Prospective, long-term evaluation of steroid-induced glaucoma

Sihota, Ramanjit; Konkal, V L; Dada, Tanuj; Agarwal, Harish; Singh, Rajinder

doi:10.1038/sj.eye.6702474

Cited by 63 publications

(34 citation statements)

References 11 publications

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“…The mean baseline IOP in the eyes requiring surgery was 49.67 8 13.28 mm Hg, and in the eyes managed medically 30.36 8 7.51 mm Hg (p = 0.002). In addition, patients ^ 20 years old with greater glaucomatous optic neuropathy were more likely to need surgery [74] .…”

Section: Surgical Managementmentioning

confidence: 99%

“…Nearly all patients who develop steroid-induced iatrogenic glaucoma can be controlled with topical antiglaucoma therapy [18,31] . Sihota et al [74] reported that in 25 of 34 patients (73.5%), IOP could be controlled by topical medications alone. At 6, 12, and 18 months' follow-up, 22 (64.7%), 33 (97.1%), and all 34 (100%) patients were off treatment, respectively.…”

Section: Medical Managementmentioning

confidence: 99%

“…In a series with 34 cases of steroid-induced iatrogenic glaucoma, topical steroid use was the most frequent (73.5%) mode of administration [74] . Tragically, many cases of steroid-induced glaucoma are produced by treatment for trivial conditions such as contact lens discomfort or red eye.…”

Section: Topical Steroidsmentioning

confidence: 99%

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Steroid-Induced Iatrogenic Glaucoma

Lj²

2011

Ophthalmic Res

218

160

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Steroids in susceptible individuals can cause a clinical condition similar to primary open-angle glaucoma. Five percent of the population are high steroid responders and develop an intraocular pressure (IOP) elevation of more than 15 mm Hg above baseline. IOP elevation may occur as early as 1 day to as late as 12 weeks after intravitreal triamcinolone in 20–65% of patients. On average, 75% of eyes with steroid implants require IOP-lowering therapy at some point within 3 years of follow-up. The exact mechanism of steroid-induced glaucoma is not totally understood, but decreased trabecular meshwork outflow is regarded as the main cause of IOP elevation. High-risk patients who receive steroids should be monitored closely and if they develop elevated IOP, steroids with lower potency or steroid-sparing agents should be used. The IOP usually returns to normal within 2–4 weeks after stopping the steroid. About 1–5% of patients do not respond to medical therapy and need surgery. Trabeculectomy, trabeculotomy, shunt surgery, and cyclodestructive procedures are among the methods employed. Removal of residual sub-Tenon or intravitreal steroids may help hasten the resolution of the steroid response. Early results with anecortave acetate, an analog of cortisol acetate with antiangiogenic activity, in controlling IOP have been promising.

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Section: Surgical Managementmentioning

confidence: 99%

Section: Medical Managementmentioning

confidence: 99%

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Steroid-Induced Iatrogenic Glaucoma

Lj²

2011

Ophthalmic Res

218

160

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“…In humans, withdrawal of glucocorticoid in most cases returns elevated IOP to baseline (18,38). Therefore, we examined whether a similar phenomenon occurred in our mouse model.…”

Section: Withdrawal Of Dexamethasone Leads To Reduction Of Elevated Imentioning

confidence: 99%

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

Zode¹,

et al. 2014

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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.

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“…Typically, instability of the eyelid is caused by either horizontal laxity at the lateral canthus (or occasionally the medial canthus) or disinsertion or attenuation of the lower eyelid retractors to the inferior tarsal border. Surgery to correct these malpositions of the lower lid must address the underlying anatomic factors responsible for the malposition [3] . So surgical procedures should be directed at correcting the horizontal and vertical instability of the lid by medial and lateral canthal tendon stabilization [4] , tarsal strip procedure or other horizontal lid shortening procedures, everting or inverting sutures, plication or reinsertion of the lower lid retractors, tumor excision, or combined techniques [5,6] .…”

Section: Cicatrical Ectropion Discussionmentioning

confidence: 99%