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Y.-B. Shui, N. M. Holekamp, F. Bai, A. Almony, D. C. Beebe; Ischemic Diabetic Retinopathy Protects Against Nuclear Cataract After Vitrectomy. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5385.
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Patients with diabetes have significantly lower vitreous pO2 and are less likely to have cataract surgery after vitrectomy than non-diabetics. Based on the hypothesis that oxygen exposure to the lens is a major risk for nuclear cataract, we performed a prospective interventional cohort study to determine whether diabetes mellitus protects against nuclear cataract after vitrectomy surgery.
Phakic diabetics and non-diabetics undergoing vitrectomy surgery for a variety of retinal conditions underwent Scheimpflug lens photography (NIDEK EAS-1000, Japan) in the operated and fellow eye before, and 6 and 12 months after surgery. Images were analyzed with the EAS-1000 analysis software. Nuclear opacity was quantified using average light scattering per pixel on the central line between the anterior surface of adult nucleus and the clear zone at the center of the lens.
Of 55 patients included in the analysis, 24 had diabetes, 16 of which had surgery for complications of ischemic retinopathy. The remaining 8 diabetics did not have ischemic retinopathy. At baseline, patients with ischemic diabetic retinopathy had significantly less nuclear opacity than non-ischemic diabetic and non-diabetic subjects (p=0.001 in surgical eyes, p=0.002 in fellow eyes). After vitrectomy surgery, non-ischemic diabetic eyes and non-diabetic eyes developed nuclear cataract (p<10-6 compared to baseline at 6 and 12 months). However, eyes with ischemic diabetic retinopathy showed no significant progression of nuclear opacification and, therefore, had significantly less post-vitrectomy nuclear cataract at 6 (p<0.0001) and 12 months (p=0.0002) than non-diabetic and non-ischemic diabetic eyes. Adjusting for baseline opacity and age did not alter this result. The cataract surgery rate was 50% in the non-ischemic eyes and 16% in the ischemic eyes at the end of one year.
Ischemic diabetic retinopathy, but not diabetes alone, protected against nuclear opacity at baseline and the development of nuclear cataract following vitrectomy. These findings are consistent with the hypothesis that increased exposure to oxygen is responsible for nuclear cataract formation in humans.
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