Arnold-Chiari type I malformation. CTA was negative for large vessel occlusion, aneurysm, or vascular malformation. She was given hypertonic saline followed by normal saline to correct her sodium at a rate of 8 to 10 mEq per 24 hours, treated as acute severe hyponatremia. Endocrinology and nephrology teams were consulted. Her random cortisol was 0.9 ng/dl [2-25], and ACTH of 1620 pg/ml [7.2-63.3], which raised concern for primary adrenal insufficiency. An ACTH stimulation test was done which showed no cortisol response. CT abdomen showed small adrenal glands with no evidence of hemorrhage. After the administration of hydrocortisone, her sodium began to normalize. To prevent overcorrection of her sodium, she received one dose of DDAVP to help maintain sodium stability and address polyuria. 21-hydroxylase antibody was negative. FSH, LH, and prolactin levels were normal. Her presentation was attributed to the initiation of levothyroxine in the context of previously undiagnosed adrenal insufficiency. The patient was started on hydrocortisone and fludrocortisone, which she continued as outpatient therapy with stability in her labs and clinical status. Conclusion: The initiation of levothyroxine in this patient, who had an underlying undiagnosed adrenal insufficiency, likely triggered her severe adrenal crisis. Although rare, this serious and life-threatening presentation underscores the importance of a comprehensive approach to the evaluation and treatment of adrenal crisis. Presentation: Monday, July 14, 2025