SUN-010 - Hidden in Plain Sight: Unmasking Cushing Disease after Acute Ischemic Stroke

Cushing Disease (CD) is associated with an increased risk off developing multiple metabolic comorbidities including hypertension, dyslipidemia, obesity, and diabetes. CD can also lead to a hypercoagulable state which can result in arterial and venous thrombosis, including DTV and acute ischemic strokes. The incidence of strokes in a patient with underlying CD is 2.0-4.5%, which is higher than the general population. Patients who are diagnosed with CD have increased incidence up to 4.5% higher in the following 3 years, even after successful surgery. This opens a debate for thromboprophylaxic therapy but also raises concerns of peri-and post-operative complications risk. Therefore, it is imperative to have a high degree of clinical suspicion to diagnose CD, to prevent fatal outcomes as a consequence of unrecognized, hidden in plain sight, disease.

A 36-year-old male who was previously healthy presented to the emergency department with sudden bilateral peripheral vision loss. About 9 months ago, he gained 30 lbs, and developed bilateral swelling of arms and legs, facial flushing, abdominal wide purple stretch marks, easy bruising, and muscle weakness. Patient saw his PCP but his symptoms were false reassured. In the ED he was hypertensive with blood pressure at 160/93 mmHg. Brain MRI showed an evolving area of infarction within the right temporal lobe extending posteriorly and medially with a 7 mm hypo-enhancing right pituitary microadenoma. CTA of head and neck showed a right internal carotid artery occlusion with atherosclerotic soft plaque. He was treated with Tenecteplase and thrombectomy with two stents placement and discharged on aspirin, clopidogrel, and atorvastatin. His vision on the right returned but his left remained affected with left homonymous hemianopsia. In hospital lab work up: morning cortisol 21.6 ug/dL and 24 hours urine cortisol 5911 mcg. Referred to a neuroendocrinologist and further lab showed elevated morning cortisol at 26.3 ug/dL, ACTH at 128 pg/mL, two 24-hours urine cortisol at 829 mcg and 3629 mcg, LNST 0.24, and 1 mg DST that failed to suppress levels with elevated morning cortisol at 59.4 ug/dL. Patient referred to neurosurgery and due to recent stroke and anticoagulation status, transsphenoidal surgery was postponed for 6 months and osilodrostat started. Surgery was done 6 months later, and then laboratory showed morning cortisol at 0.5 ug/dL, and ACTH at 8 pg/mL. Pathology report showed a pituitary neuroendocrine tumor/adenoma with TPIT and SF-1 positivity. Repeated brain MRI 8 weeks post-surgery noted no residual tumor.

Stroke can be the first manifestation of CD given its pro-thrombotic propensity. Underlying undiagnosed CD should be considered in the differential diagnosis as possible etiology, especially in young patients with atypical acute cerebrovascular events. Therefore, it is imperative to adopt heightened clinical hypervigilance of possible CD.

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