Eye (2006) 20, 407–416

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Corticosteroid- JP Kersey, DC Broadway

induced glaucoma:
a review of the

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,
mechanisms, and genetics of the condition and UK
to present management options.
A rise in intraocular pressure (IOP) can occur as Correspondence: DC
an adverse effect of corticosteroid therapy. If the Broadway
Risk factors
Tel: 01603 288064;
ocular hypertensive effect is of sufficient Fax: 01603 288856.
Although only partially understood, a number
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. Received: 29 November
IOP induced by systemic administration of
adrenocorticotrophic hormone (ACTH). After 4
History of glaucoma/glaucoma suspect Accepted in revised form:
years, Francois2 described the first case of 28 February 2005
elevated IOP induced by local administration of In 1963, Becker and Mills6 demonstrated that Published online: 6 May
steroid (cortisone). Since that time, investigators patients who had glaucoma, or had been 2005

although it has been shown that corticosteroid response in patients with certain types of depot intravitreal administration of triamcinolone can connective tissue disease. systemic hypertension. The ratio was steroid treatment.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. Eye .16. others have described corticosteroid. and much less.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).18 described the pressure rise after topical use.20 could not be used as a screening method to exclude any chronic nasal or inhaled steroid. 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. from a mean of 13. Since Herschler28 investigated 12 patients who demonstrated Francois2. caused by nightly from a mean of 16. In the same year (1963). populations.14. sex. and greater in therapy. Corticosteroid-induced glaucoma JP Kersey 408 diagnosed as glaucoma suspects. this outweighing a of clinically significant subretinal fluid and macular smaller reduction in aqueous production. but these changes have not been shown to correlate with an ocular hypertensive response. although intractable glaucoma has been that have been reported include an increase in corneal reported.10 a first-degree produce IOP rises.21 subconjunctival. with he eventually required bilateral glaucoma filtration patients in this group falling into two distinct surgery. Herschler’s Steroid-induced ocular hypertension has been reported findings implied that topical corticosteroid treatment in association with topical application to the eyelids. 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.22 injections. repository steroid injection and. Fortunately.24 These new techniques involve the use of a glaucomatous compared with nonglaucomatous eyes. Users of nasal corticosteroids were shown Age to be at increased risk of ocular hypertension or glaucoma with an odds ratio of 1. then adjusted for age. 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.3 mmHg. 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.26 thickness and a slight mydriasis.25 the majority of affected patients relative with primary open-angle glaucoma (POAG). and use of ophthalmic or systemic steroids. glaucoma suspect group rose from a mean of 17. and systemic administration of corticosteroid.6 to only 18.44.1 to The associated glaucoma was refractory to medical 28.15 Other steroid-induced ocular effects therapy. The odds ratio of patients who had a facility during the period of steroid treatment. related to preparation solubilityFthis was despite 10 of induced ocular hypertension following other methods of the patients having had extensive topical treatment prior administration. Armaly oedema. 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.23. diabetes. The IOP for the glaucoma group rose an elevated IOP of 60 mmHg. However.1 mmHg and that for the application of fluocinolone acetonide for 7 years. Armaly7. while there is an increasing body of evidence to suggest this can improve visual outcome in these patients.2 mmHg.11–13 have been controlled with topical ocular hypotensive or high myopia.8 showed that the ocular More recently. to the injection without a pressure rise. and subsequent pressure response with depot steroid sub-Tenon’s injection of steroid.9 to 32.9 type I diabetes.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. in the normal group the IOP rose therapy despite cessation of steroid therapy.

nuclear size and DNA content.25% 1. effects of systemic steroids and found that there stromelysin.44 Clark et al44 discovered that steroid-induced glaucoma patients. A steroid-induced material in the trabecular meshwork (TM).42. Furthermore. a more acute onset rise can found to bind specifically to the nuclei of cells in the occur within hours of starting intensive topical outflow channels. this resulting in a relative Medrysone 1. Structural changes in the TM cells have also deposition have been described in the TM of been proposed.27 and Armaly showed this with donor eye models. concentration has been shown to be high in ocular using the left eye as a control. provocation testing administering dexamethasone eye In rabbit eyes glucocorticosteroid receptor drops three times a day to the right eye for 4 weeks.1% 6. and leading to the formation of networks within cultured Eye . dexamethasone treatment has also been shown to inhibit TM cell arachadonic acid metabolism35 Suggested mechanisms of the corticosteroid response and reduce phagocytic activity.5% 3.38 and the activity of several TM was an increase in IOP in a group of patients treated metalloproteases32.36 A further study has often years. In addition.071. and effect being seen within weeks with potent drugs and fibronectin have been shown to increase in tissue culture only after several months with the weaker agents. In addition.43 so contributing to steroid-induced in outflow resistance.1% 22. leading to their accumulation in Dexamethasone 0. deposition of material in the uveal meshwork.0% 1.41 than a year.31 Two patterns of extracellular glaucoma.271.36.005% 8. elastin. excessive accumulation of sex-matched control group. the The amounts of glycosaminoglycans. Golgi common than following topical treatment.0% 10.871.32 Francois18 and Armaly7 both suggested that the Dexamethasone 0.8 Weinreb et al29 have tissue33 and intravenously administered steroid has been reported that.and Furthermore.271. the function of which is to clear inhibiting degradation of extracellular matrix the outflow channels of debris. It was proposed that corticosteroids. cause retention of water (‘biological oedema’) and subsequent narrowing of the trabecular Timing of response spaces.32 TM cells have Corticosteroids are believed to decrease outflow by phagocytic properties. Corticosteroid-induced glaucoma JP Kersey 409 Table 1 IOP elevations for different steroid preparations accumulation of fine fibrillar material in the Preparation Average pressure rise (mmHg) juxtacanalicular region.18 Francois18 found the incidence of steroid shown that steroids also induce proliferation and glaucoma following systemic treatment to be much less activation of the endoplasmic reticulum. apparatus.34 in a similar manner to the binding dexamethasone.171. an acute onset response has of dexamethasone reported to occur in cultured human been reported in association with intensive systemic TM cells. although rare.7 of mucopolysaccharides.4 Hydrocortisone 0.072. it was glycosaminoglycans has been identified in human reported that those who had been on systemic steroids trabecular meshwork specimens obtained from steroid- for more than 4 years had significantly higher IOPs responders.9 response might be due to an alteration of the metabolism Prednisolone 1.3 inhibition of hyaluronate depolymerisation. preparations in response to dexamethasone treatment Bernstein and Schwartz30 examined the long-term while the levels of tissue plasminogen activator. Support for a steroid-induced effect within the outflow Topical steroids have been shown to produce a steroid channels has come from animal studies.7 the TM.3 of lysosomal hyaluronidase. could reduce the release Tetrahydrotriamcinolone 0.071.40 confirming similar findings in a rabbit than those who had been on systemic steroids for less model. which Fluoromethalone 0. leading inhibition of phagocytosis within the meshwork could to aggregation of an excessive amount of the material result in accumulation of channel debris and decreased within the outflow channels and a subsequent increase facility of outflow.35 Glucocorticocoids have been shown to steroid therapy. with systemic steroid when compared to an age. fingerprint-like dexamethasone caused cross-linkage of actin fibres.39 have been shown to fall.0 stabilise lysosomal membranes. and increase deposition of extracellular Francois18 reported that the time of onset of the IOP matrix material. although the IOP response to systemic alter TM cell morphology by causing an increase in steroids typically occurs over a much longer period. The subsequent accumulation of mucopolysaccharides could.32.37 elevation was dependent on corticosteroid potency. experiments response over a period of weeks in both normal7 and with cultured human TM cells and perfusion-cultured glaucomatous eyes8. it was suggested.7.30 In support of the evidence for extracellular matrix deposition.

one set were both high responders. morphological changes response groups did show quite large degrees of included. Schwartz highly expressed in trabecular cells exposed to et al48 found no significant difference in the frequency of glucocorticoids. it was 2–3 weeks. In those eyes in which However. Becker dexamethasone-treated TM cells. However. Children of glaucoma patients. a neuroprotective factor (pigment autosomal mechanism. which transducer within the eye. has been shown to be induced in human glaucoma patients and five of the six showed a negative cultured TM cells after exposure to dexamethasone for response. Patients reversible following cessation of corticosteroid were divided into three groups depending on their administration to the cultures. while the low-response group exposure.11 epithelium-derived factor). Several authors have proposed a genetic susceptibility Several genes have been shown to be upregulated in for corticosteroid glaucoma. perfusion-cultured response reassessed.53. the effect of such an alteration of 6 mmHg. of the near future. It is hoped that recent advances in novel molecular chance 58%). gene product). In another perfusion-cultured and chance (6%) values. thickened trabecular beams.52 the was hypothesised that parents of high-response gene being identical to GCL1A and now referred to as the glaucoma patients should show at least a medium myocilin gene. Armaly47 and Becker. and protein myocilin (initially referred to as TM-inducible tested both parents and children of glaucoma patients. but when ocular hypertension has been proposed because: (1) it is 87 were tested. He tested six parents of protein. would all show a medium response. IOP was measured using a pressure population studied over the two tests was 73%. the intermediate group showed a rise of 6– cellular cytoskeleton on TM cell function remains 15 mmHg. It was suggested that the pressure response to topical corticosteroid therapy.6–8 In 1964. The actin network structure was reproducibility of the corticosteroid response. Indeed. By show good reproducibility in the high-response group. 415 mmHg. it did mechanisms causing the steroid-induced glaucoma. The authors felt that while topical testing genetic methods will allow a better understanding of the had limited effectiveness in whole populations.32 corticosteroid response. only 29 showed a response. it was noted that the intermediate and low- there was a pressure increase. suggested that medium responders (cornea-derived transcript factor 6) and a prostaglandin were heterozygotes while high responders were synthase (prostaglandin D2 synthase) enzyme. Linkage analysis of a large single family with juvenile Palmberg et al49 have offered an explanation for the onset POAG has shown that mutations in a gene on apparent discrepancy in findings. which is a 55 kDa response according to the theory. of the individual subgroups. It gene deletion or overexpression studies. (2) the delay in its expression is similar corticosteroid response between monozygotic and to the delay in the pressure rise in glucocorticoid-treated dizygotic twin groupsFthis perhaps implying that there eyes and (3) the dose required to cause the protein is an environmental influence on the development of a expression is similar to that required to raise IOP. the exact role of was suggested that the less-than-perfect reproducibility individual genes responsible for the modulation of might explain to an extent the low concordance identified meshwork extracellular material may be identified in the in Schwartz’s twin study. so that the measurement was was significantly higher than expected by chance (47%). It glucocorticoid response or TIGR. thickened juxtacanalicular tissues. homozygotes. an antiangiogenesis factor in refining this. while the high-response group had a rise of unclear. The concordance value for the total human eyes. but meshwork increased with increasing duration of steroid still statistically higher. However. The intermediate group had a human eye model glycosaminoglycan deposition in the concordance (74%) that was closer to chance (36%). and none were twins of low Genetics responders.50 including genes and Hahn12 suggested that patient response to representing a serine protease inhibitor (alpha-1- corticosteroids could be explained by a monogenic antichymotrypsin). not affected by corneal thickness. decreased crossover.46 showed no statistical difference (concordance 71%.38 four identical twins who were high responders. Corticosteroid-induced glaucoma JP Kersey 410 human TM cells. the most extensively studied gene is that representing the Francois18 argued against this simplistic theory. The testing was repeated using either the Clark et al45 went on to demonstrate histological and ipsilateral eye or the contralateral eye and the pressure pressure changes in steroid treated. in the twin study.51. The role of myocilin in corticosteroid-induced proposed. Concordance values were examined for each intertrabecular spaces.32 The myocilin gene. The high-response group and increased amounts of amorphous granular showed a marked difference in the concordance (79%) extracellular material. by investigating the chromosome 1q are responsible for most cases of Eye . The response might be mediated by the TM glucocorticoid low-response group showed a pressure rise of less than receptor. and the other two were twins of intermediate responders.

patients requiring long-term systemic patients with corticosteroid-responsive glaucoma corticosteroid therapy should have glaucoma screening have a history of significant corticosteroid use. with the exception that Ideally. Different mutations within myocilin lead to management. then methods of of all potential adverse effects. The chronic are prone to steroid-responsiveness and may be tipped corticosteroid response resolves in 1–4 weeks. prevention is ideal. while viral-mediated transfer of myocilin in TM cells caused an overexpression POAG First-degree relative with POAG of myocilin and lead to reduction in outflow Glaucoma suspect High myopia Previous steroid response Type I diabetes resistance. whenever possible. produces the protein any early changes that would necessitate a change in myocilin. similar to those of POAG. Health-care professionals should aim to prevent or minimise the chance of inducing irreversible damage by Cessation of corticosteroid treatment paying careful attention to patients’ medical histories It is ideal to ensure that the suspected corticosteroid is and with judicious use of steroids. recombinant myocilin increased outflow resistance.4% of patients receiving triamcinolone show a pressure rise to greater Clinical aspects than 24 mmHg over at an average of 100 days after The clinical features of corticosteroid glaucoma are treatment. Glaucoma screening can be damage. into a state of significant visual loss by such therapy.59 Further investigation of myocilin and other steroid. then 6-monthly if therapy is to patients most likely to develop steroid-induced continue. Patients undergoing intravitreal triamcinolone should be monitored for several months following the steroid injection. or in local nerve changes indistinguishable from those associated ophthalmic departments should there be a suspicion of with POAG. minimising the risk therapy is not possible. This gene. since these patients corticosteroid should be stopped. In perfused human anterior segment cultures. Monitoring of IOP induced gene products is needed to enhance our A baseline measurement of IOP should be taken prior to understanding of the role that steroids play on TM cells commencement of corticosteroid therapy. Fingert et al59 could not find statistically significant evidence of a link Management of corticosteroid-induced glaucoma (see between myocilin mutations and steroid-induced ocular also Appendix A) hypertension.56 Increasing age Connective tissue disease (eg RhA) Mice that have been genetically engineered to overexpress myocilin have not shown an increase in intraocular pressure. then every 4 clinicians in being able to predict more accurately those weeks for 2–3 months. induced as part of the corticosteroid should have their IOP checked at 1. established glaucoma. whereas the rare acute response may resolve within In all situations. requires careful monitoring of patients at risk to identify previously called the TIGR gene. Eye . use of the patients with pre-existing glaucoma. glaucoma. Patients on and outflow resistance. 3. and 6 months and response. to be surgically removed. increases the risk of optic nerve fibre 6 monthly thereafter. Corticosteroid-induced glaucoma JP Kersey 411 autosomal dominant juvenile onset POAG.29 In the case of avoided. As with all iatrogenic conditions. The typically insidious reducing the effects of the corticosteroid need to be nature of progressive steroid-induced glaucoma considered.55 The role of myocilin Patients at higher risk than average (see risk factors remains poorly understood and experiments altering its above) expression have provided conflicting results.57. leading to characteristic visual field and optic performed by optometrists in the community. the steroid may have has a therapeutic effect at the lowest possible dose. It is particularly responsible for the glaucoma and if glaucoma is important.28 If cessation of steroid administered by the safest route. widely variable glaucoma phenotypes54 involved in both juvenile and adult onset POAG. and those receiving 10 mg or more of prednisolone daily The elevated IOP. when steroid therapy cannot be a few days of steroid cessation. Of equal importance will be the topical therapy should then have their IOP measured findings of future genetic studies that may aid again 2 weeks after initiation of treatment. to avoid use of steroids in established (and especially if progressive). the choice of drug should be of one that repository corticosteroids. Smithen et al60 found that 40.58 In monkeys.

introducing or effective short-term treatment for the control of IOP in all increasing steroid-sparing agents such as forms of glaucoma. and in particular when there is a Argon laser trabeculoplasty (ALT) family history of glaucoma and/or chronic use of steroid This treatment has been tried both before and after (at least 4 years).17 Furthermore. this inducing some doubt exercised when prescribing prostaglandin analogues in as to whether there was a true effect of the cortico- such eyes. the ocular hypertensive response has commencing corticosteroid therapy and has not been been shown to be irreversible. 28% of the patients developed a pressure to be relatively refractory to miotics while the steroid has rise of 6 mmHg or more. as always. undergoing trabeculectomy in whom it appeared However. in addition to being less reported by Becker and Mills6 for ‘normal’ eyes that had popular than more modern agents.62 preferably following therapy and are refractory to medical therapy. Prostaglandin analogues Concomitant latanoprost has It. seems unlikely that a steroid response occurs been shown to be as effective as cessation of therapy in following successful filtration surgery.61 The management of shown to be effective in preventing corticosteroid- such cases is no different from that for POAG.18. They described an increase in uveitic glaucoma.68 cessation of steroid therapy and are a popular first-line However. are of use in the control of IOP due to corticosteroid- induced glaucoma.62 Irreversible steroid-induced ocular hypertension/glaucoma In about 3% of cases. However. latanoprost has been reported to induce that an ocular hypertensive response developed to uveitis64.66 fluoromethalone 0. such as those they require extensive monitoring.67 Galin et al attempted to prevent a corticosteroid response in myopic eyes undergoing radial keratotomy by using ALT. Corticosteroid-induced glaucoma JP Kersey 412 Alternative corticosteroid formulations have been reports of brimonidine-induced uveitis in a Topical treatments can be changed to preparations such as minority of patients. miotics are also not undergone ALT. Over longer periods. steroid or simply an effect of postoperative inflammation. contraindicated in inflamed eyes (ie those that may require topical steroid therapy) since they can exacerbate the formation of posterior synechiae.27 or in certain situations to nonsteroidal anti-inflammatory drugs (NSAIDs).1% or rimexolone 1%.65 and is relatively contraindicated in eyes with postoperative steroid.67 which was similar to the rises still been used. However. although controlling the IOP rise associated with corticosteroids63 Thomas and Jay69 described a small group of patients so can be useful if steroid treatment must be continued. of trabeculectomy or other forms of drainage surgery should be considered in relation to the potential benefits. including that induced by cyclophosphamide or methotrexate may allow the corticosteroids. excision of depot periocular patients with steroid-induced glaucoma. the adverse consequences agent for the condition. so their use should be with renal impairment. It was reported that Medical antiglaucomatous therapy when ALT was performed prior to therapy with topical Miotics Corticosteroid-induced glaucoma has appeared corticosteroid. topical carbonic discussed with a physician unless the ophthalmologist has anhydrase inhibitors (dorzolamide and brinzolamide) specific experience with such medications. Alpha agonists Brimonidine can be useful in many Although rarely necessary. although there or intraocular steroid may be indicated in patients Eye . Latanoprost has been shown to cause IOP in 17% of the postoperative eyes at around cystoid macular oedema in certain pseudophakic eyes in 4 weeks following surgery.65 so caution should be showed a further rise. which are claimed to have less effect on IOP. the side effect corticosteroid dosage to be reduced. during a later the early postoperative period (when steroids are likely challenge only three of eight previous ‘responders’ to have been prescribed). For Carbonic anhydrase inhibitors Oral acetazolamide is an patients prescribed systemic corticosteroids. induced pressure rises. Steroid-sparing profile of acetazolamide tends to make it poorly tolerated medications have their own significant adverse effects and and it is contraindicated in certain patients.62 Filtration surgery Trabeculectomy remains an effective treatment for glaucoma in those patients who have a persistently Beta-blockers Topical beta-blockers can be used to control raised IOP following cessation of corticosteroid corticosteroid-induced glaucoma.

accumulation of cellular to be undertaken. angle closure through anterior and it appears that a number of gene loci interact in synechiae formation and. Trans Am should be considered. useful potential therapeutic agents for treating 92: 1971. Nootens RH. has been shown 6 Becker B. are to It is possible that further development of nonsteroidal minimise the use of steroid appropriately and apply anti-inflammatory therapies will provide effective standard antiglaucomatous therapy.70–72 With the increasing corticosteroid-induced ocular hypertensive rabbits. Glaucoma secondary corticosteroid-induced glaucoma. (RU 486-6). Better identification of patients at risk of determine which of these factors is most important and it corticosteroid-induced IOP rises would allow them to be differs significantly between eyes.63 although determine whether an elevation in IOP is due to the cessation of corticosteroid therapy is the ideal course of steroid therapy or the uveitic disease process itself. Corticosteroids and intraocular to reduce IOP in both normotensive76 and pressure.74 a rise occurs if this effect is exceeded by obstruction of the Although there has been marked progress in the last few TM outflow pathway. Cortisone et tension oculaire. 4 Bayer JM. Cushing-syndrom und Glucocorticoid receptor blockers have been proposed as erhohter augeninnen druck. 2 Francois J. A significant minority (10%) of changes. 252: Future therapies 239–244. management of uveitic glaucoma. Am J Med Sci 1966.79 have inhibited dexamethasone- induced ocular hypertension in rabbits using tetrahydrocortisol. in part. corticosteroid response is suspected. debris in the TM. it is rarely possible to inheritance. patients with uveitis show a rise in IOP. response rather than it following simple Mendelian For individual patients. Southren et al78. In most cases. cessation of the antiglaucomatous therapy (as well as the steroid) 1 McLean JM. Clark et al80 believe Uveitic glaucoma that the action of tetrahydrocortisol is not due to its action as a glucocorticoid antagonist but due to a direct Uveitic glaucoma provides a particular therapeutic effect that alters the dexamethasone-induced TM challenge. an iatrogenic controlling the corticosteroid-induced glaucoma corticosteroid response. Corticosteroid-induced glaucoma JP Kersey 413 refractory to medical therapy.75 An increase in outflow years in understanding the mechanisms behind resistance can be due. 187: 805. Ann D’Oculist 1954. Deutsch Med Wochenschr 1967. First-line therapy alternatives to corticosteroids. However. selected cases. to the increase in corticosteroid-induced glaucoma. Am J Ophthalmol 1974. including Prostaglandins have been used successfully in the POAG. particularly if a temporary Ophthalmol Soc 1950.65 After episodes of uveitis complicated References by elevation in IOP requiring therapy.75 more closely monitored than others. in addition. Mifepristone to benign adrenal adenoma. Use of ACTH and cortisone. further research needs aqueous protein content. Mills DW. Neuner NP. The principles of management. 3 Smith CL. carbonic anhydrase inhibitors or may result in the development of novel therapies adrenergic agonists being used as second-line agents. 5 Haas JS. since they may exacerbate intraocular inflammation. responsiveness. The genetics are not fully understood. Arch Ophthalmol 1963.73 Although IOP often falls in an acutely inflamed eye (due to a reduction in aqueous production and a four-fold Conclusions increase in uveo-scleral outflow). action. antiglucocorticoid properties. 70: 500–507. this mode of therapy has not yet been used vitrectomy may prove useful in preventing glaucoma in in human subjects. but monitoring of induced pressure rise early enough to prevent them from IOP is critical. It is also hoped that for lowering IOP in eyes with uveitis is usually with a a full understanding of the steroid-induced response beta-blocker. 48: 293–296. therefore. Eye .23.77 popularity of intravitreal triamcinolone injections. It is important to Corticosteroids remain the mainstay of therapy for identify those patients who have a corticosteroid- uveitis in controlling inflammation. a peripheral progesterone blocker with 78: 497. Corticosteroid glaucoma: A summary and review of the literature.75 for the treatment of other types of glaucoma.64. but their use is cautioned. With respect to corticosteroid developing permanent visual loss. the management of uveitic glaucoma corticosteroid-induced glaucoma can be treated can be difficult because it is usually impossible to successfully by topical antiglaucoma therapy.24 However.

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Corticosteroid-induced glaucoma JP Kersey 416 Appendix A: management principles Start Steroid Therapy Topical Systemic Depot Check at 2 weeks Check at 4 weeks Check at one week No Is IOP > 21 mmHg? Regular review Yes No Initially 2 monthly then 6 monthly Are there signs of Glaucoma? or Is the pressure >30 mmHg? Yes Stop steroid if possible In Uveitic glaucoma Start first line medical treatment • Avoid Prostaglandins • Reduce steroids if possible Recheck IOP at 4 weeks Add further medical treatment No Yes No No Is IOP < target? Max Medical treatment? Yes Yes Recheck at 6/12 Consider surgery/ cyclo-destruction Eye .