Endogenous hypercortisolism inducing reversible ocular hypertension.

Cushing's syndrome Endogenous hypercortisolism Glaucoma Glucocorticoid Ocular hypertension Trabecular meshwork

Journal

American journal of ophthalmology case reports
ISSN: 2451-9936
Titre abrégé: Am J Ophthalmol Case Rep
Pays: United States
ID NLM: 101679941

Informations de publication

Date de publication:
Dec 2019
Historique:
received: 28 02 2019
revised: 10 09 2019
accepted: 05 11 2019
entrez: 27 11 2019
pubmed: 27 11 2019
medline: 27 11 2019
Statut: epublish

Résumé

To describe the clinical findings of two patients with reversible ocular hypertension secondary to endogenous hypercortisolism. Retrospective, observational case series. A 65-year-old man (patient 1) and a 21-year-old woman (patient 2) were both found to have Cushing's syndrome after presentation to our clinic with elevated intraocular pressures (IOP). Clinical histories, ophthalmic examinations including IOP measurements, optical coherence tomography of the retinal nerve fiber layer, visual field testing, magnetic resonance imaging and computerized tomography of two patients were reviewed between 2007 and 2019. Patient 1 demonstrated elevated IOP (maximum 26 mmHg OD and 22 mmHg OS) and bilateral disc edema. Following diagnosis of Cushing's syndrome, the patient underwent two pituitary resections and bilateral adrenalectomy, with subsequent resolution of his hypercortisolism and ocular hypertension (OHT). Patient 2 presented with blurred vision and found to have OHT (maximum 32 mmHg OU). Following diagnosis of Cushing's disease and two resections of her adrenocorticotropic hormone (ACTH) producing pituitary adenoma, her IOPs normalized. Both patients maintained normal IOPs after resolution of their endogenous hypercortisolism and discontinuation of topical IOP-lowering medication. Ocular hypertension induced by endogenous hypercortisolism is, in some cases, fully reversible following normalization of cortisol levels. These findings suggest that the physiologic changes to the trabecular meshwork induced by endogenous hypercortisolism may be fully reversible.

Identifiants

pubmed: 31768472
doi: 10.1016/j.ajoc.2019.100573
pii: S2451-9936(19)30098-2
pii: 100573
pmc: PMC6872801
doi:

Types de publication

Case Reports

Langues

eng

Pagination

100573

Subventions

Organisme : NEI NIH HHS
ID : P30 EY010572
Pays : United States

Informations de copyright

© 2019 The Authors.

Déclaration de conflit d'intérêts

The following authors have no financial disclosures: SG, TB, BE, WH, MG, ST.

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Auteurs

Shane Griffin (S)

Casey Eye Institute, Department of Ophthalmology, Oregon Health & Science University, Portland, OR, USA.

Timothy Boyce (T)

Casey Eye Institute, Department of Ophthalmology, Oregon Health & Science University, Portland, OR, USA.

Beth Edmunds (B)

Casey Eye Institute, Department of Ophthalmology, Oregon Health & Science University, Portland, OR, USA.

William Hills (W)

Casey Eye Institute, Department of Ophthalmology, Oregon Health & Science University, Portland, OR, USA.

Marjorie Grafe (M)

Department of Pathology, Oregon Health & Science University, Portland, OR, USA.

Shandiz Tehrani (S)

Casey Eye Institute, Department of Ophthalmology, Oregon Health & Science University, Portland, OR, USA.

Classifications MeSH