How Diabetics Lose Vision: Molecular and Biochemical Mechanisms Associated With Hyperglycaemic Damage in the Retina

Abstract

Diabetic patients are at risk of increased morbidity and mortality from macrovascular and microvascular complications. The increased risk of the vascular complications includes genetic factors, hyperglycaemia, hypertension, hyperlipidaemiaand oxidative stress. The mechanisms by which hyperglycaemia causes vision loss and blindness and other diabetic complications include the polyol pathway, accumulation of AGEs, activation of PKC, increased oxidative stress, increased flux through the hexosamine pathway and vascular inflammation. All these pathways play critical roles in the development and progression of diabetic retinopathy and other diabetic complications.There is an individual variation in the presentation and course of diabetic retinopathy, and other diabetes-induced complications. Some patients, after many years with diabetes, never develop sight threatening retinal changes, thus maintaining good visual acuity. However, there are patients who after only a few years of diabetes show diabetic retinopathy that progresses rapidly and may not respond to available treatment. Some patients do not lose their vision even with poor metabolic control; others develop vision loss despite good metabolic control. The threat of vision loss requires a lot of patient education and psychological support, not only after a loss but also before any loss is recognized by the patient. Care for patients with diabetes requires an understanding that the diabetic eye is an end-organ response to a general metabolic disease.

Keywords: Diabetes, Hyperglycaemia, Retinopathy, Retinal Cells, Vision Loss