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Diabetic retinopathy is still the leading cause of blindness in people of working age. It is one of the most common complications of diabetes, affecting 80–100% of type 1 patients and being present at the diagnosis of diabetes in around one third of type 2 patients.
The earliest detectable lesions of diabetic retinopathy are microaneurysms. These are associated with excessive vascular permeability and result in exudate formation. There is occlusion of the vessels and stimulation of growth factors, which in turn promote the proliferation of new blood vessels and the growth of fibrous tissue. This may contract and lead to haemorrhage. The process of angiogenesis, however, occurs right through the evolution of diabetic retinopathy.
Until very recently, treatment was confined to relatively late in the pathology of diabetic retinopathy, when there was already some proliferative disease. Photocoagulation has been successful in preventing blindness and, more recently, studies have shown the importance of tight blood glucose control.
The diabetes control and complications trial (DCCT) in patients with type 1 diabetes emphasised the importance of tight glycaemic control in reducing the progression of retinopathy and also reducing the incidence of retinopathy (fig 1).1
Importantly, even patients receiving intensive treatment had some progression of retinopathy. Also, it took three years before a clear difference between intensive and conventional treatment was observed. Clearly, while tight glycaemic control is successful, other treatments are still required. There is now strong evidence that agents that modulate the renin-angiotensin system (RAS) may be one of these treatments.
RAS and retinopathy
A local RAS exists in the eye that is independent of …
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