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36 EW FEATURE February 2011 Retinal pharmacotherapy for the anterior segment surgeon January 2013 A new era in pharmacologic vitreolysis by Michelle Dalton EyeWorld Contributing Writer AT A GLANCE • Posterior vitreous detachment is a relatively benign process that occurs with aging. • Gel liquefaction can exceed the pace of vitreoretinal dehiscence that results in anomalous PVD. • Ocriplasmin is the first FDA-approved treatment for vitreomacular adhesion, one manifestation of anomalous PVD. • Ocriplasmin is injected once into the vitreous and has an approximate 40% success rate. Armed with the knowledge that the vitreous plays a larger role in retinal disease than realized, retinal specialists are rapidly embracing ocriplasmin as a treatment for the right patient Pravin U. Dugel, M.D. P osterior vitreous detachment (PVD) is an age-related occurrence that usually is asymptomatic or mildly symptomatic. But an incomplete (or anomalous) PVD can cause vision loss, experts say. "People with relatively good vision—say 20/40 to 20/50—who were symptomatic were usually followed rather than treated surgically," said Jeffrey S. Heier, M.D., director, Vit- What is PVD? Posterior vitreous detachment—much like presbyopia and cataract—is an age-related phenomenon. A ccording to Dr. Sebag, who first described the phenomenon1: "Posterior vitreous detachment (PVD) requires two concurrent events. First is that the gel vitreous that we're born with has to liquefy sufficiently so it destabilizes and is prone to collapse moving away from the inside of the back of the eye. Second is a weakening of the adhesion of the vitreous to the retina. When both of those occur, you get an innocuous PVD. The overwhelming majority of people get an innocuous PVD, meaning they get some floaters, but that's the end of the story. This occurs in 40-60s age range. Studies have shown after age 65, two of every three people have a PVD. Most of the time, it's innocuous. If, however, you have liquefaction of the gel that promotes collapse of vitreous without weakening of the vitreoretinal adhesion, an anomalous PVD will result. The manifestations of this PVD will vary depending upon where the vitreous is most firmly adherent to the retina and where the gel is most liquefied. Those variables are different from person to person." In some syndromes (Wagner's, Stickler's, Marfan's) anomalous PVD is common, but little is known about the genetic component, he said. Marfan's syndrome patients also have very lax joints (suggesting that abnormal type II collagen is the cause of joint disease) and also very abnormal vitreous with a higher rate of retinal detachment. Reference 1. Sebag J. Anomalous posterior vitreous detachment: a unifying concept in vitreo-retinal disease. Graefes Arch Clin Exp Ophthalmol. 2004; 242:690-698. Jeffrey S. Heier, M.D. reoretinal Service, Ophthalmic Consultants of Boston, and co-director, vitreoretinal fellowship, Ophthalmic Consultants of Boston. Jetrea (ocriplasmin, ThromboGenics, Heverlee, Belgium) provides "a relatively atraumatic means to help patients without surgery," Dr. Heier said. Jetrea has been approved in the U.S. for symptomatic vitreomacular adhesion (VMA), which occurs as a result of anomalous PVD and can sometimes lead to edema, metamorphopsia, visual impairment, and/or severe vision loss. Ocriplasmin has been in development for more than a decade, and almost 1,000 people have been injected with the drug in the course of the clinical studies, said Pravin U. Dugel, M.D., managing partner, Retinal Consultants of Arizona, Phoenix, and clinical associate professor of ophthalmology, Doheny Eye Institute, Los Angeles. "There are really three forces that are colliding at this moment— one is the drug itself. Second, imaging—the importance of vitreomacular traction (VMT) or VMA was not well known before we had sophisticated imaging. Third—treatment burden," Dr. Dugel said. Because anti-vascular endothelial growth factor (VEGF) doesn't confer any permanent structural change in the retina, patients need continuous dosing, Dr. Dugel said. The introduction of Jetrea may prove useful in combination with the anti-VEGFs like Lucentis (ranibizumab, Genentech, San Francisco) and might be able to decrease the treatment burden in patients with both VMA and chronic diseases such as diabetic macular edema, neovascular macular J. Sebag, M.D. degeneration, or retinal vein occlusion, he said. J. Sebag, M.D., founding director, VMR Institute, Huntington Beach, Calif., and professor of clinical ophthalmology, University of Southern California, Los Angeles, first described anomalous PVD more than a decade ago (for more on his description, see sidebar). It's imperative ophthalmologists continue to think about the vitreous as an organ, not a space, Dr. Sebag said. Surgery had become the de facto standard method for removal when necessary, but with the development of ocriplasmin, retinal specialists are experiencing a transition to pharmacotherapy, he added.1 "In a patient with anomalous PVD that has caused any of a variety of vitreoretinopathies [see sidebar], we hope to be able to use Jetrea to treat it, rather than doing surgery," Dr. Sebag said. Simplifying treatment for VMA by using intravitreal injections in lieu of surgery is "doing patients a great service," Dr. Dugel said. PVD pharmacotherapy The "biggest issue" with macular holes currently is that while surgery has a "very high" success rate, it involves patients having to face the floor post-op so that a bubble can tamponade the hole closed. "That is incredibly arduous for the patient," Dr. Sebag said. An intravitreal injection mandates no surgery center or hospital visit and no need to face the floor. Remarkably, Jetrea is successful in 40-60% of cases, he said. "This drug does not give us the ability to treat something we could not treat before, but it does give us