More from the AAO 2006 Annual Meeting

Peter Kaiser presented an update on new treatments for wet AMD that have not yet been approved. I thought the most promising new therapy was the VEGF Trap. The VEGF trap is a small protein that tightly binds VEGF. It prevents VEGF from binding to receptors on other cells such as vascular endothelial cells. In addition the VEGF trap is small and can penetrate the retina. A preliminary study showed that six weeks after an intravitreal injection of the VEGF trap, patients had average gain of almost 5 letters. The advantage of the VEGF trap is that it lasts longer in the eye and may have to be injected only every three months.

Squalamine was isolated from shark cartilage and also has an anti-VEGF effect. It’s given intravenously once a week. The advantages of this drug would be that it would eliminate the need for injection into the eye and, since it is given IV, it could work on both eyes. The initial results showed that 39/40 patients had improved or stable vision and ten patients had three or more lines of improvement. The drug was well tolerated. The FDA has granted fast-track status to this drug. Another trial is underway.

John Thompson discussed a RNA interference drug called bevasiranib. This drug interferes with the production of VEGF. A small study showed that patients who had intraocular injections of this drug continued to have visual loss over the next three months. This loss was thought to be due to VEGF that was already present in the retina. Bevasiranib may be able however, to prevent the production of new VEGF for a long period of time. Therefore a patient could be injected with Avastin or Lucentis to block the VEGF that is already present along with bevasiranib to prevent the future production of VEGF. The combination may result in long-term control of the neovascularization without the need for multiple injections.

Dr. Ronald Danis presented the results of the Rheophoresis Study for Age-Related Macular Degeneration. Rheophoresis involves the pumping of a patient’s blood through a set of filters and is analogous to hemodialysis for patients with kidney failure. The rheophoresis removes high-density macromolecules and possibly inflammatory mediators from the blood. The problem is that these molecules come back to their normal levels a few days after the procedure and we don’t even know if they play a major role in AMD. The study contained 183 patients who were randomized to sham treatment or rheophoresis. They found no difference in the visual acuity between these groups of patients. They then “removed” patients who had cataract surgery during the study, advanced AMD, or who didn’t meet the original study guideline. When they analyzed the remaining 121 patients, there was a modest gain of almost one line of vision in the treated group. It’s dangerous to start analyzing subgroups in any study and then make conclusions. Overall I was not impressed with the results.