I would like to thank Dr. Rupak Roy for his interest in our recent article entitled "Role of hyperglycemia-mediated erythrocyte redox state alteration in the development of diabetic retinopathy."1 In our previous study, we had collected control vitreous samples from 36 normal individuals without diabetes and retinopathy for the estimation of vitreous lactate and pyruvate level. Among these 36 controls, 15 subjects had traumatic dislocation of crystalline lens and 21 subjects had per-operative complication of phacoemulsification. We had excluded trauma cases with vitreous hemorrhage because hemorrhage into the vitreous body results in rapid clot formation and clears at a rate of ~ 1 % per day. Erythrocytes exit through the trabecular meshwork, undergo hemolysis and phagocytosis within the vitreous, and may impair in the chemical nature of the vitreous.2 Emergency vitrectomy was performed for all the subjects, and vitreous were collected through pars plana vitrectomy during removal of dropped nucleus, which occurred accidentally after blunt trauma and peropera-tive complication of phacoemulsification.
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