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membrane is thickened from the progressive accumulation of lipid or lipoprotein deposits, leading to increased hydro- phobic resistance to the normal active transport of fluid and resulting in fluid accumulation beneath the RPE. These hypotheses concerning the pathogenesis of PED are believed not to be mutually exclusive.8

The visual prognosis for patients with CNV-associated PED may be especially poor. In a study that followed 55 eyes of 53 patients for an average of 2.2 years, 62% of patients were reported to have lost 6 or more lines of vision, with 75% having a final visual acuity of 20/200 or worse.9 Elman et al10 reported in a retrospective analysis of the natural history of PED in patients without CNV that 52% of patients maintained an initial visual acuity of 20/20–20/40 through an average of 32.8 months.10 Another study involving 101 eyes reported a similar course of vision loss irrespective of PED type.11 Although patients without CNV may have a better prognosis at the onset, they are at high risk of developing CNV and sub- sequent vision loss. In the Elman et al study,10 32% of patients eventually developed CNV while in another series,12 67% of patients with serous PED developed CNV after a maximum of 19 months. Since serous PED may obscure the extent of any existent CNV, it should be noted that proper assessment of patients with sub-RPE fluid is often rendered difficult.1

The management of AMD patients with PED is contro- versial due to the difficulty in determining the presence of associated CNV and the inability to reliably identify those patients with serous PED who are likely to develop CNV and experience severe vision loss. In addition, treatment options for PED are limited and usually of poor outcome. While one trial13 of angiographically directed laser pho- tocoagulation involving 35 eyes reported stabilization or improvement of vision in 60%, other attempts14,15 with both unguided and guided photocoagulation reported much infe- rior results, with treated eyes faring worse than untreated controls. Results of studies of photodynamic therapy (PDT) with verteporfin have also not been encouraging. Although patients with PED were not specifically studied in either the Treatment of Age-related Macular Degeneration with Pho- todynamic Therapy (TAP) or Verteporfin in Photodynamic Therapy (VIP) trials,16,17 a recent study18 enrolling lesions of 2 months’ duration found that 60% of patients had improved or stabilized vision over a 16-month follow-up. In contrast, other groups19,20 have reported that PDT with verteporfin conferred little treatment benefit, even when combined with intravitreal triamcinolone acetonide.21 In these trials, treatment was also complicated by subretinal hemorrhage and RPE tears.


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Based on the suboptimal treatment outcomes with laser and PDT with verteporfin there is a need for a therapeutic approach that improves the prognosis of PED secondary to AMD. One promising avenue involves agents that inactivate vascular endothelial growth factor (VEGF), the most potent known promoter of angiogenesis22 and vascular permeability23 both of which appear to play a role in the pathogenesis of PED. Two intravitrealVEGF antagonists indicated for the treatment of all angiographic subclasses of CNV are commercially available: pegaptanib, an RNA aptamer, which has high affinity and speci- ficity for the 165 amino acid isoform of VEGF while sparing VEGF121,24,25 and ranibizumab, an Fab antibody fragment that inactivates all VEGF isoforms.26–28 In addition, bevacizumab, an antibody related to ranibizumab, which is indicated for intravenous treatment of cancer in combination with chemo- therapeutic agents (see prescribing information at: http://www. gene.com/gene/products/information/oncology/avastin/ insert. jsp# indications) and which also inactivates allVEGF isoforms, has been used in off-label studies to treat neovascular AMD.29 The present pilot study examined the effectiveness of pegap- tanib and bevacizumab in the treatment of PED associated with occult CNV secondary to AMD. The results are encouraging and merit further study in an appropriately designed random- ized clinical trial.


This prospective, comparative, nonrandomized pilot study included patients with PED comprising 50% of the total lesion in the subfoveal location. Eligible patients had visual acuity between 20/40 and 20/400, and lesions that either had not been treated previously or had been treated only with PDT with verteporfin. Visual acuity (Early Treatment Dia- betic Retinopathy Study [ETDRS]), a complete ophthalmic examination, indocyanine green angiography, fluorescein angiography, and optical coherence tomography (OCT) were evaluated at baseline. Examinations were completed 5–7 days before the administration of the first intravitreal injection.

The first seven patients presenting with PED received intravitreal injections of commercially available pegaptanib sodium 0.3 mg (Macugen®; [OSI] Eyetech, Inc and Pfizer Inc, New York, USA). The following eight patients received intravitreal injections of bevacizumab 1.25 mg in 0.05 mL prepared in a sterile compounding environment by the pharmacy service of our hospital. Injection procedures were identical for both therapies and included use of povidone iodine 5%, a sterile drape and gloves, and an eyelid speculum. Follow-up visits for each patient occurred every 4 to 6 weeks for 6 months. Each visit included a complete ophthalmic

Clinical Ophthalmology 2010:4

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