Corticosteroids and Intraocular Pressure

Becker, Bernard; Mills, Donald W.

doi:10.1001/archopht.1963.00960050502012

Cited by 313 publications

(130 citation statements)

References 13 publications

Supporting

Mentioning

122

Contrasting

Unclassified

Order By: Relevance

“…Glucocorticoids induce ocular hypertension in a subset of the human population (10,12). Differential glucocorticoid responsiveness is also observed in several animal models, including nonhuman primate eyes (41), rabbits (44), mice (47), and the bovine perfusion cultured anterior segment model (48).…”

Section: Discussionmentioning

confidence: 99%

“…Approximately 30%-40% of the general population can develop IOP elevation after topical ocular administration of a potent glucocorticoid (such as dexamethasone or betamethasone) for 4-6 weeks (10)(11)(12)(13)(14)(15)(16). If undetected, glucocorticoid-induced ocular hypertension can lead to secondary open-angle glaucoma that mimics POAG (14).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Ocular-specific ER stress reduction rescues glaucoma in murine glucocorticoid-induced glaucoma

Zode¹,

et al. 2014

View full text Add to dashboard Cite

Administration of glucocorticoids induces ocular hypertension in some patients. If untreated, these patients can develop a secondary glaucoma that resembles primary open-angle glaucoma (POAG). The underlying pathology of glucocorticoid-induced glaucoma is not fully understood, due in part to lack of an appropriate animal model. Here, we developed a murine model of glucocorticoid-induced glaucoma that exhibits glaucoma features that are observed in patients. Treatment of WT mice with topical ocular 0.1% dexamethasone led to elevation of intraocular pressure (IOP), functional and structural loss of retinal ganglion cells, and axonal degeneration, resembling glucocorticoid-induced glaucoma in human patients. Furthermore, dexamethasoneinduced ocular hypertension was associated with chronic ER stress of the trabecular meshwork (TM). Similar to patients, withdrawal of dexamethasone treatment reduced elevated IOP and ER stress in this animal model. Dexamethasone induced the transcriptional factor CHOP, a marker for chronic ER stress, in the anterior segment tissues, and Chop deletion reduced ER stress in these tissues and prevented dexamethasone-induced ocular hypertension. Furthermore, reduction of ER stress in the TM with sodium 4-phenylbutyrate prevented dexamethasone-induced ocular hypertension in WT mice. Our data indicate that ER stress contributes to glucocorticoid-induced ocular hypertension and suggest that reducing ER stress has potential as a therapeutic strategy for treating glucocorticoid-induced glaucoma.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Ocular-specific ER stress reduction rescues glaucoma in murine glucocorticoid-induced glaucoma

Zode¹,

et al. 2014

View full text Add to dashboard Cite

show abstract

“…[6][7][8] In 1964, Becker and Hahn 12 suggested that patient response to corticosteroids could be explained by a monogenic autosomal mechanism. Armaly 47 and Becker,11 in refining this, suggested that medium responders were heterozygotes while high responders were homozygotes.…”

Section: Geneticsmentioning

confidence: 99%

Corticosteroid-induced glaucoma: a review of the literature

Kersey

Broadway

2005

Eye

382

228

View full text Add to dashboard Cite

The intraocular pressure rise that can complicate the use of topical or systemic corticosteroid has been recognised for 50 years. More recently, following isolation of the myocilin gene (previously known as the trabecular meshwork inducible glucocorticoid response or TIGR gene), there has been renewed interest in this steroid-responsive phenomenon. Furthermore, the currently fashionable use of injectable intraocular steroids in the management of clinically significant subretinal fluid and macular oedema has resulted in an increased incidence. Animal studies, cell biology, molecular biology, and an improved knowledge of genetics have provided a better understanding of the mechanisms behind the response. The purpose of this review is to describe the risk factors for developing corticosteroid-induced glaucoma, to discuss the underlying mechanisms and genetics of the condition and to present management options.

show abstract

“…(1) Uptake of tritiated thymidine between 2 Figure 4). Table 1 shows that for Series I the normals have a significantly higher number of whites and men than the POAG groups.…”

Section: Poag11mentioning

confidence: 99%