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Endocrine Abstracts (2025) 110 EP161 | DOI: 10.1530/endoabs.110.EP161

ECEESPE2025 ePoster Presentations Adrenal and Cardiovascular Endocrinology (170 abstracts)

Cushing’s disease in a patient presenting for oculomotor palsy-a diagnostic and management conundrum

Theodora Nistor 1 , Sebastian Botezatu 2 , Dorin Bica 3 , Marian Mitrica 2 , Serban Radian 1,4 & Catalina Poiana 1,4


1National Institute of Endocrinology CI Parhon, Bucharest, Romania; 2Central Military University Emergency Hospital, Bucharest, Romania; 3NeuroHope Hospital, Bucharest, Romania; 4Carol Davila University of Medicine and Pharmacy, Bucharest, Romania


JOINT3437

Background: Oculomotor palsy is an infrequent presentation in Pitnet patients, due to pituitary apoplexy or tumour compression, with other causes being exceedingly rare. We present a case of Cushing’s disease (CD) which associated a vascular cause of oculomotor palsy.

Aim: To describe the diagnosis and management challenges due to concomitant pituitary and parasellar disease.

Case presentation: A 66-year-old woman presented to the ER in Dec 2024 for recent onset unilateral right eye blindness and ophthalmoplegia. A CT scan demonstrated bilateral cavernous sinus masses with intense contrast uptake and she was referred to our endocrine department, following neurosurgical consultation. On examination there was complete right sided ophtalmoplegia and blindness, and pre-existing right hemiplegia from an ischemic stroke (2012). The history was not suggestive of pituitary apoplexy. No obvious signs of endocrine disease were noted. Prolactinemia was minimally elevated (25.3 ng/ml) and there was no pituitary insufficiency. Baseline cortisolemia was 809,65 nmol/l and ACTH=48.81 pg/ml. 11PM cortisol was high and unsuppressed by 1mg overnight dexamethasone (744 nmol/l) and LDDST (670,3 nmol/l), suggesting an invasive corticotropinoma. Contrast-enhanced head MRI demonstrated bilateral cystic parasellar masses highly suggestive of intracavernous carotid aneurysms. The pituitary appeared compressed between the cavernous sinuses and presented a T1-hypointense micronodule. Pituitary MDT recommended cerebral angiography with the aim of flow-diverter treatment of aneurysms (pending). We initiated ketoconazole treatment, well-tolerated at 400 mg/day.

Conclusion: The differential diagnosis of compressive parasellar masses includes other lesions besides PitNet. Our patient presented bilateral intracavernous carotid aneurysms and CD, mimicking an invasive corticotropinoma. Aneurysm treatment is prioritary. When pituitary surgery is not feasible, as in this case, medical treatment is necessary for hypercortisolism. Pituitary surgery and radiotherapy remain therapeutic options following carotid aneurysm endovascular repair.

Volume 110

Joint Congress of the European Society for Paediatric Endocrinology (ESPE) and the European Society of Endocrinology (ESE) 2025: Connecting Endocrinology Across the Life Course

European Society of Endocrinology 
European Society for Paediatric Endocrinology 

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