Refractory Cystoid Macular Edema Research Articles

Werner syndrome with refractory cystoid macular edema and immunohistochemical analysis of WRN proteins in human retinas

BackgroundTo present our findings in a case of Werner syndrome with refractory cystoid macular edema (CME) and to determine the expression and the distribution of WRN proteins in human retinas.Case presentationA 35-year-old man with Werner syndrome who developed CME after YAG laser treatment was studied. Optical coherence tomographic (OCT) scans were used to examine the CME in the right eye. The patient received topical eye drops (0.1% bromfenac sodium hydrate twice daily and 1% dorzolamide hydrochloride thrice daily), sub-Tenon triamcinolone injection thrice, intravitreal bevacizumab injection twice, and pars plana vitrectomy of the right eye. Genetic analyses were performed to diagnose the disease. To examine the expression and distribution of WRN proteins in the retinas, immunohistochemistry for WRN proteins was performed in human retinas. The CME in the right eye was not improved by any of the treatments. During the follow-up period, CME developed in the left eye. Genetic analyses detected compound heterozygosity, Mut4 and Mut11, in the WRN gene and the individual was diagnosed with Werner syndrome. Immunohistochemical analysis of WRN proteins expression in human retinas showed that WRN proteins were expressed in the parts of the Müller cells in the inner nuclear layer and outer nuclear layer.ConclusionPatients with Werner syndrome can develop severe CME after laser treatment. A pathological link may exist between mutations in the WRN gene and the development of CME in patients with Werner syndrome.

Anti-TNF-α agents for refractory cystoid macular edema associated with noninfectious uveitis

The use of anti-tumor necrosis factor (TNF)-α agents for uveitis has been increasing since the first efficacy studies in 2004. However, information on their specific role in cystic macular edema remains sparse. The aim of this study was to evaluate the efficacy of anti-TNF-α agents for the treatment of uveitis-related refractory cystoid macular edema. The files of 23 consecutive patients treated for cystoid macular edema at the uveitis services of two tertiary medical centers in 2006-2011 were reviewed for demographic data, visual acuity, and optical coherence tomography measurements at baseline and 3, 6, and 12 months after treatment. Changes in mean visual acuity and macular thickness were analyzed. Findings were compared between patients treated with a conventional immunosuppressive regimen only (n = 18, 27 eyes) and patients treated with an anti-TNF-α agent after proving refractory to conventional treatment (n = 9, 15 eyes). Mean duration of cystoid macular edema before initiation of anti-TNF-α therapy was 12 ± 8 months. The two groups had similar baseline values of mean central macular thickness and visual acuity. Significant improvement in macular thickness was noted at 3 months in both groups, with a maximal effect at 6 months for the anti-TNF-α group (p = 0.002). Maximal improvement in visual acuity was achieved at 3 months in both groups, with a reduced effect towards 12 months. Mean visual acuity at 12 months was similar in both groups. Anti-TNF-α agents may serve as an effective lasting treatment for long-standing refractory uveitis-related cystoid macular edema. Their role as first-line therapy in this setting warrants further investigation.

INTRAVITREAL DICLOFENAC VERSUS INTRAVITREAL TRIAMCINOLONE FOR THE TREATMENT OF UVEITIC CYSTOID MACULAR EDEMA.

PURPOSE:: To compare the effect of intravitreal diclofenac (IVD) versus intravitreal triamcinolone (IVT) on refractory uveitic cystoid macular edema. METHODS:: In this pilot, randomized, clinical trial, 15 eyes were randomly assigned to IVD group, patients (8 eyes) who received a single intravitreal injection of diclofenac (500 μg/0.1 mL), and IVT group (7 eyes) patients who received a single intravitreal injection of triamcinolone (2 mg). Change in best-corrected visual acuity in logarithm of the minimum angle of resolution at Week 36 was the primary outcome measure. Secondary outcomes included changes in best-corrected visual acuity (BCVA) at 12 weeks and 24 weeks, central macular thickness, macular leakage, and potential injection-related complications. RESULTS:: In the IVD group, BCVA was more than the baseline values in 4 eyes at 36 weeks; however, within-group analysis disclosed no statistically significant changes in the mean BCVA in this group. Nonetheless, in the IVT group, mean BCVA improved significantly at 12, 24, but not at 36 weeks compared with the baseline values. It was 0.86 ± 0.37 at baseline and 0.63 ± 0.48, 0.62 ± 0.42, and 0.43 ± 0.49 logarithm of the minimum angle of resolution at 12, 24, and 36 weeks, respectively. Mean central macular thickness diminished also significantly only in the IVT group. Nevertheless, comparing the mean BCVA and central macular thickness changes, macular leakage, and the occurrence of any injection-related complications, no significant difference was observed between the groups at any of the follow-up visits. CONCLUSION:: This pilot study demonstrated the superiority of IVT over IVD in the treatment of refractory uveitic cystoid macular edema regarding both functional and anatomical outcomes. Further studies are warranted to confirm potential benefit of IVD observed in this study.

A Pilot Study of Intravitreal Diclofenac versus Intravitreal Triamcinolone for Uveitic Cystoid Macular Edema

Purpose: To compare the effect of intravitreal diclofenac (IVD) versus intravitreal triamcinolone (IVT) on refractory uveitic cystoid macular edema (CME).Methods: In this pilot randomized clinical trial, 15 eyes were randomly assigned to an IVD group, patients (8 eyes) who received a single intravitreal injection of diclofenac (500 μg/0.1 mL), and an IVT group (7 eyes), cases who received a single intravitreal injection of triamcinolone (2 mg). Change in best-corrected VA in logMAR at week 36 was the primary outcome measure. Secondary outcomes included changes in best-corrected visual acuity (BCVA) at 12 and 24 weeks, central macular thickness (CMT), macular leakage, and potential injection-related complications.Results: In the IVD group, BCVA was more than the baseline values in 4 eyes at 36 weeks; however, within-group analysis disclosed no statistically significant changes in the mean BCVA in this group. Nonetheless, in the IVT group, mean BCVA improved significantly at 12, 24, and 36 weeks compared to the baseline values. It was 0.86 ± 0.37 at baseline and 0.63 ± 0.48, 0.62 ± 0.42, and 0.43 ± 0.49 logMAR at 12, 24, and 36 weeks, respectively. Mean CMT reduction diminished also significantly only in the IVT group. Nevertheless, comparing the mean BCVA and CMT changes, macular leakage, and the occurrence of any injection-related complications, no significant difference was observed between the groups at any of the follow-up visits.Conclusion: This pilot study demonstrated the superiority of IVT over IVD in the treatment of refractory uveitic CME regarding both functional and anatomical outcomes. Further studies are warranted to confirm potential benefit of IVD observed in this study.

Intravitreal and subtenon depot triamcinolone as treatment of retinitis pigmentosa associated cystoid macular edema.

We present a case of retinitis pigmentosa (RP) related cystoid macular edema (CME) refractory to oral acetazolamide and topical ketorolac that was treated with intravitreal and subtenon depot triamcinolone. A 32-year-old male with RP presented with complaints of bilateral decrease in visual acuity. His best-corrected visual acuity (BCVA) was 20/50 in the right eye and 20/100 in the left eye. After being informed of the available treatment options, the patient received bilateral intravitreal injection triamcinolone. The patient's BCVA improved to 20/40 in the right eye and 20/50 in the left eye and the CME was resorbed. However, 5 months after the injection in the left eye and two months in the right eye, visual acuity decreased due to recurrence of CME. We performed a second intravitreal injection in the left eye with improvement of visual and anatomic results, but we observed a recurrence of CME. Afterwards, we treated the patient with subtenon depot triamcinolone in both eyes, with the result that there was no recurrence after 4 months in OD or after 3 months in OS. We conclude that intravitreal and subtenon depot triamcinolone appear to provide at least temporary benefit in refractory CME as regards the improvement of visual acuity.

Werner syndrome accompanied with refractory CME and WRN proteins expression in human retinas

AbstractPurpose To present a case of Werner syndrome accompanied with refractory cystoid macular edema (CME), and analyze the expression and the distribution of WRN proteins in human retinas.Methods A 35‐year‐old individual with Werner syndrome exhibited CME after YAG laser treatment. Optical coherence tomography (OCT) scans were indicative of CME in the right eye. The patient received topical eye drops (0.1% bromfenac sodium hydrate twice daily and 1% dorzolamide hydrochloride thrice daily), sub‐Tenon triamcinolone injection thrice, intravitreal bevacizumab injection twice, and pars plana vitrectomy in the right eye. Genetic analyses were performed to conduct diagnosis of the individual. To examine the expression and distribution of WRN proteins in the retinas, immunohistochemistry for WRN proteins in human retinas was performed.Results CME in the right eye could not be improved by any of the treatment. During the follow‐up period, CME developed in the left eye. Genetic analyses detected compound heterozygosity of Mut4 and Mut11 in WRN gene and the individual was diagnosed with Werner syndrome. Immunohistochemical analysis of WRN proteins expression in human retinas indicated that WRN proteins were expressed in Müller cells of the inner nuclear layer and the outer nuclear layer.Conclusion Patients with Werner syndrome may develop severe CME. A pathological link may exist between the potential mutation in WRN gene and the development of CME in patients with Werner syndrome.

Intravitreal infliximab for refractory pseudophakic cystoid macular edema: results of the Pan-American Collaborative Retina Study Group

Inflammation is the major etiologic factor in the development of pseudophakic cystoid macular edema (CME). Several soluble mediators of inflammation such as tumor necrosis factor alpha (TNF-α) have been implicated in the pathogenesis of ocular inflammation. The purpose of this study is to report the short-term visual and anatomic outcomes following intravitreal injections of infliximab in eyes with refractory CME secondary to cataract surgery. An interventional, retrospective study of 7 eyes with refractory CME that were injected with 1 mg of infliximab. The main outcome measures were best-corrected visual acuity (BCVA) and central macular thickness (CMT) at 6-month follow-up. At the 6 month follow-up, BCVA improved from 1.14 ± 0.59 logMAR at baseline to 0.51 ± 0.35 logMAR (p = 0.0156). CMT also improved from 584 ± 159 μm at baseline to 327 ± 127 μm at 6 months (p = 0.0111). No systemic adverse events were reported in these patients. There was a single episode of uveitis that responded to topical steroids. Inhibition of TNF-α may be beneficial in the treatment of refractory pseudophakic CME.

Interferon alpha 2b in the Treatment of Uveitic Cystoid Macular Edema

Purpose: To determine the efficacy of interferon alpha 2b in the treatment of refractory, uveitic cystoid macular edema (CME).Methods: Retrospective chart review of 4 patients attending the uveitis clinic at the Casey Eye Institute, Oregon Health & Science University.Results: All 4 patients had uveitis and refractory CME, resistant to a variety of immunosuppressants. All patients, except one with severe scleral thinning, had tried and failed therapy with locally injected corticosteroids. Treatment with systemic interferon alpha 2b produced dramatic improvement in CME (central macular thickness: 563 to 267 µm, p = .002) and visual acuity (logMAR: +0.81 to +0.45, p = .0004) in all 4 cases. All patients have been able to reduce the interferon dosage, but none has discontinued it completely. All patients had some mild adverse response that did not necessitate stopping therapy.Conclusions: Interferon alpha 2b is an effective option to treat refractory CME secondary to uveitis.

Ranibizumab in a patient with refractory uveitis-related cystoid macular edema – a case report

BACKGROUND: A case report about a patient with refractory uveitis-related cystoid macular edema (CME), that could be treated sucessfully with ranibizumab. MATERIAL AND METHODS: 0,5 mg intravitreal ranibizumab was injected monthly via pars plana, when needed. Need of injection was defined by CME in OCT. RESULTS: After 8 intravitreal injections of ranibizumab CME was resorbed and stayed without recurrence since 7 months. CONCLUSIONS: Ranibizumab has the potential to reduce uveitis-related CME and to improve vision.

Intravitreal Adalimumab for Refractory Uveitis-Related Macular Edema

To evaluate the safety and efficacy of intravitreal adalimumab injections on refractory cystoid macular edema (CME) secondary to noninfectious uveitis. Prospective, noncomparative, interventional case series. Eight consecutive patients with controlled uveitis and chronic, refractory CME who had failed steroid treatment. Intravitreal adalimumab injections were given monthly for 3 months. Mean change in central retinal thickness (CRT) on optical coherence tomography (OCT); secondary objective was the mean change in best-corrected visual acuity (BCVA). Five of the eight patients completed the 6-month follow-up. For all 5 patients, the changes in BCVA from baseline to 3 months were not statistically significant (P=0.070). Similarly, the change in BCVA from baseline to 6 months was not statistically significant (P=1.0). The mean CRT at baseline was 692 microm. The changes from baseline to 3 months were not statistically significant (P=0.466); the changes from baseline to 6 months were also not statistically significant (P=0.808). We did not observe any ocular or systemic adverse effects. Intravitreal adalimumab showed no efficacy in improving BCVA or reducing CRT in patients with chronic uveitic macular edema.

Intravitreal Bevacizumab Versus Triamcinolone Acetonide for Refractory Uveitic Cystoid Macular Edema: A Randomized Pilot Study

To compare intravitreal bevacizumab (IVB) versus intravitreal triamcinolone acetonide (IVT) for treatment of refractory uveitic cystoid macular edema (CME). In this randomized clinical trial, 31 eyes with uveitic CME were allocated into the IVB group-eyes that received 1-3 injections of 1.25 mg bevacizumab (15 eyes) and the IVT group-eyes that received 1-3 injections of 2 mg triamcinolone (16 eyes). Primary outcome measure was change in best-corrected visual acuity (VA) at 36 weeks. Visual acuity improvement compared with baseline values was meaningful in the IVB group at 12, 24, and 36 weeks (-0.35 + or - 0.45 logMAR [P = 0.016]) and in the IVT group at 24 and 36 weeks (-0.32 + or - 0.32 logMAR [P = 0.001]). A significant central macular thickness (CMT) reduction was observed only in the IVT group at week 36 (74.6 + or - 108.0 microm [P = 0.049]). Between-group analysis disclosed no significant difference in any outcome measure. By statistically removing the factor of cataract, the IVT group had more improvement in VA (P = 0.007). IVB was as effective as IVT in refractory uveitic CME regarding VA improvement up to 36 weeks. Irrespective of triamcinolone-induced cataract, a more beneficial effect of IVT may be attainable.

Short-term Results of a Single Intravitreal Bevacizumab (Avastin) Injection versus a Single Intravitreal Triamcinolone Acetonide (Kenacort) Injection for the Management of Refractory Noninfectious Uveitic Cystoid Macular Edema

Purpose: To report the short-term results of a single intravitreal injection of bevacizumab (IVB) versus a single intravitreal injection of triamcinolone acetonide (IVT) to treat refractory noninfectious uveitic cystoid macular edema (CME).Methods: Twenty-eight consecutive patients (36 eyes) were retrospectively included. Patients received either 2.5 mg of IVB (16 eyes) or 4 mg of IVT (20 eyes).Results: In the IVT group, baseline best-corrected visual acuity (BCVA) was logMAR 1.1 ± 0.2, and improved to 0.7 ± 0.3 (p < .001) at 6 months. In the IVB group, baseline BCVA was logMAR of 1.2 ± 0.4 and improved to 0.8 ± 0.4 at 6 months (p = .031). At 6 months, central macular thickness (CMT) in the IVT group improved from 454.8 ± 238.9 μm to 296 ± 134.4 μm (p < .0001).Conclusion: A single IVT injection improves BCVA and reduces CMT more effectively than IVB in refractory noninfectious uveitic CME at 6 months.

Intravitreal Bevacizumab for Refractory Pseudophakic Cystoid Macular Edema: The Pan-American Collaborative Retina Study Group Results

To determine the feasibility, safety, and clinical effect of intravitreal (IVT) bevacizumab (Avastin; Genentech, Inc., San Francisco, CA) in patients with refractory cystoid macular edema (CME) after cataract surgery. Interventional, retrospective, multicenter study. Thirty-six eyes of 31 patients with refractory CME after cataract surgery and with a mean age of 68.2 years (range, 67-87 years). Patients were treated with at least 1 IVT injection of 1.25 or 2.5 mg bevacizumab. Patients were followed up for 12 months. Best-corrected visual acuity (BCVA) and central macular thickness (CMT) by optical coherence tomography (OCT). Twenty-six eyes (72.2%) demonstrated improvement of BCVA (> or =2 Early Treatment Diabetic Retinopathy Study [ETDRS] lines), and no eye experienced worsening of visual acuity (> or =2 ETDRS lines). Mean baseline BCVA was 20/200 (0.96 logarithm of the minimum angle of resolution [logMAR] units), and the mean 12-month BCVA was 20/80 (0.62 logMAR units; P<0.0001). Optical coherence tomography demonstrated that mean CMT at baseline was 499.9 microm (range, 298-784 microm) and decreased to a mean of 286.1 microm (range, 168-499 microm) at 12 months (P<0.0001). Four (11%) eyes received 2 injections, 10 (27.8%) eyes received 3 injections, 10 (27.8%) eyes received 4 injections, 1 (2.8%) eye received 5 injections, and 1 (2.8%) eye received 6 injections. The mean number of injections was 2.7 (range, 1-6), and the mean interval between injections was 15.1 weeks (range, 4-45 weeks). No ocular or systemic adverse events were observed. Short-term results suggest that IVT bevacizumab is well tolerated in patients with refractory pseudophakic CME. Treated eyes had a significant improvement in BCVA and decrease in macular thickness by OCT at 12 months.

Ranibizumab for Refractory Uveitis-related Macular Edema

To evaluate the effect of intravitreal ranibizumab injections (Lucentis; Genentech Inc, South San Francisco, California, USA) on refractory cystoid macular edema (CME) in patients with controlled uveitis who have failed oral and regional corticosteroid treatment, the mainstays of current medical therapy. Prospective, noncomparative, interventional case series. Seven consecutive patients with controlled uveitis and refractory CME who had failed corticosteroid treatment were studied. One eligible patient chose not to participate and another did not complete follow-up for nonmedical reasons. Intravitreal ranibizumab injections (0.5 mg) were given monthly for 3 months, followed by reinjection as needed. The primary outcome was the mean change in best spectacle-corrected visual acuity (VA) from baseline to 3 months, and the secondary objective was the mean change in central retinal thickness (CRT) on ocular coherence tomography. Six-month outcomes were also assessed. At 3 months, the mean increase in acuity for the 6 patients who completed follow-up was 13 letters (2.5 lines), and the mean decrease in CRT was 357 mum. Both VA and CRT improved significantly between baseline and 3 months (P = .03 for each). Although most patients required reinjection, this benefit was maintained at 6 months. There were no significant ocular or systemic adverse effects. Intravitreal ranibizumab led to an increase in VA and regression of uveitis-associated CME in patients refractory to or intolerant of standard corticosteroid therapy. Further studies of this promising treatment are warranted.

SHORT-TERM SAFETY AND EFFICACY OF INTRAVITREAL BEVACIZUMAB FOR PSEUDOPHAKIC CYSTOID MACULAR EDEMA

: To determine the feasibility, safety, and clinical effect of intravitreal bevacizumab (Avastin) in patients with refractory cystoid macular edema after uncomplicated cataract surgery. : Ten eyes of 10 patients affected by pseudophakic cystoid macular edema refractory to medical treatment treated with at least one intravitreal injection of 1.25 mg of bevacizumab were enrolled in the study. Follow-up visits included Early Treatment Diabetic Retinopathy Study visual acuity testing, optical coherence tomography imaging, and ophthalmoscopic examination. : The follow-up was 6 months. All eyes had improved best corrected visual acuity, and no eye had worse visual acuity (>/=2 Early Treatment Diabetic Retinopathy Study lines). The mean baseline best corrected visual acuity was 20/80 and the mean final best corrected visual acuity 20/32, the difference was statistically significant (P < 0.0001). The mean central macular thickness at baseline (546.8 mm; range, 359-720 mm) decreased significantly (228.7 mm; range, 190-280 mm) by the end of follow-up (P < 0.0001). No ocular or systemic adverse events were observed. : Short-term results suggest that intravitreal bevacizumab is safe and well tolerated in patients with pseudophakic cystoid macular edema. Treated eyes had a significant improvement in best corrected visual acuity and decrease in macular thickness by optical coherence tomography.

Efficacy and complications of intravitreal injection of triamcinolone acetonide for refractory cystoid macular edema associated with intraocular inflammation

To assess the effects and complications of intravitreal injection of triamcinolone acetonide (IVTA) for posterior sub-Tenon injection of triamcinolone acetonide (PSTA)-resistant cystoid macular edema (CME) with intraocular inflammation. Medical records of eight eyes of six patients with PSTA-resistant CME were retrospectively examined. Each eye received a 4-mg IVTA, and an additional injection was performed when CME recurred. Visual acuity as logarithm of the minimum angle of resolution (logMAR), intraocular pressure (IOP), and central macular thickness (CMT) were assessed before and after each treatment. CME improved in six eyes (75%) with mean visual acuity recovering from 0.56+/-0.29 to 0.41+/-0.195 (logMAR, P=0.13) and mean CMT decreasing from 470 microm (range, 275-660 microm) to 297 microm (range, 150-697 microm) (P=0.04) 2 months after the initial IVTA. CME recurred an average of 9 months (range, 5-11 months) after IVTA. A higher dose (16-mg) IVTA was effective for two eyes refractory to repeated 4-mg IVTA. IOP was elevated in two eyes (25%), of which one required filtration surgery (12.5%). In phakic eyes, cataracts progressed and necessitated surgery. IVTA is effective for PSTA-resistant CME with intraocular inflammation, and its efficacy might be dose dependent.

Intravitreal pegaptanib sodium for refractory pseudophakic macular oedema

Evaluate the efficacy of intravitreal pegaptanib sodium (Macugen) in refractory pseudophakic cystoid macular oedema (CME). Prospective, nonrandomized, interventional case series. Four eyes of four patients with refractory pseudophakic CME to pars plana vitrectomy and intravitreal bevacizumab and triamcinolone, were treated with pegaptanib sodium, with a mean follow up of 4 months. Pre- and postinfection examinations included assessment of best-corrected visual acuity (BCVA) using the Early Treatment Diabetic Retinopathy Study chart (ETDRS), fluorescein angiography (FA), and optical coherence tomography (OCT). Visual acuity increased in all patients after intravitreal pegaptanib sodium. OCT showed improvement of the retinal thickness in the macular area. Intravitreal pegaptanib sodium (Macugen) is a promising treatment for pseudophakic cystoid macular oedema resistant to other medical treatment strategies. However, further study is needed to assess the treatment's long term efficacy and the need for retreatment.

INTRAVITREAL BEVACIZUMAB (AVASTIN) AS A TREATMENT FOR REFRACTORY MACULAR EDEMA IN PATIENTS WITH UVEITIS

: Bevacizumab is a monoclonal antibody to vascular endothelial growth factor (VEGF) which has been successfully used for the treatment of age-related macular degeneration with choroidal neovascularization. As VEGF is involved in the pathomechanisms of inflammation and endothelial dysfunction the authors used bevacizumab as a last resort treatment in patients with persistent uveitic cystoid macular edema (CME). : Persistent uveitic CME was defined by optical coherence tomography (OCT) measurements >250 mum despite previous treatments. The authors reviewed patients with persistent CME who subsequently had been treated with intravitreous bevacizumab 1.25 or 2.5 mg. Improvement was judged by visual acuity (VA) gain >/=2 lines and thickness reduction in OCT. : Eleven eyes of 10 patients were injected since February 2006. Median follow-up was 70 days. Reduction in central retinal thickness could be seen as early as 2 weeks with a mean foveal thickness reduction of 127.2 mum at 4 weeks. Concurrent improvement in VA was seen in 4 of 10 patients, and was unchanged in the others. Four patients received two injections and five patients received three injections. Except for progression of cataract in one eye no ocular or systemic adverse events were recorded. : Intravitreal bevacizumab seems to be an effective and safe treatment in the management of refractory inflammatory CME. The effect is transient, and reinjections may be necessary, although the time until reinjection is needed differs individually.

Intravitreal Pegaptanib Sodium for Irvine-Gass Syndrome

To report the novel use of intravitreal pegaptanib sodium for the treatment of refractory cystoid macular edema (CME) following cataract extraction. A 72-year-old man presented with decreased visual acuity in his right eye 8 months after uncomplicated phacoemulsification cataract extraction and intraocular lens implantation. His bestcorrected visual acuity (BCVA) was 20/125 in the affected eye, and fundus examination revealed CME despite 6 months of oral and topical indomethacin therapy. Fluorescein angiography (FA) showed leakage in the central region with no signs of neovascularization, and optical coherence tomography (OCT) confirmed the diagnosis with thickening of the fovea. Because of his history of glaucoma, the patient chose to be treated with intravitreal pegaptanib sodium 0.3 mg. At the 1-week follow-up, BCVA was 20/25, and the FA and OCT revealed almost total resolution of the CME with no adverse sequelae. Six months postinjection, the patient's BCVA remained 20/25 with no recurrence of CME. Perimetry revealed a stable fixation within 4 degrees with slight reduction of sensitivity. Vascular endothelial growth factor inhibition with intravitreal pegaptanib sodium appears to be of benefit in the treatment of chronic refractory CME with improvement of visual acuity. Studies evaluating pegaptanib''s use in this setting with long-term follow-up are warranted to confirm its efficacy and safety.

INTERFERON ALFA-2A: A NEW TREATMENT OPTION FOR LONG LASTING REFRACTORY CYSTOID MACULAR EDEMA IN UVEITIS?

To perform a prospective pilot study to evaluate interferon alfa-2a (IFN alfa-2a) for the treatment of refractory cystoid macular edema (CME) in endogenous uveitis. IFN alfa-2a was administered at an initial dose of 3 or 6 million IU (depending on body weight) per day subcutaneously. Afterwards IFN alfa-2a was tapered slowly over 6 months and finally discontinued. If CME relapsed IFN alfa-2a was reinstituted and tapered slowly again to evaluate the lowest maintenance dose to keep remission. A total of 15 eyes of 8 patients with refractory CME due to intermediate or posterior uveitis were included. Ineffective pretreatment consisted of systemic steroids and acetazolamide (all patients) and at least one additional immunosuppressant (6 patients). Six of 8 patients (11 eyes) responded well to IFN alfa-2a and CME resolved completely during 6 months treatment. One patient was lost to follow-up after IFN alfa-2a was stopped. In 1 patient (1 eye) even 19 months after cessation of IFN alfa-2a no recurrence of CME occurred. In 4 patients (8 eyes) IFN alfa-2a had to be reinstituted because CME relapsed. All 4 patients responded again. During a mean follow-up period of 16.4 months since restart of therapy we succeeded in all 4 patients to taper IFN alfa-2a to maintenance doses between 1.5 million IU every second and every sixth day without a recurrence of CME in any of the 8 eyes. IFN alfa-2a can be a treatment option for patients with otherwise treatment resistant uveitic CME.