PURPOSE: To determine whether diabetes mellitus is protective for nuclear sclerotic cataract at baseline and 6 and 12 months after vitrectomy surgery. DESIGN: Prospective, interventional cohort study. METHODS: Phakic diabetic and nondiabetic patients undergoing vitrectomy surgery for a variety of retinal conditions underwent Scheimpflug lens photography in the operated and fellow eye at baseline and at 6 and 12 months after vitrectomy surgery. RESULTS: Of 52 eyes included in the analysis, 23 eyes were from diabetic patients, 14 of which had surgery for ischemic retinopathy. At baseline, eyes with ischemic diabetic retinopathy had less nuclear sclerotic cataract than nonischemic diabetic and nondiabetic eyes. This was true for eyes undergoing vitrectomy surgery (P = .0001) and for fellow eyes (P = .003). Nuclear sclerotic cataract developed after vitrectomy surgery in nonischemic diabetic eyes and nondiabetic eyes at the same rate. Diabetic eyes with ischemic retinopathy showed no significant progression of nuclear opacification, and therefore had significantly less postvitrectomy nuclear cataract at 6 months (P < 1 × 10(-6)) and at 12 months (P < .001) than nondiabetic or nonischemic diabetic eyes. Normalizing to baseline opacity and adjusting for age and other comorbidities did not alter this result. CONCLUSIONS: Ischemic diabetic retinopathy, not just systemic diabetes mellitus, protected against nuclear sclerotic cataract at baseline and after vitrectomy surgery. These findings are consistent with the hypothesis that increased exposure to oxygen is responsible for nuclear cataract formation.
PURPOSE: To determine whether diabetes mellitus is protective for nuclear sclerotic cataract at baseline and 6 and 12 months after vitrectomy surgery. DESIGN: Prospective, interventional cohort study. METHODS: Phakic diabetic and nondiabeticpatients undergoing vitrectomy surgery for a variety of retinal conditions underwent Scheimpflug lens photography in the operated and fellow eye at baseline and at 6 and 12 months after vitrectomy surgery. RESULTS: Of 52 eyes included in the analysis, 23 eyes were from diabeticpatients, 14 of which had surgery for ischemic retinopathy. At baseline, eyes with ischemic diabetic retinopathy had less nuclear sclerotic cataract than nonischemic diabetic and nondiabetic eyes. This was true for eyes undergoing vitrectomy surgery (P = .0001) and for fellow eyes (P = .003). Nuclear sclerotic cataract developed after vitrectomy surgery in nonischemic diabetic eyes and nondiabetic eyes at the same rate. Diabetic eyes with ischemic retinopathy showed no significant progression of nuclear opacification, and therefore had significantly less postvitrectomy nuclear cataract at 6 months (P < 1 × 10(-6)) and at 12 months (P < .001) than nondiabetic or nonischemic diabetic eyes. Normalizing to baseline opacity and adjusting for age and other comorbidities did not alter this result. CONCLUSIONS:Ischemic diabetic retinopathy, not just systemic diabetes mellitus, protected against nuclear sclerotic cataract at baseline and after vitrectomy surgery. These findings are consistent with the hypothesis that increased exposure to oxygen is responsible for nuclear cataract formation.
Authors: Ying-Bo Shui; Nancy M Holekamp; Benjamin C Kramer; Jan R Crowley; Mark A Wilkins; Fred Chu; Paula E Malone; Shayna J Mangers; Joshua H Hou; Carla J Siegfried; David C Beebe Journal: Arch Ophthalmol Date: 2009-04
Authors: George J Harocopos; Ying-Bo Shui; Megan McKinnon; Nancy M Holekamp; Mae O Gordon; David C Beebe Journal: Invest Ophthalmol Vis Sci Date: 2004-01 Impact factor: 4.799
Authors: David C Beebe; Nancy M Holekamp; Carla Siegfried; Ying-Bo Shui Journal: Philos Trans R Soc Lond B Biol Sci Date: 2011-04-27 Impact factor: 6.237