SAT-486 A Unique Case of Pituitary Macroadenoma Unmasked by Glucocorticoid Treatment

Abstract

Abstract BACKGROUND Long-term systemic administration of exogenous steroids is the most common cause of adrenal suppression due to hypothalamic-pituitary-adrenal (HPA) axis suppression. The confounding effects of steroid therapy on HPA axis diagnoses remains a clinical challenge. We report a unique case of a 70-year-old woman diagnosed with pituitary macroadenoma which was unmasked by glucocorticoid treatment. Clinical case A 70-year-old woman with medical history of prediabetes and gastroesophageal reflux was referred to endocrinology for evaluation of inability to taper steroids. She was on prednisone for acute kidney injury due to acute interstitial nephritis (biopsy confirmed) due to omeprazole. She was started on prednisone 60mg initially, and over the last year was on gradual taper because of worsening kidney function. She developed symptoms of dizziness, nausea, and diarrhea with orthostatic hypotension immediately after completing her prednisone taper. Early morning cortisol was ordered which came back low at 1.1 (ref 2-18 ug/dl). She was started back on prednisone 1mg daily and was referred to endocrinology. Physical examination was unremarkable. Laboratory data was remarkable for ACTH 9.7 (ref: 10-60), morning cortisol 3.3, free T4 0.6 (ref 0.6-1.6) with TSH 2.08 (ref: 0.34 -3.00), prolactin 27 (2-18), FSH 5 (23-116) and LH <1 (10-54.7). An ACTH stimulation test was obtained; cortisol levels at baseline, 30-minutes and 60-minutes were 5.8, 9.7, and 9.2 ug/dL respectively (ref: peak level >18). Magnetic resonance imaging (MRI) of head revealed 1.4 x 2.3 x 2.5 cm pituitary macroadenoma with slight bulging into the bilateral cavernous sinuses, right side greater than left. She was treated with oral levothyroxine 75 mcg daily, prednisone 5 mg a day and was referred to a neurosurgeon. She underwent endoscopic transsphenoidal resection of the tumor and repeat MRI of the brain 3 months post-surgery revealed minimal soft tissue thickening about the inner periphery of the pituitary fossa. She remained clinically stable and was on prednisone 5 mg in the morning, 2.5 mg in the evening and levothyroxine daily. DISCUSSION In our literature search, there were no previously reported cases of pituitary adenoma diagnosed after failure to taper prednisone therapy. The patient in our case had been receiving external supplementation of prednisone, which was sufficient to maintain her daily activities but developed symptoms of adrenal insufficiency after completely tapering off the steroids. Failure of recovery of the HPA axis after a prolonged taper along with rapid development of symptoms was a clue that indicated workup for other secondary causes of adrenal insufficiency. Our case emphasizes the importance of neuroimaging in patients with unexpected endocrinopathies with suspected central origin and to consider secondary causes of adrenal insufficiency in patients with difficulty to taper steroids.