Corticosteroid- Induced Glaucoma: a Review of the Literature
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Eye (2006) 20, 407–416 & 2006 Nature Publishing Group All rights reserved 0950-222X/06 $30.00 www.nature.com/eye Corticosteroid- JP Kersey, DC Broadway PERSPECTIVE induced glaucoma: a review of the literature Abstract have maintained an interest in this particular form of secondary ocular hypertension/ The intraocular pressure rise that can glaucoma, both in its own right and in complicate the use of topical or systemic providing possible insights into the aetiology of corticosteroid has been recognised for 50 years. certain types of open-angle glaucoma (OAG). More recently, following isolation of the It has long been known that IOP fluctuates myocilin gene (previously known as the diurnally and it has been postulated that this trabecular meshwork inducible glucocorticoid may be linked to cortisol levels.3 The peak in response or TIGR gene), there has been diurnal IOP occurs at around 0700 hours and renewed interest in this steroid-responsive the trough during the early evening, the daily phenomenon. Furthermore, the currently fluctuation in IOP correlating closely with fashionable use of injectable intraocular plasma cortisol levels.3 Furthermore, cases have steroids in the management of clinically been described of raised IOP secondary to significant subretinal fluid and macular adrenal gland hyperplasia4,5 and although oedema has resulted in an increased incidence. direct cause and effect has not been proven, it is Animal studies, cell biology, molecular known that there is no diurnal IOP variation in biology, and an improved knowledge of patients who have had their adrenals removed.3 genetics have provided a better understanding A corticosteroid-induced IOP rise has been of the mechanisms behind the response. The shown to occur with various methods of steroid purpose of this review is to describe the risk administration (see Methods of administration, factors for developing corticosteroid-induced below), but is most commonly identified as a glaucoma, to discuss the underlying complication of topical corticosteroid mechanisms and genetics of the condition and application with drugs such as dexamethasone to present management options. or prednisolone. In responsive patients, the IOP Eye (2006) 20, 407–416. doi:10.1038/sj.eye.6701895; typically rises after several weeks of continual published online 6 May 2005 corticosteroid therapy and returns to normal following cessation of such therapy.2 Keywords: glaucoma; corticosteroid; intraocular The purpose of this review is to describe the pressure; steroid induced; myocilin; secondary Department of risk factors for developing corticosteroid- Ophthalmology, Norfolk and induced glaucoma, including the effect of Norwich University Hospital preparation type, to discuss the underlying Norwich, Norfolk NR4 7UY, UK Introduction mechanisms, and genetics of the condition and to present management options. A rise in intraocular pressure (IOP) can occur as Correspondence: DC Broadway an adverse effect of corticosteroid therapy. If the Risk factors Tel: 01603 288064; ocular hypertensive effect is of sufficient Although only partially understood, a number Fax: 01603 288856. magnitude, for an adequate duration, damage E-mail: broadway@ of risk factors for developing corticosteroid- to the optic nerve (steroid-induced glaucoma) nnuh.nhs.uk induced glaucoma or ocular hypertension have may ensue. In 1950, McLean1 reported a rise in been identified. IOP induced by systemic administration of Received: 29 November adrenocorticotrophic hormone (ACTH). After 4 2004 2 History of glaucoma/glaucoma suspect Accepted in revised form: years, Francois described the first case of 28 February 2005 6 elevated IOP induced by local administration of In 1963, Becker and Mills demonstrated that Published online: 6 May steroid (cortisone). Since that time, investigators patients who had glaucoma, or had been 2005 Corticosteroid-induced glaucoma JP Kersey 408 diagnosed as glaucoma suspects, had marked IOP rises Cubey20 described the case of a 22-year-old man in response to several weeks’ exposure to topical who had developed corneal oedema secondary to corticosteroids. The IOP for the glaucoma group rose an elevated IOP of 60 mmHg, caused by nightly from a mean of 16.9 to 32.1 mmHg and that for the application of fluocinolone acetonide for 7 years. glaucoma suspect group rose from a mean of 17.1 to The associated glaucoma was refractory to medical 28.3 mmHg. However, in the normal group the IOP rose therapy despite cessation of steroid therapy, and much less, from a mean of 13.6 to only 18.2 mmHg, with he eventually required bilateral glaucoma filtration patients in this group falling into two distinct surgery. populations; those who showed a moderate increase and Garbe et al21 described a case–control study in those who showed none. Patients who responded to the which patients were recruited from a health insurance steroids were also shown to have a reduced outflow database. The odds ratio of patients who had a facility during the period of steroid treatment. recent diagnosis of ocular hypertension or OAG was The IOP for all the patients studied returned to their calculated in patients using nasal or inhaled baseline or to a normal level after cessation of the corticosteroids relative to nonusers. The ratio was steroid treatment. then adjusted for age, sex, diabetes, systemic hypertension, and use of ophthalmic or systemic steroids. Users of nasal corticosteroids were shown Age to be at increased risk of ocular hypertension or glaucoma with an odds ratio of 1.44. In the same year (1963), Armaly7,8 showed that the ocular More recently, there has been renewed interest in the hypertensive response to topical dexamethasone was due use of injectable intraocular steroids in the management to a reduction in aqueous outflow, this outweighing a of clinically significant subretinal fluid and macular smaller reduction in aqueous production. Armaly oedema,23 this includes the novel method of combining reported that the steroid-induced effect was greater in intravitreal triamcinolone with the use of photodynamic older compared with younger eyes, and greater in therapy.24 These new techniques involve the use of a glaucomatous compared with nonglaucomatous eyes. repository steroid injection and, while there is an increasing body of evidence to suggest this can improve visual outcome in these patients,23,24 it should be Other factors remembered that the depot steroid cannot easily be It has been reported that there is a greater risk of removed. Fortunately, although it has been shown that corticosteroid response in patients with certain types of depot intravitreal administration of triamcinolone can connective tissue disease,9 type I diabetes,10 a first-degree produce IOP rises,25 the majority of affected patients relative with primary open-angle glaucoma (POAG),11–13 have been controlled with topical ocular hypotensive or high myopia.14,15 Other steroid-induced ocular effects therapy, although intractable glaucoma has been that have been reported include an increase in corneal reported.26 thickness and a slight mydriasis, but these changes have not been shown to correlate with an ocular hypertensive response.16,17 Different preparations Cantrill et al27 have reported differences in the level of Type of preparation steroid response in known high responders to steroid for different preparations and found that the higher the Methods of administration steroid potency the greater the ocular hypertensive effect Elevation in IOP has been associated with both topical (see Table 1). and systemic administration of corticosteroid. Since Herschler28 investigated 12 patients who demonstrated Francois2,18 described the pressure rise after topical use, a steroid response to injected corticosteroid and showed and Bernstein et al19 described the response to systemic that the duration and severity of response was inversely corticosteroids, others have described corticosteroid- related to preparation solubilityFthis was despite 10 of induced ocular hypertension following other methods of the patients having had extensive topical treatment prior administration. to the injection without a pressure rise. Herschler’s Steroid-induced ocular hypertension has been reported findings implied that topical corticosteroid treatment in association with topical application to the eyelids,20 could not be used as a screening method to exclude any chronic nasal or inhaled steroid,21 subconjunctival, and subsequent pressure response with depot steroid sub-Tenon’s injection of steroid.22 injections. Eye Corticosteroid-induced glaucoma JP Kersey 409 Table 1 IOP elevations for different steroid preparations accumulation of fine fibrillar material in the juxtacanalicular region.32 Preparation Average pressure rise (mmHg) Francois18 and Armaly7 both suggested that the Dexamethasone 0.1% 22.072.9 response might be due to an alteration of the metabolism 7 Prednisolone 1.0% 10.0 1.7 of mucopolysaccharides, leading to their accumulation in Dexamethasone 0.005% 8.271.7 the TM. It was proposed that corticosteroids, which Fluoromethalone 0.1% 6.171.4 Hydrocortisone 0.5% 3.271.0 stabilise lysosomal membranes, could reduce the release Tetrahydrotriamcinolone 0.25% 1.871.3 of lysosomal hyaluronidase, this resulting in a relative Medrysone 1.0% 1.071.3 inhibition of hyaluronate depolymerisation. The subsequent accumulation of mucopolysaccharides could, it was suggested, cause retention of water (‘biological oedema’) and subsequent narrowing of the trabecular Timing of response spaces. Support