MON-134 Unmasking Hypopituitarism in a Patient With a Pituitary Mass Following Aneurysmal Intracerebral Hemorrhage

Abstract Disclosure: J.Z. Lacson: None. F.C. Yap: None. J.P. de Leon: None. M.G. Famorcan: None. J.G. Sazon: None. L.F. Lopez: None. Introduction: Hypopituitarism is commonly caused by sellar or suprasellar masses that directly compress the pituitary gland, leading to disrupted hormone production. Intracerebral hemorrhage (ICH) can unmask hypopituitarism, particularly when compounded by a pre-existing pituitary lesion, which may remain asymptomatic until hemorrhage occurs and causes pituitary hypoperfusion. CASE PRESENTATION A 61-year-old male presented with sudden-onset severe headache and left complete ophthalmoplegia. Initial CT imaging revealed an acute frontal intracerebral hemorrhage (2.3 x 1.7 x 1.3 cm) and a pituitary incidentaloma (1.6 x 2.5 x 2.2 cm). A CT angiogram confirmed a ruptured saccular aneurysm at the distal A1 segment of the right anterior cerebral artery, which was successfully treated with endovascular coil embolization. Initial laboratory tests were consistent with hypopituitarism: FSH 1.74 mIU/mL (n, 1.5-12.4), LH 0.35 mIU/mL (n, 1.7-8.6), GH 0.187 ng/mL (n, 0.004-1.406), low TSH 0.02 uIU/mL (n, 0.35-4.94), fT3 < 1.00 pg/mL (n, 1.71-3.71), fT4 0.80 ng/dL (n, 0.70-1.48), and PRL 0.38 ng/mL (n, 4.04-15.2). Focus was placed on therapy of the cerebral hemorrhage and aneurysm and the patient was discharged without endocrine referral.In the next three weeks after discharge, the patient exhibited progressive lethargy, generalized weakness, slowed responses, and decreased appetite, with relative hypotension and fasting hypoglycemia. He became bedridden and unable to speak, prompting readmission. Laboratory evaluation showed severe hyponatremia (Na 112 mEq/L n, 135 - 145). He was then referred to endocrinology for investigation of hyponatremia. He was found to have central hypothyroidism and adrenal insufficiency as follows: low TSH 0.27 uIU/mL (n, 0.27-3.75), fT3 1.3 pM/L (n, 3.1-6.5), and fT4 3.2 pM/L (n, 9.0-23.2), and a blunted cortisol response after 250 µg ACTH stimulation test (baseline 8 AM cortisol 1.49 µg/dL, 1 hour post-ACTH 7.89 µg/dL). The patient was promptly started on steroid and thyroid hormone replacement therapy, resulting in significant clinical improvement. He was able to resume normal functioning within a few weeks of hormone replacement. Conclusion: The possibility of hypopituitarism secondary to hypoperfusion should be considered in patients with intracerebral hemorrhage, particularly those with concomitant pituitary adenomas. Symptoms of hypopituitarism, often subtle and overridden by the acute neurological event, demands heightened clinical vigilance to prevent delays in diagnosis and intervention. Integration of routine hormonal assessments into the management of cerebrovascular events can mitigate life-threatening complications and improve long-term morbidity. This case highlights the link between cerebrovascular pathology and pituitary dysfunction, advocating for a multidisciplinary approach to improve patient outcomes. Presentation: Monday, July 14, 2025