Diabetic retinopathy is the leading cause of blindness world over. Neurovascular degeneration of the retina is considered presently as the cause as against the vascular changes which are believed to be causative previously. In fact the neuronal changes are shown to ante-date the vascular changes. There is complex interaction of many cells like pericytes, mullers cells, astrocytes, vascular endothelial cells as well as factors like advanced glycation products, Oxidative and metabolic stress, inflammatory cytokines, leukotrienes, various growth factors and glycoproteins etc. in the pathogenesis of DR. Various biochemical pathways like Polyol pathway, glucosamine pathway, AGE pathway and PKC pathways interacting with one another is also recognised as having a role in the pathogenesis of DR. But the common link responsible for all these factors involvement linking to DM2 is still not clear. The mechanism explaining Benfotiamine, a thiamine analogue found to be useful in treating DR , though attractive in integrating the various biochemical pathways cited above, is not comprehensive. The concept of reactive oxygen species (ROS) is a better alternative explanations linking up all pathogenic factors concerned to chronic hyperglycaemia of DzM2. But antioxidants proved futile in treating DR. It may be useful to remember that extensive ROS production in DM2 is consequent to shift of energy metabolism from glycolysis to B-oxidation of fats. Unless this is reversed, ROS production continues. The Diabetes Control and Complications Trial (DCCT) and UKPDS are the two landmark clinical trials that clearly showed the relationship between chronic hyperglycaemia and genesis of DR. Progression in T1DM and T2DM patients, respectively. Randomized controlled trials have shown that early treatment of DM2 can reduce an individual’s risk of severe visual loss by 57%. Intensive glycaemic control appeared long lasting because of the metabolic memory, also known as ‘legacy effect’. A term which explains the beneficial effects of immediate intensive treatment of hyperglycaemia with a sustained benefit with respect to the outcomes for many years, regardless of glycaemia in the later course of diabetes. Hence the current emphasis is prevention of DR with strict glycaemic control in DM2 ab initio.
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