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Tracking Information | |||||
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First Received Date † | April 19, 2007 | ||||
Last Updated Date | December 5, 2008 | ||||
Start Date † | May 2007 | ||||
Current Primary Outcome Measures † |
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 ] | ||||
Original Primary Outcome Measures † | Same as current | ||||
Change History | Complete list of historical versions of study NCT00464581 on ClinicalTrials.gov Archive Site | ||||
Current Secondary Outcome Measures † |
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Original Secondary Outcome Measures † |
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Descriptive Information | |||||
Brief Title † | Lucentis for Cystoid Macular Edema for Non-Ischemic Retinopathy | ||||
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 | ||||
Brief Summary | 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. |
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Detailed Description | 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. |
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Study Phase | Phase II | ||||
Study Type † | Interventional | ||||
Study Design † | Treatment, Non-Randomized, Open Label, Historical Control, Single Group Assignment, Safety/Efficacy Study | ||||
Condition † | Cystoid Macular Edema | ||||
Intervention † | Drug: Lucentis (ranibizumab) | ||||
Study Arms / Comparison Groups | |||||
Publications * | |||||
* Includes publications given by the data provider as well as publications identified by National Clinical Trials Identifier (NCT ID) in Medline. |
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Recruitment Information | |||||
Recruitment Status † | Active, not recruiting | ||||
Enrollment † | 30 | ||||
Estimated Completion Date | December 2009 | ||||
Estimated Primary Completion Date | December 2009 (final data collection date for primary outcome measure) | ||||
Eligibility Criteria † | Inclusion Criteria:
Exclusion Criteria:
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Gender | Both | ||||
Ages | up to 90 Years | ||||
Accepts Healthy Volunteers | Yes | ||||
Contacts †† | |||||
Location Countries † | United States | ||||
Expanded Access Status | |||||
Administrative Information | |||||
NCT ID † | NCT00464581 | ||||
Responsible Party | Michael D. Bennett, MD, Retina Institute of Hawaii | ||||
Secondary IDs †† | |||||
Study Sponsor † | Retina Institute of Hawaii | ||||
Collaborators †† | Genentech | ||||
Investigators † |
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Information Provided By | Retina Institute of Hawaii | ||||
Verification Date | April 2007 | ||||
† Required WHO trial registration data element. †† WHO trial registration data element that is required only if it exists. |