Diabetic retinopathy and metabolic control.

Abstract

Retinopathy is probably the first long-term complication of diabetes mellitus to become clinically evident, possibly because the retina is the only microvascular bed that can be observed directly and repeatedly. This makes it a good model for studying the pathogenesis and natural history of diabetic microangiopathy. Most of the proposals to account for its pathogenesis invoke mechanisms that depend directly on the circulating and tissue levels of glucose: protein glycosylation, activation of the "polyol pathway", abnormalities of vascular endothelium, altered capillary blood flow. Several population studies and clinical trials suggest that the degree of metabolic control maintained over the years influences the rates of appearance and progression of retinopathy. However, on an individual basis, factors independent of control may intervene, making some patients more or less prone to this complication. Animal models also suggest that the progression of retinopathy may become irreversible from its very early stages. From a clinical point of view, it is difficult to establish a satisfactory definition of "good" control and approaching it may increase the risk of dangerous hypoglycemia and weight gain. Diabetes and eye specialists are thus left to strive for the best possible, sensible, metabolic control but must also rely on early diagnosis and treatment for the sight-threatening complications of diabetes.