Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2025) 110 EP94 | DOI: 10.1530/endoabs.110.EP94

ECEESPE2025 ePoster Presentations Adrenal and Cardiovascular Endocrinology (170 abstracts)

Non-arteritic anterior ischemic optic neuropathy and addison’s disease

Shyam Seshadri 1 , Jaiminkumar Patel 1 , Murtaza Rashid 1 & Michael Kouroupis 2


1Queen Elizabeth Hospital Foundation NHS Trust, Department of Diabetes and Endocrinology, Kings Lynn, United Kingdom; 2Queen Elizabeth Hospital Foundation NHS Trust, Department of Ophthalmology, Kings Lynn, United Kingdom


JOINT751

Nonarteritic anterior ischemic optic neuropathy (NAION) is the most common cause of acute optic neuropathy in adults presenting as sudden, painless vision loss due to ischemia of the optic nerve head. Risk factors that have been strongly associated with NAION include hypertension, hypercholesterolemia, diabetes mellitus, cardio- and cerebrovascular disease, and obstructive sleep apnoea. Addison’s disease which is a rare autoimmune condition leading to adrenal insufficiency, is not commonly linked to NAION. However, chronic hypotension and vascular dysregulation in Addison’s disease may contribute to ischemic complications, including NAION.

Case Presentation: We report on a 46-year-old female with known Addison’s disease who presented with acute, painless blurry vision in the right eye upon waking up. On examination at eye casualty, visual acuity was 6/18 in the right eye and 6/6 in the left eye. Fundoscopy revealed optic disc swelling. Inflammatory markers were within the normal range with a very low GCA probability score and given the young age, Giant cell arteritis was considered highly unlikely. MRI of the brain showed white matter foci in keeping with small vessel disease and empty Sella syndrome. The neurologist reviewed her, and multiple sclerosis was excluded. She had a long-standing history of Addison’s disease and autoimmune hypothyroidism. She was being treated with fludrocortisone and prednisolone and had previously experienced subjective hypotensive episodes. Lying and standing blood pressure checks in the clinic did not document postural hypotension. Adherence to corticosteroid and mineralocorticoid replacement therapy was monitored with serum prednisolone levels within the therapeutic range and plasma renin activity levels indicating sufficient fludrocortisone dosing. 24-h ambulatory blood pressure monitoring was arranged which could have detected nocturnal hypotension, however, our patient was unable to attend this. Chronic hypotension secondary to adrenal insufficiency was suspected as the precipitating factor for optic nerve head ischemia during presumed nocturnal hypotensive episodes, however, we could not conclude this due to lack of evidence of documented nocturnal hypotension. The patient did report subjective symptoms of dizzy spells, especially at night though with no other associated symptoms. Other vascular risk factors were absent, however, suggesting Addison’s disease as a possible cause.

Conclusion: This case highlights a rare but significant association between Addison’s disease and NAION. Clinicians should consider adrenal insufficiency in atypical presentations of NAION, particularly in younger patients or those without traditional vascular risk factors. Early recognition of Addison’s disease and appropriate hormonal therapy may reduce the risk of ischemic events, including NAION.

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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