Lucentis for Treatment of Macular Edema (FVF4153s)
Cystoid macular edema (CME) is the most common cause of suboptimal post-operative visual acuity in uncomplicated cataract extractions. Over two million cataract extractions are performed each year, with a reported incidence ranging from 1.5 to 6.9%, resulting in an estimated 20,000-130,000 new cases of CME annually. Clinical CME historically was associated with visual acuity of 20/40 or worse with fluorescein angiographic evidence of macular edema in a classic petaloid pattern. Angiographic CME physiologically signals an inflammatory process causing distortion of the outer plexiform layer, which if not resolved quickly could result in non-repairable visual loss. Topical, periocular, or intravitreal corticosteroids, despite their associated side effects, are the mainstay for pharmacologic treatment for patients with CME. Their efficacy has never been demonstrated in a randomized, controlled and blinded study.
This is an open-label, Phase II study of intravitreally administered ranibizumab in subjects with cystoid macular edema secondary to non-ischemic retinopathy, as seen following cataract surgery with intraocular lens implantation.
Cystoid Macular Edema
|Study Design:||Observational Model: Case-Only
Time Perspective: Retrospective
|Official Title:||A Single-center Phase 2 Trial of Intravitreous Injections of Lucentis (Ranibizumab) in Subjects With Cystoid Macular Edema Secondary to Non-ischemic Retinopathy|
- To evaluate the safety and tolerability of ranibizumab in patients with CME secondary to non-ischemic retinopathy [ Time Frame: 2 years ] [ Designated as safety issue: No ]
- Mean change in best corrected visual acuity (BCVA), as assessed by the number of letters read correctly on the ETDRS eye chart, at each month of months 0-12. [ Time Frame: 2 years ] [ Designated as safety issue: No ]
- Proportion of subjects who remained at baseline VA or gained >0 lines of vision from baseline to week 24 and 52. [ Time Frame: 2 years ] [ Designated as safety issue: No ]
- Mean change in central retinal thickness on OCT 3 from Baseline to week 24 and 52. [ Time Frame: 2 years ] [ Designated as safety issue: No ]
- Changes observed on the Fluoreosceiien Angiographs from baseline to week 24 and 52. [ Time Frame: 2 years ] [ Designated as safety issue: No ]
- Mean number of ranibizumab injections required. [ Time Frame: 2 years ] [ Designated as safety issue: No ]
- Nidek MPI measurements taken at baseline, week 24, and week 52 [ Time Frame: 2 years ] [ Designated as safety issue: No ]
- Proportion of subjects who demonstrate complete resolution of macular edema as seen on OCT testing from baseline to week 52 [ Time Frame: 2 years ] [ Designated as safety issue: No ]
|Study Start Date:||May 2007|
|Study Completion Date:||December 2009|
|Primary Completion Date:||December 2009 (Final data collection date for primary outcome measure)|
Vascular endothelial growth factor (VEGF) is known to be induced by hypoxia and has been implicated in the development of iris and retinal vascularization. VEGF, however, is also known to be a potent mediator of vascular permeability in other tissues and may perform this function in retina.
Immunohistochemical VEGF staining has been identified in patients with disorders such as aphakic and pseudophakic cystoid macular edema, ocular inflammatory disease and infection. VEGF was primarily localized within retinal neurons and within the retinal pigment epithelium in these cases. In addition or in association with its role of inducing neovascularization (Wet AMD and diabetic retinopathy, VEGF may contribute to the breakdown of the blood-retinal barrier in a variety of disorders.
Ranibizumab is a pan-VEGF A blocker that has been proven highly effective for the treatment of wet macular degeneration. The underlying pathophysiology of both cystoid macular edema and wet AMD is VEGF overproduction.
To date ranibizumab has been approved only for treating wet ARMD. In this study we will explore ranibizumab for the treatment of cystoid macular edema It is hypothesized that this population will show dramatic improvement as the initial cause of VEGF production can be isolated to the surgical procedure and due to the fact that the retinal pigment epithelium is healthier in this population as compared to the macular degeneration counterparts.
|United States, Hawaii|
|Retina Institute of Hawaii|
|Honolulu, Hawaii, United States, 96815|
|Principal Investigator:||Michael D Bennett, MD||Retina Institute of Hawaii|