EyeWorld Asia-Pacific March 2013 Issue

March 2013 56 EWAP NEWS & OPINION to propose new research by comprehensive studies to integrate various components of AMD- related costs,” Dr. Azad said. “We need to provide an easy, accessible, affordable, and efficacious mode of treatment. The pricing policy should not be only profit-driven but service-driven [as well].” About AMD Dr. Azad discussed vision and economics in AMD management at the “Update on age-related macular degeneration” symposium. He outlined the story of AMD, from the epidemiology of the disease— for instance, it is a common cause of blindness in the elderly age group, and the 60+ population is the fastest growing age group in the world. The disease has serious economic ramifications for that rapidly growing age group, considerably lowering productivity from work absence, ability to earn a daily living, and reducing quality of life. The most common severe vision loss in AMD is caused by choroidal neovascular membrane (CNVM), and CNVM’s primary treatment is anti-VEGF, he said. “In the last 10, 15 years, there’s been a lot of change and a paradigm shift in AMD. For most of us sitting here, the primary treatment is anti-VEGF—others, are laser for extrafoveal CNVM and PDT for a very selective group. We have other treatment that is now historical,” he said. “Therefore, the whole treatment revolves around anti-VEGF.” Anti-VEGFs Anti-VEGFs have changed the “aim of therapy … to gain in vision in AMD, where previously the aim in treatment was to maintain vision or prevent vision loss,” he said. Therein lies the financial problem, Dr. Azad said, because while vision is gained with the drug, it not only has some complications, including systemic and others, as well as issues involved with frequent visits for treatments, but it also has the burden of the cost—the treatment is expensive. He compared prices of two commonly used anti-VEGFs, Lucentis (ranibizumab, Genentech, San Francisco, Calif., USA), U.S. Food and Drug Administration approved, and Avastin (bevacizumab, Genentech) used off- label. The two have similar profiles: The duration of action for Lucentis is four weeks, while the duration of action is four to six weeks for Avastin, and ocular and systemic safety is comparable. But the cost of the two drugs is significantly different. “It is 40,000 to 60,000 rupees per dose for ranibizumab and 2,000 to 5,000 rupees per dose for bevacizumab,” Dr. Azad said. The total estimated cost of anti-VEGFs with a four to six weeks frequency dosing at 20 expected doses for Lucentis is 800,000 to 1,200,000 rupees, while Avastin is 40,000 to 100,000 rupees—and another anti-VEGF, Macugen (pegaptanib sodium, OSI Pharmaceuticals, Melville, NY, USA), has a more initial estimated cost, at 45,000 rupees, going up to 50,000 rupees, totaling 900,000 to 1,000,000 for 20 doses. Cost burden, protocol At such costs, it is not difficult to understand how many patients cannot afford their treatment for the blinding disease, regardless of the consequences to their vision. In his own treatment protocol, Dr. Azad first diagnoses CNVM/ recurrence and then assigns three monthly dose treatment of anti- VEGF with PRN dosing based on visual acuity, OCT, and fluorescein angiography eye test, as needed. With his current protocol, for the first year, with 30% to 40% remission, five doses are expected when using any of the three drugs, dropping to four doses expected in the following years, impacting cost in a positive way by slightly reducing the overall financial burden, he said—but still, that cost does not account for other coexistent costs at present, such as OCT and fluorescein angiography eye test. The future of endothelial keratoplasty “To understand the future, you need to understand the past,” said Jodhbir S. Mehta, MD , Singapore. It has been 108 years since the first penetrating keratoplasty was performed. Penetrating keratoplasty became the gold standard for endothelial replacement, but even after more than a century of development, it remains problematic, including a corneal endothelial cell loss of up to 70% at 10 years. The trend today is increasingly toward targeted replacement of diseased corneal layers. Endothelial keratoplasty represents a shift in the paradigm that has dominated for almost a century. However, Dr. Mehta and his colleagues at the Singapore National Eye Centre (SNEC) soon found that the typically shallow Asian eye presented a particular challenge to the procedure. Using the taco folding technique for inserting donor tissue used in countries like the U.S., he and his colleagues were alarmed to find an initial endothelial cell loss of 30% post-op, going up to over 60% at one year— results that were reinforced and closely replicated in Japan. They thus introduced the sheets glide technique. Using the sheets glide, a large incision, and a pull- through technique, the SNEC team was able to reduce the initial loss to 9%, with a clear cornea at day 1. It still was not ideal—the pull- through could damage the donor rim, the sheets glide is open so the donor tissue is not protected and may slip, and requires a degree of ambidexterity. So the SNEC team developed the EndoGlide. The earliest version of the EndoGlide—the design inspired by thumb drives— produced double coiling of the donor tissue, allowing surgeons to insert larger donor tissues through smaller incisions. More importantly, the EndoGlide gave the surgeon full control of the donor tissue at all times until insertion is completed. The EndoGlide reduced one- year endothelial cell losses from 19% to 15.6%, then 14.9% as they performed more cases and surgeons grew more comfortable with the technique. The more recent preference for thinner donor tissue—such as in Descemet’s membrane endothelial keratoplasty (DMEK)—led the SNEC team to develop a new iteration of the EndoGlide. The EndoGlide Ultrathin introduces a saddle to the design to more gently curve the tissue while loading. The ideal approach to endothelial disease, however, is to cultivate human corneal endothelial cells. The first problem was to find a medium in which cultivated cells Live - from page 55 continued on page 58