Published: Sept. 1, 2009
Updated: Aug. 18, 2010
A chance meeting started it all.
Harvey DesVeaux’s youngest son, Darren, ran into an old friend, Russell Burns, who works at the Duke Reading Center. He mentioned that his father, a retired court officer living in Maine, had been told by his doctor that his bilateral wet macular degeneration (AMD) would cause him to go blind.
While Burns said that doctors at Duke had no magic pill or shot, Darren DesVeaux was impressed enough with Duke’s reputation to convince his father to come down for a second opinion.
Little did the DesVeauxs know that Duke ophthalmologist Scott Cousins, MD, would be able not only to stabilize one eye, but also actually to improve the vision in the other.
When Harvey DesVeaux arrived for his appointment in October 2008, Cousins immediately recognized that he had two sub-types of AMD that didn’t respond well to standard treatment.
“When you look at the real-world results with ranibizumab (Lucentis) and bevacizumab (Avastin) injections, it controls the leakage in about 90 percent of people and it makes the vision better in about 30 percent of people. But it doesn’t work very well in about 10 percent of people,” says Cousins. “He unfortunately was one of those 10 percent.”
Cousins was able to determine this through dynamic ICG angiography, a technology he says Duke excels at using. This imaging test allowed him to identify the blood vessel type in the eye so he could determine the most appropriate treatment.
“This technology has been around for 20 years,” he says, “but it fell out of fashion because it’s difficult to interpret and people didn’t know how to use the information. Over the last four years, we’ve tried to resurrect the technology and understand it better. With the technology, we now understand the actual flow and size of new blood vessels forming in wet AMD.”
He recommended immediate photodynamic therapy to dry out DesVeaux’s right eye, the worse one, and a more frequent course of anti-VEGF injections in his left eye. DesVeaux’s right eye, which was previously completely unresponsive, is now dry; though the vision is not great, at least it’s stable.
His left eye, however, now boasts 20/30 vision. "His left eye bounced back to spectacularly good vision, where he’s reading and driving again,” says Cousins. “Before, he was essentially legally blind because the drugs weren’t working in him.”
DesVeaux continues to fly back from Maine every four to five weeks for injections. These trips have a happy bonus -- he and his wife get extra time with their son and daughter-in-law, and their two young grandchildren.
Although each appointment can last hours, the treatment he gets is worth it, DesVeaux says. “They’ve done a lot for me here. If they can keep my vision where it is, I’m happy.”
DesVeaux is also doing a lot for patients like him -- by participating in research
Cousins is doing in the lab. By analyzing blood samples from patients such as DesVeaux, Cousins is hoping to predict who will get the types of AMD that don’t respond well to conventional treatment.
He says that specific types of circulating stem cells in the blood and an inappropriately activated immune system seem to contribute to the growth of the big blood vessels that are harder to treat conventionally.
Cousins’s goal is to pair findings from that analysis with clinical outcomes data to help personalize current AMD treatment protocols. Doctors typically guess at AMD treatment regimens based on their own experience, Cousins says. “No one really has a regimen that’s designed specifically for an individual patient’s disease activity. That’s what we’re trying to develop,” he says.
DesVeaux’s case is a good example of the difference that such personalized approaches can make. “The ideas that we’re coming up with are the result of cross-fertilization between what we study in the test tube, what we study in rats, and what we study in the patient as a living laboratory. The goal is to make patients better by coming up with better tests and better treatments.”