Study of Intravitreal Microplasmin in Relieving Vitreo-Macular Adhesion in Neovascular Age-related Macular Degeneration (AMD)
The purpose of this study is to determine whether microplasmin given by intravitreal injection is effective and safe for the treatment of wet age-related macular degeneration (AMD) in patients who have focal vitreomacular adhesion (VMA)
|Study Design:||Allocation: Randomized
Endpoint Classification: Safety/Efficacy Study
Intervention Model: Parallel Assignment
Masking: Double Blind (Subject, Caregiver, Investigator, Outcomes Assessor)
Primary Purpose: Treatment
|Official Title:||Resolution of Vitreomacular Adhesion (VMA) Associated With Neovascular Age Related Macular Degeneration (AMD) With Intravitreal Microplasmin|
- The primary outcome is the proportion of patients in whom there is release of vitreomacular traction as assessed by ultrasonography, optical coherence tomography and physical examination [ Time Frame: Day 28 ] [ Designated as safety issue: No ]
- Total number of ranibizumab injections following microplasmin in those with PVD compared with those without PVD [ Time Frame: 12 months ] [ Designated as safety issue: No ]
- Change in mean macular thickness [ Time Frame: Day 28 and month 12 ] [ Designated as safety issue: No ]
- Mean change in ETDRS visual acuity [ Time Frame: Day 28 and Month 12 ] [ Designated as safety issue: No ]
- Incidence and severity of ocular adverse events [ Time Frame: Day 28 and Month 12 ] [ Designated as safety issue: Yes ]
- Incidence and severity of nonocular adverse events [ Time Frame: Day 28 and Month 12 ] [ Designated as safety issue: Yes ]
|Study Start Date:||October 2009|
|Estimated Study Completion Date:||December 2011|
|Estimated Primary Completion Date:||September 2011 (Final data collection date for primary outcome measure)|
Experimental: microplasmin, intravitreal injection
Subjects will receive one intravitreal injection of microplasmin on Day 0.
Microplasmin, 1.875 mg, will be given by intravitreal injection,on Day 0.
Placebo Comparator: Placebo
Subjects will receive one intravitreal injection of the placebo on Day 0.
Drug: Placebo control
The placebo control will be the microplasmin vehicle without the microplasmin.
The human vitreous gel undergoes progressive liquefaction with age. Concurrent with the process of vitreous liquefaction, there is a weakening of the adhesion at the vitreoretinal interface between the cortical vitreous gel and the inner limiting lamina. Posterior vitreous detachment (PVD) is a separation of the cortical vitreous get from the inner limiting lamina. PVD is usually a sudden event during which liquefied vitreous from the center of the vitreous body bursts through a hole in the posterior vitreous cortex and then dissects the residual cortex gel away from the inner limiting lamina. If there is residual vitreoretinal traction around the break, this process may induce a tear in the retina that can in turn result in rhegmatogenous retinal detachment, macular hole, or cystoid macular edema. The importance of the vitreous in the progression of diabetic retinopathy may also extend beyond tractional considerations. For example, it is believed that the vitreous serves as scaffolding for new vessel formation and may also contribute to molecular imbalances that lead to retinopathy progression. Therefore, total PVD, by releasing vitreoretinal traction as well as other potential mechanisms, may be beneficial in various vitreoretinal diseases such as neovascular AMD.
Vitreomacular adhesion (VMA) in exudative (wet) AMD may be associated with poor prognosis in patients with AMD. This trial is primarily aimed at showing that release of VMA can be induced by microplasmin, a proteolytic enzyme, in patients with wet AMD, and that microplasmin is safe in patients w/ neovascular (wet) AMD. Secondary endpoint will be assessment of improved AMD outcomes.
|Contact: Rosaleen M Ostrick, MPH, MAemail@example.com|
|Contact: Logan Hitchcock, B.S.||firstname.lastname@example.org|
|United States, California|
|Jules Stein Eye Institute/UCLA||Recruiting|
|Los Angeles, California, United States, 90095|
|Principal Investigator: Steven D Schwartz, M.D.|
|Sub-Investigator: Jean-Pierre Hubschman, M.D.|
|Principal Investigator:||Steven D Schwartz, M.D.||University of California, Los Angeles|