SUN-047 - Here Today, Gone Tomorrow: Spontaneous Regression of a Growth Hormone-Secreting Pituitary Macroadenoma Following Apoplexy

Background: Pituitary apoplexy is a medical emergency requiring prompt surgical evaluation. When surgery is deferred, spontaneous tumor regression can occur; however, hypopituitarism and tumor recurrence may still follow.

Clinical

Case: A 70-year-old female with hypertension, type 2 diabetes, obstructive sleep apnea, and osteoporosis presented with acute severe headache, nausea, vomiting, and diplopia. Neurologic evaluation revealed a left cranial nerve VI palsy. An MRI of the sella demonstrated a 2.2 cm heterogeneous mass with evidence of evolving hemorrhage, optic chiasm compression, and cavernous sinus involvement.

Endocrine evaluation showed elevated growth hormone (GH = 14 ng/mL; reference range < 10 ng/mL) and insulin-like growth factor (IGF-1 = 654 ng/mL; reference rage 26-226 ng/mL) consistent with acromegaly. A random serum cortisol level of 46.4 µg/dL (obtained at 12:32 PM) was appropriately elevated for acute illness, ruling out adrenal insufficiency.

The hospital course was complicated by stress-induced cardiomyopathy triggered by claustrophobia during the MRI, leading to the deferral of planned transsphenoidal resection. The patient was treated with octreotide for three months, resulting in biochemical improvement. Treatment was subsequently held for two months prior to planned transsphenoidal surgery. No viable tumor was identified intraoperatively, consistent with infarction of the adenoma from apoplexy and potential treatment effect from prior medical therapy. Pathology revealed blood clots and fibrotic tissue with only scant, crushed pituitary cells and no viable adenoma.

Postoperative imaging confirmed a reduction in the size of the sellar mass. Somatostatin analog therapy was restarted due to biochemical persistence, suggestive of residual microscopic functioning adenoma despite the absence of a gross tumor on pathology. Two months after the operation and reinitiation of therapy, IGF-1 decreased to 230 ng/mL.

Conclusion: This case highlights three main teaching points. First, regression can occur in pituitary apoplexy, driven by ischemic necrosis and hemorrhage as the tumor outgrows its blood supply. Despite spontaneous regression clinicians should monitor for hypopituitarism and recurrence. Secondly, acromegaly is associated with hypertension, concentric hypertrophy, and diastolic dysfunction, but does not cause stress-induced cardiomyopathy. Lastly, endocrine disorders associated with stress-induced cardiomyopathy are typically mediated by catecholamine excess, increased catecholamine sensitivity, or impaired stress buffering (e.g., adrenal insufficiency), highlighting that her cardiomyopathy was stress-mediated rather than hormonally driven.

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