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        Drug May Reduce Risk of Diabetic Retinopathy: Presented at ARVO

        By Earl R. Nichols

        FT. LAUDERDALE, F.L. -- May 3, 2006 -- The insulin sensitizer rosiglitazone (Avandia) could offer some degree of protection for patients with diabetes who are at risk of developing diabetic retinopathy, suggests a study reported here at the Association for Research in Vision and Ophthalmology (ARVO) annual meeting.

        Proliferative diabetic retinopathy is characterized by angiogenesis of the retinal vasculature. Along with diabetic macular edema, these represent the leading causes of severe vision loss among patients with diabetes mellitus. Rosiglitazone increases insulin sensitivity by acting on the PPAR-gamma receptors in adipose and other tissues.

        Lucy Q. Shen, MD, investigator, surgical research unit, Harvard University Medical School, Boston, Massachusetts, and colleagues conducted a chart review of 124 patients who had been treated with rosiglitazone and 158 controls whose diabetes was treated with other agents. Study subjects had diabetes for a mean of 15 years and were matched for baseline ocular characteristics.

        After a mean of 2.8 years of follow-up, the vision of 2.7% of patients receiving rosiglitazone worsened by 3 or more lines on the Early Treatment of Diabetic Retinopathy Study (ETRDS) scale while 6.6% of those in the control group experienced such a worsening.

        Overall, progression to severe nonproliferative diabetic retinopathy occurred in 7.1% of rosiglitazone subjects compared with 20.8% of controls. Diabetic retinopathy becomes proliferative when retinal vascular dysfunction progresses into full-blown pathological retinal angiogenesis.

        An important difference was seen when patients were stratified as to whether their retinopathy was mild, moderate, or severe at baseline. For example, among patients who had either mild or moderate retinopathy at baseline, there was no statistical difference between those who went on from having nonproliferative diabetic retinopathy to develop proliferative disease (11% and 12.5% in the rosiglitazone and the control groups, respectively). Patients who had severe nonproliferative diabetic retinopathy at baseline, however, were more likely to progress to the proliferative form of the disease (14.3% and 45.8%, respectively).

        There was no statistical between-group difference in the number of patients who went on to develop clinically significant macular edema, regardless of baseline macular status.

        Dr. Shen said she could not explain why rosiglitazone should have such an ocular effect, but it was not related to better glycemic control. Nor did it appear to be because rosiglitazone had a pro-apoptotic effect.

        Recent reports in the literature have suggested that rosiglitazone may actually cause macular edema in some patients, although this is controversial, she said, and 1 large study involving more than 3000 patient failed to show any greater likelihood of developing macular edema whether the patient was or was not being treated with rosiglitazone.


        [Presentation title: Rosiglitazone May Delay Progression to Proliferative Diabetic Retinopathy. Abstract 2333]



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