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Scribe Winter 2000 |
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MRI used to predict retinopathy risk
All insulin-dependent diabetics are warned that they may go blind because of diabetic retinopathy, but not all do. So can you predict who will lose their vision? Bruce Berkowitz, PhD, with funding from Juvenile Diabetes Foundation International, has developed a non-invasive technique using magnetic resonance imaging that may predict the risk of developing diabetic retinopathy, the leading cause of blindness in those under the age of 45 in developed countries. “This is kind of a stress test for the retinal vessels,” said Dr. Berkowitz, an associate professor at Wayne State University School of Medicine with a joint appointment in the departments of anatomy/cell biology and ophthalmology (Kresge Eye Institute). The technology, which also received funding from the National Eye Institute, may also work in predicting retinopathy of prematurity, a condition causing blindness in children born premature, as well as other types of proliferative retinopathies (for example, macular degeneration) and glaucoma damage. Proliferative retinopathy occurs when blood vessels grow off of the surface of the retina and into the vitreous, a pocket behind the eye’s lens filled with a semigelatinous substance. The blood vessels rupture or cause retinal detachment, leading to blindness. Experts assume the new blood vessels develop because the retina is not getting enough oxygen. With that in mind, Dr. Berkowitz decided to compare MRI scans done at two-minute intervals on rats when they were breathing room air and then again when they were breathing carbogen, a mixture of 95 percent oxygen and 5 percent carbon dioxide. He hypothesized that the MRI scans from rats in a control group would register a vast difference in oxygenation of the retina between the intervals of room oxygen and carbogen. Rats that had been fed galactose, a chemical that would induce proliferative retinopathy in them but not other effects of diabetes, would not show much, if any, contrast in their MRI scans done while breathing room air and carbogen. Dr. Berkowitz’s hypothesis proved to be correct. After about 15 months on the diet, the control group’s change in oxygen in the retina was about 200 percent higher than that of the galactose-fed rats. Not only did the MRI scans show a significant difference in oxygenation at the 15-month stage, when the galactose-fed rats were starting to show early signs of retinopathy, but they showed a substantial gap between the two groups when they were 3.5 months old. Both groups appeared to have healthy retinas, but the MRI scans of the control group showed a change in oxygenation 67 percent higher than that of the galactose-fed rats. The doctors next step is to test the hypothesis on rats whose pancreases have been compromised, leading to true insulin-dependent diabetes. Over the summer, Dr. Berkowitz began work to get similar MRI data in humans. This project is just beginning and most of his work will be confined to the rats for now. Ideally, if the technology proves to be reliable in humans, drugs could be prescribed early on to reduce the progression of retinopathy or, if laser surgery is necessary, it could be confined to areas where the blood vessels are growing into the vitreous, limiting the loss of peripheral vision caused by the surgery. “Usually, we wait until the development of the vessels to treat retinopathy. It’s kind of like waiting for a crash to put up a traffic light,” Dr. Berkowitz said. “What we’re trying to do is develop a measure of risk that’s clinically useful.”
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