Abstract
Purpose of Review
In this article, we discuss the pathophysiology underlying intraocular pressure elevation associated with corticosteroid use as well as targeted therapies for treatment.
Recent Findings
Several signaling pathways at the level of the trabecular meshwork are altered by steroid exposure. A pre-existing diagnosis of glaucoma is the best-established risk factor for development of steroid-associated ocular hypertension. Topical, local, and systemic steroids have all been associated with ocular hypertension.
Summary
Current management is directed at steroid-sparing alternatives to treatment, steroid cessation, IOP-lowering medications, and interventional lasers and surgery.
Similar content being viewed by others
Avoid common mistakes on your manuscript.
Introduction
Synthetic glucocorticoids and analogs are commonly used to treat many medical conditions [1]. Specific to the eye, we use steroids to reduce post-procedural inflammation and for inflammatory diseases, such as uveitis. Studies in cellular models and in humans (some of which will be reviewed in this paper) have demonstrated that steroids increase intraocular pressure (IOP). If left untreated, elevated IOP can lead to progressive glaucomatous optic nerve damage and vision loss [2]. This disease entity has been called by several names, including “steroid glaucoma,” “steroid-associated glaucoma,” and “steroid-induced glaucoma.” Recent research has focused on elucidating structural alterations and molecular signaling underlying steroid-induced glaucoma as well as on therapeutics and surgical interventions.
Historical Perspective
Ocular hypertension in patients treated with steroids was first reported in the 1950s [2, 3]. In a 1951 review article describing use of steroids for ophthalmic conditions ranging from allergic conjunctivitis to optic neuritis, the authors noted several cases of ocular hypertension after steroid exposure, but they hedged that the relationship might be coincidental. In 1958, Lester Covell published three cases and definitively warned the reader to the adverse effects of steroids on IOP [4]. Then, in the 1960s, Mansour Armaly at the University of Iowa published several elegant studies demonstrating the hypertensive effect of topical steroids [4, 5]. In a study comparing patients with glaucoma versus those without, he reported that nearly all eyes of patients with baseline IOP of 25–30 mmHg reached an elevated IOP near 40 mmHg within three weeks of steroid exposure. Within three weeks of steroid withdrawal, IOP decreased to pre-exposure levels. A single patient in this group did not have a hypertensive response to steroid. His data showed that the hypertensive response was greater in eyes with glaucoma compared to those without. Additionally, he demonstrated that pilocarpine, epinephrine, and acetazolamide successfully lowered IOP in eyes with steroid-induced hypertension; however, steroid use could still induce hypertension in eyes concurrently treated with IOP-lowering medications. In these publications, he also conjectured that steroids could unmask a predisposition for glaucoma in patients with a family history of glaucoma. Dr. Armaly’s work continues to be the cornerstone for research related to steroid glaucoma.
Pathophysiology
Decades of research have reproducibly demonstrated that steroids are associated with increased outflow resistance in the pressure-dependent pathway. Since the 1960s, electron microscopy has been used to demonstrate thickening of the trabecular meshwork with alterations in glycosaminoglycans in eyes treated with steroids. In these post-mortem and in vitro studies, it could not be determined whether alterations of the trabecular meshwork were a cause or a result of elevated intraocular pressure or simply an association with exposure to steroid [6,7,8]. Protein assays further demonstrated altered levels of specific glycosaminoglycans in eyes treated with steroids compared with control eyes [9]. In addition to glycosaminoglycans, other components of the extracellular matrix (e.g., actin) have been implicated in decreased permeability of trabecular meshwork treated with steroid [10, 11]. Phagocytosis and autophagy have also been shown to be dysregulated in steroid-exposed trabecular meshwork [12•].
Several protein signaling pathways have been studied in tissue culture and animal models. Rho-associated protein kinase (ROCK) signaling contributes to cytoskeletal remodeling in steroid-treated trabecular meshwork, and ROCK inhibitors reverse this remodeling [13, 14•, 15]. A long-noncoding RNA called ANRIL and the p15 gene are differentially expressed in mice with steroid-induced glaucoma, and it has been proposed that ANRIL/p15 control of TM cell senescence has a role in the pathophysiology of steroid-induced glaucoma [16]. Aside from their role in pressure-independent uveoscleral outflow, prostaglandins might increase TM outflow [17]. Transforming growth factor β (TGFβ) signaling has also been implicated [18].
With an increase in minimally invasive glaucoma surgery, steroid-associated IOP elevation has been reported following excision of the trabecular meshwork (i.e., goniotomy), suggesting steroids might additionally alter the pressure-independent pathway [19]. Alternatively, remnants of the trabecular meshwork that persist after trabecular meshwork excision might still play a role in control of the intraocular pressure.
Epidemiology
Studies do not demonstrate one hundred percent incidence of ocular hypertension after steroid exposure; in other words, not all eyes are steroid-responders. A history of glaucoma is the best-established risk factor for a predisposition to steroid-associated ocular hypertension. In Armaly’s early work, eyes with pre-existing glaucoma had higher incidence and higher magnitude of IOP elevation following exposure to topical steroids [4, 20]. In a study of 929 eyes undergoing intravitreal triamcinolone injection, eyes with pre-existing glaucoma were more likely to develop elevated IOP after steroid injection [21].
Several retrospective studies report an association of steroid-associated ocular hypertension with younger age and axial length [22, 23]. There are likely many confounders and uncontrolled variables due to the retrospective nature of these studies, such as the nature of the underlying disease/surgery, dosing versus body size, and ocular angle anatomy.
Route of Administration
Armaly’s historical studies provide strong evidence for the IOP-elevating effect of topical steroids. There is a multitude of heterogenous evidence—ranging from case reports to clinical trials—demonstrating the hypertensive effect of steroids administered into the vitreous, intranasally, orally, and intravenously [24].
Intravitreal
Elevated IOP following intravitreal injection of steroid is well described in case series and randomized controlled trials. Singh et al. published three cases that developed elevated IOP within one week of intravitreal triamcinolone that all required surgical intervention for IOP-lowering [25]. The Standard of Care versus COrticosteroid for REtinal Vein Occlusion (SCORE) Study compared doses of intravitreal triamcinolone with laser/observation in 682 patients with macular edema from retinal vein occlusions [26]. Eyes with a history of glaucoma were excluded, and management of elevated IOP was at the discretion of the treating physician during the study. In the SCORE study, a 1 milligram dose of intravitreal triamcinolone conferred an increased risk of IOP elevation compared with laser/observation, and a 4 milligram dose of intravitreal triamcinolone conferred an even higher risk of IOP elevation. In this study, the median time to elevated IOP was approximately 1–2 months after injection of intravitreal steroid. The GENEVA Study Group compared an intravitreal steroid implant (DEX implant; OZURDEX, Allergan, Inc., Irvine, CA) with sham in 1267 eyes with macular edema from retinal vein occlusions [27]. In this study group, elevated IOP was shown to occur significantly more in the steroid-treated group, with a peak in IOP change at two months after injection. In this study, five patients required procedural intervention for pressure.
Inhaled
Inhaled corticosteroids have been shown to elevate IOP, but the effect is likely dependent on dosing and length of use [28]. In a large case-control study of more than 35,000 patients, treatment with high dose or chronic intranasal steroids were associated with a diagnosis of glaucoma or ocular hypertension [29]. Many other studies conclude that intranasal and inhaled steroids do not increase intraocular pressure, but these studies are limited by small sample size, variability in dose and length of use, and exclusion of patients with comorbid POAG [30, 31]. Given that not all eyes are steroid responders, the small studies are likely missing steroid responders and limit conclusions that can be drawn.
Systemic
Several studies describe dramatic elevation of IOP in children treated with systemic (oral or intravenous) steroids. In a study of nine babies treated for infantile spasms, five required IOP-lowering treatment after initiating systemic steroids [32]. In a study of 33 children treated with oral prednisone for autoimmune hepatitis, 20 developed elevated IOP by one month [33]. In another study of 37 children treated for autoimmune disease, 22 children developed a diagnosis of steroid-induced ocular hypertension [34]. Additionally, there are multiple published case reports of IOP elevation develo** after initiation of systemic steroids. Elevated intraocular pressure has also been reported after intraarticular steroid injections [35].
One of the challenges in studying the effect of steroids on IOP is that the comorbidities in eyes treated with steroids can also contribute to IOP elevation and glaucoma. For example, intraocular inflammation can elevate IOP (e.g., herpetic) and can cause aqueous outflow dysregulation due to synechiae. Also, there is moderate evidence that intravitreal injections of non-steroidal medications are a risk factor for elevated IOP, so it is important to consider both the pharmacological effect of steroid and the mechanical effect of the injection when determining the risk of intravitreal steroid injections [36].
Management
The first step in management of steroid-induced ocular hypertension is to eliminate the offending agent. It is important to involve the patient’s care team (e.g., primary care physician, rheumatologist, otolaryngologist) to determine if an alternative steroid-sparing therapy can be used in place of systemic or inhaled steroids. When an ophthalmic steroid is the culprit, alternatives such as non-steroidal anti-inflammatory drugs (NSAIDs) and anti-VEGF agents should be considered for inflammation and/or macular edema. For post-operative ophthalmic steroids in patients with glaucoma, we recommend either topical steroids (that can be tapered) or injection of a depot that can be removed (e.g., subconjunctival triamcinolone) instead of a depot that cannot be easily removed (e.g., intra-punctal insert). In cases where the steroid cannot be withdrawn topically, there are different types of glucocorticoids to consider.
If medically appropriate, we recommend fluorometholone (FML) in cases where there is an elevated response to other agents. Multiple studies demonstrate that FML does not elevate IOP to the same extent that dexamethasone does, possibly because FML penetrates the eye less than other topical steroids [37,38,39,40].
Medical management of steroid-induced IOP elevation includes all the IOP-lowering agents used for primary open-angle glaucoma. Netarsudil is a ROCK inhibitor that was approved by the FDA in 2017. In anecdotal reports, netarsudil can lower IOP in steroid-associated glaucoma refractory to other medications, perhaps by modulating trabecular outflow that has been dysregulated by steroids [41]. From 2009 to 2012, several published studies (including a randomized clinic trial) discussed anecortave acetate as a possible treatment for steroid-induced IOP elevation [42, 43]. Anecortave acetate is a synthetic compound derived from cortisol but without glucocorticoid activity. As far as we are aware, there has been no more recent development published on the use of anecortave acetate for IOP.
Interventional treatment of steroid-induced IOP elevation includes selective laser trabeculoplasty (SLT) and surgery. SLT directly targets the dysregulated trabecular meshwork. Although SLT can cause intraocular inflammation, SLT has been successful for IOP lowering in eyes with quiescent uveitis [44]. Surgical options for steroid-induced glaucoma include angle-based surgery and/or trabecular bypass surgery. For example, goniotomy has been found to be effective in eyes with steroid-induced glaucoma [45, 46]. Trabecular bypass surgery is also an important tool for management of steroid-induced glaucoma, particularly tube implants for patients with uveitis and refractory elevated IOP. We prefer a valved tube in uveitic glaucoma patients given markedly elevated pre-treatment IOP and risk for long-term hypotony. There still remains little surgical data on glaucoma outcomes for patients with uveitic glaucoma and/or steroid-induced glaucoma.
Conclusion
Steroids continue to be an important treatment for inflammation control and immunosuppression in the eye. Steroids are also a risk factor for increased IOP and development of glaucoma. From decades of research, underlying structural changes at the level of the trabecular meshwork are now better understood. Current research focuses on targeted therapeutics. Physicians prescribing steroids need to be prepared for close monitoring of IOP and modifications to treatment plans to adequately care for these patients.
References
Papers of particular interest, published recently, have been highlighted as: • Of importance •• Of major importance
Vandewalle J, Luypaert A, De Bosscher K, Libert C. Therapeutic mechanisms of glucocorticoids. Trends Endocrinol Metab. 2018;29(1):42–54. https://doi.org/10.1016/j.tem.2017.10.010.
Covell LL. Glaucoma induced by systemic steroid therapy. Am J Ophthalmol. 1958;45(1):108–9. https://doi.org/10.1016/0002-9394(58)91403-X.
Gordon DM, McLEAN JM, Koteen H, et al. The use of ACTH and cortisone in ophthalmology. Am J Ophthalmol. 1951;34(12):1675–86. https://doi.org/10.1016/0002-9394(51)90032-3.
Armaly MF. Effect of corticosteroids on intraocular pressure and fluid dynamics: II. The effect of dexamethasone in the glaucomatous eye. Arch Ophthalmol. 1963;70(4):492–9. https://doi.org/10.1001/archopht.1963.00960050494011.
Armaly MF, Becker B. Intraocular pressure response to topical corticosteroids. Fed Proc. 1965;24(6):1274–8.
Kayes J, Becker B. The human trabecular meshwork in corticosteroid-induced glaucoma. Trans Am Ophthalmol Soc. 1969;67:9–54.
Spaeth GL, Rodrigues MM, Weinreb S. Steroid-induced glaucoma: A. Persistent elevation of intraocular pressure B. Histopathological aspects. Trans Am Ophthalmol Soc. 1977;75:353–81.
Clark AF, Wilson K, de Kater AW, Allingham RR, McCartney MD. Dexamethasone-induced ocular hypertension in perfusion-cultured human eyes. Invest Ophthalmol Vis Sci. 1995;36(2):478–89.
Johnson DH, Bradley JM, Acott TS. The effect of dexamethasone on glycosaminoglycans of human trabecular meshwork in perfusion organ culture. Invest Ophthalmol Vis Sci. 1990;31(12):2568–71.
Clark AF, Wilson K, McCartney MD, Miggans ST, Kunkle M, Howe W. Glucocorticoid-induced formation of cross-linked actin networks in cultured human trabecular meshwork cells. Invest Ophthalmol Vis Sci. 1994;35(1):281–94.
Clark AF, Brotchie D, Read AT, et al. Dexamethasone alters F-actin architecture and promotes cross-linked actin network formation in human trabecular meshwork tissue. Cell Motil Cytoskeleton. 2005;60(2):83–95. https://doi.org/10.1002/cm.20049.
• Sbardella D, Tundo GR, Coletta M, Manni G, Oddone F. Dexamethasone downregulates autophagy through accelerated turn-over of the Ulk-1 complex in a trabecular meshwork cells strain: insights on steroid-induced glaucoma pathogenesis. Int J Mol Sci. 2021;22(11):5891. https://doi.org/10.3390/ijms22115891. This study demonstrated the downregulation of autophagy with use of steroid therapy, this leads to metabolic dysregulation at the level of the trabecular meshwork and likely contribute to elevated intraocular pressure.
Yuan Y, Call MK, Yuan Y, et al. Dexamethasone induces cross-linked actin networks in trabecular meshwork cells through noncanonical wnt signaling. Invest Ophthalmol Vis Sci. 2013;54(10):6502–9. https://doi.org/10.1167/iovs.13-12447.
• Ren R, Humphrey AA, Kopczynski C, Gong H. Rho kinase inhibitor AR-12286 reverses steroid-induced changes in intraocular pressure, effective filtration areas, and morphology in mouse eyes. Invest Ophthalmol Vis Sci. 2023;64(2):7. https://doi.org/10.1167/iovs.64.2.7. This study demonstrates the importance of RhoKinase inhibitors for treatment of steroid induced ocular hypertension.
Fujimoto T, Inoue T, Kameda T, et al. Involvement of RhoA/Rho-associated kinase signal transduction pathway in dexamethasone-induced alterations in aqueous outflow. Invest Ophthalmol Vis Sci. 2012;53(11):7097–108. https://doi.org/10.1167/iovs.12-9989.
Wan P, Huang S, Luo Y, Deng C, Zhou J, Long E, Zhuo Y. Reciprocal regulation between lncRNA ANRIL and p15 in steroid-induced glaucoma. Cells. 2022;11(9):1468. https://doi.org/10.3390/cells11091468.
Bahler CK, Howell KG, Hann CR, Fautsch MP, Johnson DH. Prostaglandins increase trabecular meshwork outflow facility in cultured human anterior segments. Am J Ophthalmol. 2008;145(1):114–9. https://doi.org/10.1016/j.ajo.2007.09.001.
Kasetti RB, Maddineni P, Patel PD, Searby C, Sheffield VC, Zode GS. Transforming growth factor β2 (TGFβ2) signaling plays a key role in glucocorticoid-induced ocular hypertension. J Biol Chem. 2018;293(25):9854–68. https://doi.org/10.1074/jbc.RA118.002540.
Abtahi M, Rudnisky CJ, Nazarali S, Damji KF. Incidence of steroid response in microinvasive glaucoma surgery with trabecular microbypass stent and ab interno trabeculectomy. Can J Ophthalmol J Can Ophtalmol. 2022;57(3):167–74. https://doi.org/10.1016/j.jcjo.2021.04.008.
Armaly MF. Effect of corticosteroids on intraocular pressure and fluid dynamics: I. The effect of dexamethasone* in the normal eye. Arch Ophthalmol. 1963;70(4):482–91. https://doi.org/10.1001/archopht.1963.00960050484010.
Roth DB, Verma V, Realini T, Prenner JL, Feuer WJ, Fechtner RD. Long-term incidence and timing of intraocular hypertension after intravitreal triamcinolone acetonide injection. Ophthalmology. 2009;116(3):455–60. https://doi.org/10.1016/j.ophtha.2008.10.002.
Choi W, Kim JD, Bae HW, Kim CY, Seong GJ, Kim M. Axial length as a risk factor for steroid-induced ocular hypertension. Yonsei Med J. 2022;63(9):850–5. https://doi.org/10.3349/ymj.2022.63.9.850.
Bojikian KD, Nobrega P, Roldan A, Forrest SL, Tsukikawa M, Chen PP. Incidence of and risk factors for steroid response after cataract surgery in patients with and without glaucoma. J Glaucoma. 2021;30(4):e159–63. https://doi.org/10.1097/IJG.0000000000001785.
Acar M, Gedizlioglu M, Koskderelioglu A, Ozturk F, Kilinc S, Talay N. Effect of high-dose intravenous methyl-prednisolone treatment on intraocular pressure in multiple sclerosis patients with relapse. Eur Neurol. 2012;68(1):20–2. https://doi.org/10.1159/000337615.
Singh IP, Ahmad SI, Yeh D, et al. Early rapid rise in intraocular pressure after intravitreal triamcinolone acetonide injection. Am J Ophthalmol. 2004;138(2):286–7. https://doi.org/10.1016/j.ajo.2004.03.001.
Aref AA, Scott IU, Oden NL, et al. Incidence, risk factors, and timing of elevated intraocular pressure after intravitreal triamcinolone acetonide injection for macular edema secondary to retinal vein occlusion: SCORE study report 15. JAMA Ophthalmol. 2015;133(9):1022–9. https://doi.org/10.1001/jamaophthalmol.2015.1823.
Haller JA, Bandello F, Belfort R, et al. Randomized, sham-controlled trial of dexamethasone intravitreal implant in patients with macular edema due to retinal vein occlusion. Ophthalmology. 2010;117(6):1134–1146.e3. https://doi.org/10.1016/j.ophtha.2010.03.032.
Desnoeck M, Casteels I, Casteels K. Intraocular pressure elevation in a child due to the use of inhalation steroids--a case report. Bull Soc Belge Ophtalmol. 2001;280:97–100.
Garbe E, LeLorier J, Boivin JF, Suissa S. Inhaled and nasal glucocorticoids and the risks of ocular hypertension or open-angle glaucoma. JAMA. 1997;277(9):722–7.
Moss EB, Buys YM, Low SA, et al. A randomized controlled trial to determine the effect of inhaled corticosteroid on intraocular pressure in open-angle glaucoma and ocular hypertension: the ICOUGH study. J Glaucoma. 2017;26(2):182–6. https://doi.org/10.1097/IJG.0000000000000429.
Wijnants D, Stalmans I, Vandewalle E. The effects of intranasal, inhaled and systemic glucocorticoids on intraocular pressure: a literature review. J Clin Med. 2022;11(7):2007. https://doi.org/10.3390/jcm11072007.
Friling R, Weinberger D, Zeharia A, et al. Elevated intraocular pressure associated with steroid treatment for infantile spasms. Ophthalmology. 2003;110(4):831–4. https://doi.org/10.1016/S0161-6420(02)01890-0.
Prasad D, Poddar U, Kanaujia V, Yachha SK, Srivastava A. Effect of long-term oral steroids on intraocular pressure in children with autoimmune hepatitis: a prospective cohort study. J Glaucoma. 2019;28(10):929–33. https://doi.org/10.1097/IJG.0000000000001352.
Yan H, Tan X, Yu J, et al. The occurrence timeline of steroid-induced ocular hypertension and cataract in children with systemic autoimmune diseases. Int Ophthalmol. 2022;42(7):2175–84. https://doi.org/10.1007/s10792-022-02217-5.
Taliaferro K, Crawford A, Jabara J, et al. Intraocular pressure increases after intraarticular knee injection with triamcinolone but not hyaluronic acid. Clin Orthop. 2018;476(7):1420–5. https://doi.org/10.1007/s11999.0000000000000261.
Levin AM, Chaya CJ, Kahook MY, Wirostko BM. Intraocular pressure elevation following intravitreal anti-VEGF injections: short- and long-term considerations. J Glaucoma. 2021;30(12):1019–26. https://doi.org/10.1097/IJG.0000000000001894.
Akingbehin AO. Comparative study of the intraocular pressure effects of fluorometholone 0.1% versus dexamethasone 0.1%. Br J Ophthalmol. 1983;67(10):661–3. https://doi.org/10.1136/bjo.67.10.661.
Kass M, Cheetham J, Duzman E, Burke PJ. The ocular hypertensive effect of 0.25% fluorometholone in corticosteroid responders. Am J Ophthalmol. 1986;102(2):159–63. https://doi.org/10.1016/0002-9394(86)90137-6.
Kwok AK, Lam DS, Ng JS, Fan DS, Chew SJ, Tso MO. Ocular-hypertensive response to topical steroids in children. Ophthalmology. 1997;104(12):2112–6. https://doi.org/10.1016/s0161-6420(97)30052-9.
Kupferman A, Leibowitz HM. Penetration of fluorometholone into the cornea and aqueous humor. Arch Ophthalmol Chic Ill 1960. 1975;93(6):425–7. https://doi.org/10.1001/archopht.1975.01010020439008.
Li G, Lee C, Read AT, et al. Anti-fibrotic activity of a rho-kinase inhibitor restores outflow function and intraocular pressure homeostasis. eLife. 10:e60831. https://doi.org/10.7554/eLife.60831.
Stalmans I, Callanan DG, Dirks MS, et al. Treatment of steroid-induced elevated intraocular pressure with anecortave acetate: a randomized clinical trial. J Ocul Pharmacol Ther. 2012;28(6):559–65. https://doi.org/10.1089/jop.2012.0063.
Reduction of intraocular pressure with anecortave acetate in eyes with ocular steroid injection–related glaucoma | Glaucoma | JAMA Ophthalmology | JAMA Network. Accessed April 8, 2023. https://jamanetwork.com/journals/jamaophthalmology/fullarticle/421022.
**ao J, Zhao C, Liang A, Zhang M, Cheng G. Efficacy and safety of high-energy selective laser trabeculoplasty for steroid-induced glaucoma in patients with quiescent uveitis. Ocul Immunol Inflamm. 2021;29(4):766–70. https://doi.org/10.1080/09273948.2019.1687730.
Boese EA, Shah M. Gonioscopy-assisted transluminal trabeculotomy (GATT) is an effective procedure for steroid-induced glaucoma. J Glaucoma. 2019;28(9):803–7. https://doi.org/10.1097/IJG.0000000000001317.
Van Rijn LJR, Eggink CA, Janssen SF. Circumferential (360°) trabeculotomy for steroid-induced glaucoma in adults. Graefes Arch Clin Exp Ophthalmol Albrecht Von Graefes Arch Klin Exp Ophthalmol. 2023;21. https://doi.org/10.1007/s00417-023-06012-5.
Author information
Authors and Affiliations
Corresponding author
Ethics declarations
Conflict of Interest
Erin Sieck has served on an Advisory Board and received an honorarium for participation for Allergan. Ariana Levin declares that she has no conflicts of interest.
Human and Animal Rights and Informed Consent
This article does not contain any studies with human or animal subjects performed by any of the authors.
Additional information
Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Rights and permissions
Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
About this article
Cite this article
Levin, A.M., Sieck, E.G. New Concepts in Steroid Glaucoma. Curr Ophthalmol Rep 11, 78–82 (2023). https://doi.org/10.1007/s40135-023-00316-9
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s40135-023-00316-9