Pathogenesis Of Microvascular Disease

From a pathogenic viewpoint a number of different molecular mechanisms have been proposed for the development of the various manifestations of diabetic retinopathy. The underlying abnormalities may also play a role in the microvascular disease that results in nephropathy and possibly neuropathy. Many of these theories have been studied extensively in animals and humans using both in vitro and in vivo methods. The primary goal of these studies was to try and identify the underlying mechanisms through which hyperglycemia and other metabolic factors cause damage to vascular cells, that in turn lead to specific organ damage and ultimately the long-term complications.

This type of evidence is very important and will provide the clinician with a scientific basis for advocating tight glycemic control. This in turn will also be a major factor in shaping the healthcare policies for patients with diabetes. However, it is also apparent that our current therapies do not allow us to optimally control the blood sugars into the normal range for prolonged periods. Therefore an understanding of the basis for the microvascular disease can have far-reaching implications. If we can identify other areas where hyperglycemia induces further metabolic changes that lead to vascular damage, inhibiting or blocking the enzymes or products that cause this damage can become additional therapies. This approach can be additive to the initial goal of trying to achieve normoglycemia by the traditional treatments. It is of interest that there have been reports in the literature of patients who develop all the microvascular complications but who do not have overt clinical diabetes at the time (5). Abdella et al. reported on a 47-year-old man who presented with the nephrotic syndrome and renal failure with proliferative retinopathy on fundoscopy. The patient did not have overt hyperglycemia but did have impaired glucose tolerance on testing. These case reports serve to remind us that while hyperglycemia is critical to the development of diabetic complications, milder degrees of glucose intolerance can also play a role through other mechanisms.

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