Steroid-induced Glaucoma Research Articles

Intraocular Pressure Effects of Common Topical Steroids for Post-Cataract Inflammation: Are They All the Same?

The efficacy of topical corticosteroids as ocular anti-inflammatory agents following cataract surgery is well-documented. They also help to prevent a number of complications associated with post-operative ocular inflammation, including corneal edema and cystoid macular edema. However, topical corticosteroids are associated with side effects, such as increased intraocular pressure (IOP). Indeed, corticosteroid-induced ocular hypertension and the potential for steroid-induced glaucoma remain the leading drawbacks of topical corticosteroid therapy. Some individuals are known to experience a high degree of IOP elevation with low doses or short durations of treatment with topical corticosteroids. Careful monitoring of IOP in such individuals is essential. Few randomized, controlled studies are available on the comparative safety and efficacy of common topical corticosteroids in the treatment of post-operative ocular inflammation. Furthermore, the lack of consistent reporting criteria for clinically significant IOP increases across clinical studies makes meaningful comparisons among corticosteroids difficult. This review aims to examine data from available published studies, including studies in steroid responders, to determine whether topical corticosteroids are the same in terms of their effect on IOP. Early generation corticosteroids, such as dexamethasone and prednisolone, are more likely to result in clinically significant increases in IOP. Newer corticosteroids, such as rimexolone and the retro-metabolically designed corticosteroid, loteprednol etabonate, offer similar anti-inflammatory efficacy to older corticosteroids with less effect on IOP. However, randomized controlled trials of newer corticosteroids are needed. The proportion of patients exhibiting an increase of ≥10 mmHg IOP in clinical studies has emerged as the most clinically relevant parameter for ophthalmologists to consider when deciding on which topical corticosteroid to use.

Effects of Thailanstatins on Glucocorticoid Response in Trabecular Meshwork and Steroid-Induced Glaucoma

Elevated intraocular pressure (IOP) is a major risk factor in glaucoma. Various changes in the trabecular meshwork (TM) are responsible for elevated IOP. Glucocorticoids (GCs) increase IOP and mediate biochemical changes in the TM, similar to those associated with primary open-angle glaucoma (POAG). There are differences in steroid responsiveness among the population. Approximately 40% of individuals significantly elevate IOP (i.e., responders) upon GC administration, while others do not (i.e., nonresponders). The responders are at higher risk of developing POAG compared to the nonresponders. In addition, almost all POAG patients are steroid responders. GC responsiveness is regulated by the relative levels of the active GC receptor alpha (GRα) and the alternatively spliced dominant negative regulator isoform GRβ. Glaucomatous TM cell strains have a lower GRβ-GRα ratio compared to normal TM cells, making them more sensitive to GCs. Our purpose was to investigate the role of a special class of natural products called thailanstatins (TSTs) in GR alternative splicing and GC response in cultured human TM cells. Quantitative RT-PCR and Western immunoblotting were used to study the effect of TSTs on GRβ-GRα ratios in human TM cell strains. Effects of TSTs on dexamethasone (DEX) responsiveness were assessed by GRE-luciferase reporter activity assay and fibronectin (FN) induction in TM cells. TSTs increased the GRβ-GRα ratio in TM cells. Increased GRβ-GRα ratios were associated with decreased DEX-mediated FN induction and GRE-luciferase activity. TSTs modulate the GR splicing process to enhance GRβ levels and thereby decrease the GC response in cultured human TM cells. These TSTs, or similar compounds, may potentially be new glaucoma therapeutic agents.

Comparative Genomic and Proteomic Analysis of Cytoskeletal Changes in Dexamethasone-Treated Trabecular Meshwork Cells

Changes in the actin cytoskeleton, especially the formation of cross-linked actin networks (CLANs) are thought to contribute to the increased intraocular pressure observed in primary open-angle and steroid-induced glaucoma. To better understand the effects of glucocorticoids, we employed a shotgun method to analyze global changes in the cytoskeleton and integrin signaling pathways following dexamethasone (DEX) treatment of human trabecular meshwork (HTM) cells. RNA and cell lysates were obtained from HTM cells incubated with or without DEX. Changes in protein expression were determined by mass spectrometry (MS) following differential centrifugation of cell lysates to enrich for low-abundance cytoskeletal and signaling proteins, proteolytic digestion, and a titanium dioxide column to enrich for phosphopeptides. Results were validated by Western blots. Changes in RNA levels were determined with gene arrays and RT-PCR. Overall, MS identified 318 cytoskeleton associated proteins. Five of these proteins (PDLIM1, FGFR1OP, leiomodin-1, ZO-2 and LRP16A) were only detected in DEX-treated cells by MS. However, only PDLIM1 showed a statistically significant increase at the RNA level. Other proteins with differences at both the RNA and protein levels included β3 integrin, caveolin-1, Borg2, raftlin1, PI-3 kinase regulatory subunit α, transgelin, and filamin B. By immunofluorescence microscopy filamin B and PDLIM1 showed enhanced expression in human trabecular meshwork cells, but only PDLIM1 demonstrated significant localization within CLANs. Finally, MS showed that some of the cytoskeleton proteins (Borg2, leiomodin-1, LRP16A, raftlin1 and CKAP4) contained phosphorylated residues. This study suggests that DEX affects the expression of cytoskeleton proteins at the transcriptional and translational level and shows that a combined genomic and proteomic approach can be used for rapid analysis of proteins in the TM. It also shows that DEX altered the expression of components (PDLIM1 and β3 integrins) involved in CLAN formation and provides new findings into the effects of glucocorticoids on the cytoskeleton.

Intraocular pressure elevation and post-DSEK glaucoma after Descemet`s stripping endothelial keratoplasty

Intraocular pressure (IOP) elevation is a common problem in penetrating keratoplasty (PK), and possibly leads to graft failure. IOP elevation and secondary glaucoma may also be present after Descemet`s stripping endothelial keratoplasty (DSEK). This retrospective study analyzes the risk factors for IOP elevation and the functional outcome in those patients with post-DSEK glaucoma. A retrospective analysis of case records of 72 DSEKs between 2007 and 2010 was performed. A total of 59 operated eyes were included. The assessment included the pre-operative history of corneal disease and glaucoma. Furthermore, the response to antiglaucoma treatment, the graft failure, the IOP, and visual acuity development were evaluated. The incidence of IOP elevation was 28.8 % and of post-DSEK glaucoma 11.9 %. Steroid-induced IOP elevation was the most frequent cause, with an incidence of 18.6 %. Patients with pre-existing glaucoma showed a significantly higher risk of developing IOP elevation, steroid-induced glaucoma and post-DSEK glaucoma (p = 0.006, p = 0.023, p = 0.009). In all cases, IOP elevation was treated effectively by tapering down steroid medication and initiating or increasing antiglaucoma medication. Visual acuity after 6 and 12 months improved significantly in cases with and without pre-existing glaucoma (p < 0.0001). After 24 months, clear grafts were achieved in 53 eyes (89.9 %). There was no significant difference in graft failure rates between cases with or without pre-existing glaucoma (p = 0.581) and with or without post-DSEK glaucoma (p = 0.306). IOP elevation after DSEK shows a high incidence. Pre-existing glaucoma increased the risk of developing IOP elevation and post-DSEK glaucoma. Although steroid-induced IOP elevation was the most frequent cause and could be treated effectively by tapering down steroid medication; there are other reasons why post-DSEK glaucoma developed. Management by medical treatment results in good visual acuity and graft survival.

Amyloid Fibril Formation by the Glaucoma-Associated Olfactomedin Domain of Myocilin

Myocilin is a protein found in the extracellular matrix of trabecular meshwork tissue, the anatomical region of the eye involved in regulating intraocular pressure. Wild-type (WT) myocilin has been associated with steroid-induced glaucoma, and variants of myocilin have been linked to early-onset inherited glaucoma. Elevated levels and aggregation of myocilin hasten increased intraocular pressure and glaucoma-characteristic vision loss due to irreversible damage to the optic nerve. In spite of reports on the intracellular accumulation of mutant and WT myocilin in vitro, cell culture, and model organisms, these aggregates have not been structurally characterized. In this work, we provide biophysical evidence for the hallmarks of amyloid fibrils in aggregated forms of WT and mutant myocilin localized to the C-terminal olfactomedin (OLF) domain. These fibrils are grown under a variety of conditions in a nucleation-dependent and self-propagating manner. Protofibrillar oligomers and mature amyloid fibrils are observed in vitro. Full-length mutant myocilin expressed in mammalian cells forms intracellular amyloid-containing aggregates as well. Taken together, this work provides new insights into and raises new questions about the molecular properties of the highly conserved OLF domain, and suggests a novel protein-based hypothesis for glaucoma pathogenesis for further testing in a clinical setting.

Steroid-Induced Iatrogenic Glaucoma

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.

OCULAR MANIFESTATIONS OF TAKAYASU ARTERITIS

To detail the spectrum of eye manifestations in Takayasu arteritis and factors predisposing to its development. In this cross-sectional study, 61 patients with proven Takayasu arteritis who were identified during a 16-month period were evaluated for disease- and treatment-related eye manifestations. A fundus fluorescein angiography examination was performed where indicated and with the patients consent. The mean (±standard deviation) duration of illness before ophthalmic evaluation was 55 ± 69 months. Decreased vision was the most common ocular symptom (30%). Thirty-five patients underwent fundus fluorescein angiography examination. Takayasu retinopathy was seen in 9 (15%), ocular ischemic syndrome in 4 (7%), and hypertensive retinopathy in 10 (16%) patients. The most common treatment-related ocular complication was steroid-induced cataract (23%). Other manifestations included iris neovascularization (n = 3), anterior ischemic optic neuropathy (n = 2), steroid-induced glaucoma (n = 1), neovascular glaucoma (n = 1), and uveitis (n = 1). Those manifesting Takayasu retinopathy and ocular ischemic syndrome had significantly (P < 0.05) lower blood pressure in both upper limbs compared with patients not manifesting ischemic retinopathy. A significant (P < 0.03) proportion of patients with Takayasu retinopathy and ocular ischemic syndrome had a nonrecordable right upper limb blood pressure. Disease- and treatment-related ocular complications are not infrequent in Takayasu arteritis. Arteritis involving the aortic arch and its branches favors the development of ischemic ocular complications.

Komplikationskaskade nach hyperoper LASIK

This report concerns the case of a 28-year-old female patient who was treated with topical steroids for 2 years following complicated hyperopic LASIK surgery with a re-treatment including a re-lift of the flap. A steroid-induced rise in the intraocular pressure (IOP) was subsequently observed on the treated eye, together with a glaucomatous subtotal destruction of the optic nerve, resulting in a residual vision of 1/15. An erroneously low IOP measurement, which was probably the reason for the delay in detecting steroid-induced glaucoma, has been reported in several cases concerning LASIK patients. The reason for the unusually severe course in the case in question can only be presumed, namely a possible accumulation of fluid at the interface or altered biomechanics following hyperopic LASIK surgery. The need for a thorough postoperative examination following refractive surgery must be emphasized. This case shows a cascade of complications following hyperopic LASIK surgery resulting in the functional blindness of one eye.

Success Rates of Trabeculotomy for Steroid-Induced Glaucoma: A Comparative, Multicenter, Retrospective Cohort Study

To evaluate the surgical outcomes of trabeculotomy for steroid-induced glaucoma. Multicenter, retrospective cohort study. At 17 Japanese clinical centers, 121 steroid-induced glaucoma patients who underwent trabeculotomy between 1997 and 2006 were reviewed. Surgical failure was defined by the need for additional glaucoma surgery, deterioration of visual acuity to no light perception, or intraocular pressure ≥21 mm Hg (criterion A) and ≥18 mm Hg (criterion B). Surgical outcomes were compared with those of 108 primary open-angle glaucoma (POAG) patients who underwent trabeculotomy and 42 steroid-induced glaucoma patients who underwent trabeculectomy. Prognostic factors for failure were evaluated using the Cox proportional hazards model. The probabilities of success at 3 years for trabeculotomy for steroid-induced glaucoma vs trabeculotomy for POAG was 78.1% vs 55.8% for criterion A (P = .0008) and 56.4% vs 30.6% for criterion B (P < .0001), respectively. At 3 years, the success of trabeculotomy for steroid-induced glaucoma was comparable to trabeculectomy for steroid-induced glaucoma for criterion A (83.8%; P = .3636), but lower for criterion B (71.6%; P = .0352). Prognostic factors for failure of trabeculotomy for steroid-induced glaucoma were previous vitrectomy (relative risk [RR] = 5.340; P = .0452 on criterion A, RR = 3.898; P = .0360 for criterion B) and corticosteroid administration other than ocular instillation (RR = 2.752; P = .0352 for criterion B). Trabeculotomy is effective for controlling intraocular pressure <21 mm Hg in steroid-induced glaucoma eyes.

Ocular complications of severe vernal keratoconjunctivitis (VKC) in Yemen

Objectives The objective of this study was to assess the ocular complications and visual loss among patients with severe vernal keratoconjunctivitis (VKC). Methods Four hundred and thirty-one patients with VKC seen at Ibn Al-Haitham Eye Center were the study group. This is a retrospective non-comparative observational study between 01 January 2002 and 31 December 2002. Visual acuity was measured with the standard Snellen visual acuity chart and for children under 5 years of age Kay pictures were used. Visual impairment was assessed by means of the World Health Organization criteria for visual disabilities. Cases with severe VKC that developed ocular complications leading to blindness and severe visual impairment were analyzed. Results The majority of VKC patients were males (75.9%) with a male:female ratio of 3.1:1. A total of 68 (15.7%) patients (54 boys and 14 girls) had severe VKC. The ocular findings among 20 patients with severe VKC that led to blindness and severe visual impairment included keratoconus (7); steroid-induced cataract (5), central corneal scars (5) and steroid-induced glaucoma (3). Two of the keratoconus cases developed acute hydrops. Conclusion Severe VKC in developing countries including Yemen is a potentially blinding disease. Visual loss may be due to keratoconus and corneal scars, as well as complications of the unsupervised use of topically administered corticosteroids.

Do reducing regimens of fluorometholone for paediatric ocular surface disease cause glaucoma?

Background/aimsAlthough fluorometholone (FML) is considered a steroid of minimal ocular penetration, reports in children have shown dose-dependent intraocular pressure (IOP) rise. The authors aimed to assess whether reducing regimens of...

Intraocular pressure variation in patients on long-term corticosteroids

Background:Long-term use of topical and systemic steroids produces secondary open-angle glaucoma similar to chronic simple glaucoma. The increased intraocular pressure [IOP] caused by prolonged steroid therapy is reversible but the damage produced by it is irreversible.Materials and Methods:In this study, we analyzed 200 patients with steroid-induced glaucoma, who were on systemic and topical corticosteroids for various dermatological conditions. The variation in IOP caused by different steroid preparations was studied.Results:Two hundred patients who were on systemic steroids for more than 8 weeks developed raised IOP. Three of these patients also developed bilateral posterior subcapsular cataract.Conclusion:We conclude that systemic steroids can induce rise of IOP and cataract formation. If it is not detected and treated in time, rise in IOP can lead to irreversible damage to the eyes.

Inflammatory glaucoma

Glaucoma is seen in about 20% of the patients with uveitis. Anterior uveitis may be acute, subacute, or chronic. The mechanisms by which iridocyclitis leads to obstruction of aqueous outflow include acute, usually reversible forms (e.g., accumulation of inflammatory elements in the intertrabecular spaces, edema of the trabecular lamellae, or angle closure due to ciliary body swelling) and chronic forms (e.g., scar formation or membrane overgrowth in the anterior chamber angle). Careful history and follow-up helps distinguish steroid-induced glaucoma from uveitic glaucoma. Treatment of combined iridocyclitis and glaucoma involves steroidal and nonsteroidal antiinflammatory agents and antiglaucoma drugs. However, glaucoma drugs can often have an unpredictable effect on intraocular pressure (IOP) in the setting of uveitis. Surgical intervention is required in case of medical failure.Method of Literature Search:Literature on the Medline database was searched using the PubMed interface.

Control of steroid-induced glaucoma with surgical excision of sub-Tenon triamcinolone acetonide deposits: A clinical and biochemical approach

Objet: Évaluation de l’efficacité de l’excision chirurgicale des dépôts sousténoniens d’acétonide de triamcinolone (AT) pour contrôler le glaucome induit par les stéroïdes. Nature: Série de cas interventionnels prospectifs et non randomisés. Participants: Dix-huit yeux de 14 sujets qui, ayant une hausse de pression dans les 6 mois suivant une injection d’AT sousténonienne, n'ont pas répondu au traitement médical antiglaucomateux. Méthodes: Sous anesthésie topique, les dépôts de stéroïde ont été entièrement excisés et placés dans de l’alcool éthylique pour déterminer la quantité d’AT par chromatographie liquide à haute performance. Les patients ont été suivis pendant 6 mois et un test t à appariement d’échantillons a servi à comparer la moyenne de PIO avant et après l’excision des dépôts d’AT sousténoniens. Résultats: Les moyennes de PIO avant et après les injections sousténoniennes de stéroïdes étaient 15,9 (ÉT 2,9) mm Hg et 36,4 (ÉT 8,4) mm Hg, respectivement ( p < 0,001). Les niveaux de PIO ont baissé de façon significative après le retrait des dépôts (moyenne 15,3 [ÉT 2,1] mm Hg) ( p < 0,001). Dans les 6 mois de suivi, tous les médicaments pour le glaucome furent arrêtés chez 9 sujets sans autre hausse éventuelle de PIO, alors que chez 5 sujets le contrôle de la PIO a demandé le recours aux médicaments antiglaucomateux. La quantité médianne d’AT était de 7,35 mg (écart 3,3–29,68 mg). La baisse de PIO après l’excision n'a pas montré de corrélation avec la quantité d’AT ( p = 0,8). Conclusions: L’excision chirurgicale des dépôts sousténoniens de stéroïdes devrait être considérée comme traitement primaire pour le glaucome induit par les stéroïdes réfractaire au traitement médical.

Ultrastructural changes of the trabecular meshwork in glucocorticoid induced glaucoma

Steroid-induced glaucoma in rabbit ocular was established to observe the ultrastructural changes in trabecular meshwork,and to preliminarily study the mechanisms of increased resistance of aqueous outflow in steroid-induced glaucoma. Forty New Zealand white rabbits were randomly divided into four groups, namely,control group (n = 10 rats),drops drug group(n = 10 rats), Injecting drug group(n = 10 rats) and drug combination group (n=10 rats). For three consecutive days before the experiment,using the Schitoz's tonometer to measure intraocular pressure(IOP) at 8am, 10am, and 12am each day,obtained the average,and finally calculated basis IOP of these rabbits. The rabbits eyes in drug combination group of were treated with dexamethasone sodium phosphate solution (0.5%)for 8 weeks,three times a day, and given injection of triamcinolone endure (3 mg) weekly. While the rabbits eyes in the control group were treated with sterile saline in the same period of experiment.After 4 days,IOP of the rabbit was measured by Schitoz's tonometer weekly( the IOP was measured at 8am, 10am, 12am each day for the average value).The rabbit whose IOP was more than 21.97 mmHg and continued for one week is regarded a successful animal model as Corticosteroid. After 8 weeks,the eyes of control group and Corticosteroid rabbits was made for Transmission electron microscopy(TEM) specimen which was used to study the ultrastructural of trabecular meshwork cell. 1.The Rabbit-based IOP was (18.082±2.398) mmHg（n=80）,in the drug combination group The IOP of rabbit is up to (24.056±1.245) mmHg after three weeks，which was significantly higher compared with that of(18.254 ± 3.465) mmHg in the control group,the difference had significance(p<0.05),after six weeks, which reached the peak, up to (30.214±0.766) mmHg,in the eighth week, up to (29.144±0.685) mmHg, the IOP of 16 rabbit eyes from 20 rabbit eyes in the exprimental group increased.The positive rate was 80%.2. After treatment with dexamethasone,the abnormality of nucleus of the trabecular meshwork cell was increased, microfilament and microtubules among interstitial cells also increased ,cytoplasmic vacuolation, rough endoplasmic reticulum expansion, as well as an increase in intercellular amorphous material. 1.The glucocorticoid-induced high intraocular pressure rabbit model has been successfully established in drug combination group.2.A series of changes in the cytoskeleton observed under the transmission electron microscopy are an important part of glucocorticoid-induced elevation of intraocular pressure.

Historical Review of Steroid-Induced Glaucoma

This article briefly reviews the literature of steroid-induced ocular hypertension and glaucoma. An insight in the prevalence, risk factors and pathophysiology of this entity can help the clinicians prevent, monitor and treat this secondary form of glaucoma.

Little evidence for association of the glaucoma gene MYOC with open-angle glaucoma

Background/aimTo determine if overexpression of the glaucoma gene MYOC is involved in the development of open-angle glaucoma (OAG) and if its promoter variants are associated with glaucoma in the Korean...

Morphologic Changes in the Outflow Pathways of Bovine Eyes Treated with Corticosteroids

To analyze morphologic changes in the trabecular meshwork (TM) of bovine eyes treated with topical prednisolone and exhibiting elevated intraocular pressure for 4 weeks. The TM of four adult Braford cow eyes treated with 0.5% prednisolone eye drops three times daily for 7 weeks and their contralateral eyes treated with artificial tear preparation and that of two adult untreated Braford cows and untreated young calves eyes were analyzed with light and electron microscopy. Increased extracellular matrix (ECM) under the outflow loops was evaluated quantitatively. Additionally, deparaffinized tissue of treated eyes was labeled with an antibody against type VI collagen for immunocytochemistry. In steroid-treated eyes ECM (plaques) accumulated under the endothelium of the inner wall of the outflow loops. On electron microscopy, this material contained fine fibrils that labeled for type VI collagen. Plaques were also seen in the contralateral controls of the treated animals but here they were significantly less in amount. In the untreated Braford controls and in untreated calf eyes, plaques were nearly absent. In the TM cells of the treated eyes there was a loss of glycogen from the cytoplasm and an increase in basement membrane-like material. These changes were not seen in contralateral eyes or eyes of untreated animals. Accumulations of ECM in the treated eyes resembled morphologic changes in human eyes with primary open-angle glaucoma and steroid-induced glaucoma. This animal model, therefore, provides a good tool in which to further study the pathogenesis of TM changes in glaucoma.

Steroid-induced Glaucoma in Children With Acute Lymphoblastic Leukemia

To evaluate the ocular hypertensive response to repetitive cycles of high-dose systemic corticosteroid in young patients with acute lymphoblastic leukemia (ALL). Five patients up to 6 years of age with ALL who received chemotherapy between November 2003 and March 2005 were examined. As maintenance therapy, they received oral or intravenous dexamethasone 6 to 12 mg/m²/day for 2 weeks, followed by 1-week taparing and 5 weeks break were used in 1 cycle. The duration of maintenance therapy was 15 cycles for 2.5 to 3 years. Comprehensive ophthalmic check-up, including best-corrected visual acuity, intraocular pressure (IOP), and slit-lamp and fundus examinations, were performed. All patients were followed up until final cycle. Symmetrical IOP rise >21 mm Hg was observed in all patients. Right IOP increased to a maximum of mean 39.6 ± 7.2 mm Hg. (range: 28 to 47). The range of cycle to reach a maximal IOP was 5th to 11th. All patients were maintained IOP control with antiglaucoma medications. However, 1 patient already had severe glaucomatous optic atrophy at the time of consultation. Systemic corticosteroid in childhood-ALL treatment has a risk for IOP elevation. Periodical and careful ophthalmic check-up is necessary, especially in patients with dexamethasone.

Sudden refractive change 1 month after phakic intraocular lens implantation

Editor, This letter describes a case of corticosteroid-induced hypertension detected because of a sudden refractive change as late as 1 month following phakic intraocular lens (IOL) implantation with 1-year follow-up data. Sudden astigmatic refractive changes can be caused by a preliminary suture break or cheese-wiring. Usually, a with-the-wound shift occurs 1–3 months after surgery depending on the incision size, location, wound construction and the suture material used. Corticosteroid-induced hypertension is a serious complication that occurs as early as 2 weeks after ocular surgery. It is usually reversible within 3–7 days (Deng et al. 1999) when treatment is limited to a period of less than 12 months (Sapir-Pichhadze & Blumenthal 2003). A 24-year-old woman presented to our refractive clinic with a best-corrected visual acuity (BCVA) of 20/20 with the refraction −8.0–3.5 × 172° (right eye) and −10.0–1.5 × 167° (left eye), intraocular pressure (IOP) 11 mmHg (both eyes) and a regular with-the-rule corneal astigmatism (both eyes) in the corneal topography. Preoperatively, an Nd-YAG-iridotomy was performed in the left eye. Phakic IOL implantation (Verisyse™; AMO, Ettlingen, Germany; −11.5 D) via a 6.1 mm limbal incision closed by a running 10.0-nylon suture was uneventful in the left eye. Dexamethasone 0.1% and ofloxacin four times daily (qid) were given postoperatively. One week after surgery, uncorrected visual acuity was 20/25 and BCVA 20/16 with a refraction of +0.25–1.5 × 148°, IOP 18 mmHg. Examination showed a well-centred phakic IOL with an unremarkable incision suture and no irritation. Local treatment was reduced to dexamethasone twice daily (bid). An uneventful Mitomycin-C-augmented LasEk was performed on the right side. Postoperative fluorometholone 1% was used in the right eye. One month after phakic IOL implantation, the patient presented with a sudden subjective loss of visual acuity on the left phakic IOL side, no other discomfort, an uncorrected visual acuity of 20/32 (decreased), BCVA of 20/16 (unchanged) with refraction of +0.75–1.75 × 100° (astigmatic change of roughly 3 D of cyl in comparison to the previous examination), no irritation, corneal oedema or flare on slit-lamp examination (Fig. 1). Wound architecture and the suture looked perfectly normal. Remarkably, the IOP was 45 mmHg. A quiet eye with a centred phakic iris-claw intraocular lens. Steroid treatment was discontinued; the new treatment was a non-steroidal anti-inflammatory agent three times daily (tid) on the right side, apraclonidine bid on the left side and oral acetazolamide 250 mg bid. Three days later, uncorrected visual acuity was 20/20 and IOP 10 mmHg so oral acetazolamide was discontinued. One week and 1 month after hypertension, IOP was 13 mmHg in the left eye. Apraclonidine treatment was discontinued after 1 month. At the 1-, 3- and 12-month follow-up visits, uncorrected visual acuity remained at 20/20 and BCVA 20/16 with a returned refraction of +0.25–0.75 × 120°. IOP was normal without anti-glaucoma treatment. Slit-lamp examination showed a perfect postoperative situation. At all follow-up visits the right eye showed a normal IOP. This is a rare case of a sudden astigmatic change of almost 3 D cyl as the only presenting manifestation of a corticosteroid-induced hypertension after 1 month of steroid treatment. The condition is definitely related to a large sutured corneal incision relaxed by high IOP. Nowadays a foldable phakic lens design with a sutureless sclerocorneal or clear corneal incision can solve this problem. An extremely large refractive shift (−8.0 D) has been described with malignant glaucoma (Sii & Shah 2006) but no cases similar to ours exist. This case demonstrates the difference between weak (fluorometholone right eye) and strong (dexamethasone left eye) steroids on IOP. In conclusion, the case presented illustrates that a sudden change in refraction as late as 1 month after the implantation of a phakic IOL could be the first manifestation of a late-onset, steroid-induced glaucoma.