Search the Health Library
Get the facts on diseases, conditions, tests and procedures.
I Want To...
Find a Doctor
Find a doctor at The Johns Hopkins Hospital, Johns Hopkins Bayview Medical Center or Johns Hopkins Community Physicians.
I Want To...
Find Research Faculty
Enter the last name, specialty or keyword for your search below.
Johns Hopkins Medicine
Media Relations and Public Affairs
Media Contact: Jeff Ventura
Dec. 15, 2006
DRUG TREATMENT SLOWS MACULAR VISION LOSS IN DIABETICS
A drug commonly used to slow the loss of central vision has shown promise in stemming a common precursor of blindness in diabetics, which involves the same central light-sensitive area of retina, Johns Hopkins Wilmer Eye Institute scientists report.
Encouraged by the effect of ranibizumab in people with macular degeneration, the Hopkins researchers injected the drug into the eyes of 10 people losing their sight from macular edema, one of many complications of diabetes and a first stage of diabetic retinopathy.
Over the course of several months of therapy, every patient in the preliminary Hopkins study could read at least two more lines on the standard eye chart, the researchers said. Moreover, the thickness of the patients’ maculae, the central part of the retina responsible for seeing fine details, decreased an average of 85 percent. The American Journal of Ophthalmology published the team’s findings in their December issue.
“The results are impressive,” says Quan Dong Nguyen, M.D., M.Sc., an assistant professor of ophthalmology at the Wilmer Eye Institute at Johns Hopkins, “although we will not know until we begin a larger clinical trial what the long-term benefits of the drug might be.”
The Hopkins group believes that ranibizumab interferes with a protein that spurs the growth of unwanted blood vessels in the back of the eye. Vascular endothelial growth factor, or VEGF, is released when the oxygen supply in the eye is restricted by blood vessel damage related to diabetes.
In a self-preserving attempt to acquire more oxygen, the VEGF signals for the creation of new blood vessels, which almost always damage, rather than improve, vision by blocking light’s entry onto the retina.
“We’ve suspected for awhile that ranibizumab’s ability to shut down VEGF’s signaling would do the trick because it’s highly likely that VEGF is the culprit when it comes to diabetic macular edema,” says Nguyen.
More than 4 million diabetics in the United States have diabetic retinopathy and, according to the National Eye Institute, one in 12 of those experience at least some vision loss.
Macular edema, a first stage of retinopathy, occurs when, over time, excess uncontrolled blood sugar damages the tiny blood vessels in the eye, causing fluid and fat to leak onto the retina at the back of the eye. The swelling interferes with focus and blurs vision. Making matters worse, a lack of oxygen often then triggers VEGF’s production cycle.
All 10 subjects in the study had some vision loss at the start of the clinical trial, in which ranibizumab was administered at the one, two, four and six month marks. The thickness of each patient’s macula was also measured at each point in the study using an advanced digital imaging technique.
“Within a week, several patients experienced dramatic reductions in the thickness of their maculas, and there were further improvements with each injection,” says Peter Campochiaro, M.D., the Dolores and George Eccles Professor of Ophthalmology at The Johns Hopkins University School of Medicine, who is also an investigator in the study.
Ranibizumab is marketed for treatment of neovascular macular degeneration by Genentech Inc. under the brand name of Lucentis.