Prevention and reduction in progression of microvascular complications requires intensive management of glucose, blood pressure and lipids
Diabetes mellitus (DM) is characterized by organ dysfunction arising directly or indirectly from the effects of chronic hyperglycemia. The chronic complications of diabetes are traditionally classified as macro- or micro vascular depending on the underlying pathophysiology. The micro vascular triad of retinopathy, nephropathy and neuropathy is unique to diabetes.1 Most patients with diabetes will have one or more of these as overt or sub clinical manifestations during the course of their disease.
The underlying driver of micro vascular disease is tissue exposure to chronic hyperglycemia. clinical trials have established a clear relationship between micro vascular disease and glucose control. Microvascular disease tends to occur predominantly in tissues where glucose uptake is independent of insulin activity (eg kidney, retina and vascular endothelium) because these tissues are exposed to glucose levels that correlate very closely with blood glucose levels. The development of disease is the result of a combination of direct glucose-mediated endothelial damage, oxidative stress due to superoxide overproduction, and the production of sorbitol and advanced glycation end-products due to the prevailing state of hyperglycemia. These metabolic injuries cause altered blood flow and changes in endothelial permeability, extra vascular protein deposition and coagulation resulting in organ dysfunction. Current evidence demonstrates a clear relationship between blood pressure (BP) and progression of nephropathy and retinopathy. These are now established as independent risk factors for micro vascular disease progression.
Long term diabetic complications are the result of one or more parts of your body becoming damaged as a result of diabetes.
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