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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 ranibuzumab 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 teams 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 ranibuzumab 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 lights entry onto the retina.

"Weve suspected for awhile that ranibuzumabs ability to shut down VEGFs signaling would do the trick because its highly likely that VEGF is the culprit when it comes to diabetic macular edema," says Nguyen.

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Contact: Jeff Ventura
jventur4@jhmi.edu
410-955-7832
Johns Hopkins Medical Institutions
15-Dec-2006


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