Prophylactic Medical Treatment of Diabetic Retinopathy

Diabetic retinopathy (DR) is a leading cause of visual loss and blindness in adults in developed and developing countries (Friedman et al., 2011). Clinical trials have shown that intensive glycemic control reduces the incidence and progression of DR (Reichard et al., 1993; Stratton et al., 2001; DCCT, 2002 ). Other metabolic factors also affect the progression and development of DR. The UK Prospective Diabetes Study Group reported that tight blood pressure control is effective for reducing the incidence of DR (UK Prospective Diabetes Study Group, 1998a, 1998b). The EUCLID study group reported that inhibitors of angiotensin-converting enzyme drugs decreased the progression of retinopathy in patients without hypertension who had type 1 diabetes with little or no nephropathy (Chaturvedi et al., 1998). Lipid-lowering therapy with fenofibrate also might reduce the progression of DR (Chew et al., 2010; Keech et al., 2007). Among the metabolic factors, although glycemic control seems to be the most important, achieving acceptable glucose homeostasis is difficult, even when patients are highly compliant. Furthermore, DR continues to develop and progress even in patients who are treated intensively to achieve better glycemic control. Therefore, it is important to find medical options other than glycemic control to prevent diabetic ocular complications. The metabolic changes that accompany hyperglycemia, such as activation of the polyol pathway (Gabbay, 1973; Lorenzi, 2007; Robison et al., 1988; 1989), activation of protein kinase C (PKC) (Frank, 2002; Liang et al., 2005; Shiba et al., 1993), increased oxidative stress (Gurler et al., 2000; Jennings et al., 1991; Pan et al., 2008; Pinto et al., 2007), leukocyte adhesion to the endothelial cells (McLeod et al., 1995; Miyamoto et al., 1996; Schroder et al., 1991), and accumulation of advanced glycation end products (AGEs)