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The individuals are at a high risk for cardiovascular events, and this increased risk does not appear to be completely explained by the association of IGT or type II diabetes with such classical risk factors as hypertension, hypercholesterolemia, or cigarette smoking.

Introduction

The early events appear to involve macrophage adherence to endothelium, followed by macrophage migration to the sub-endothelial space. Here, macrophages may be transformed into foam cells. While these signs may also be present, proximal diabetic neuropathy causes pain and weakness that develops more rapidly and affects nerves closer to the torso. This disease most often affects people with type 2 diabetes, but it can also affect people who do not have diabetes (nondiabetic lumbosacral radiculoplexus neuropathy). A history of type 2 diabetes is the most important risk factor. It can happen to people who have never had diabetes before or who have diabetes type 1 on rare occasions. Infections, strokes, trauma, some drugs, and heart attacks are all potential triggers. Blood tests reveal a blood sugar level of more than 30 mmol/L (600 mg/dL), an osmolarity level of more than 320 mOsm/kg, and a pH level of less than 7. A variety of growth factors and cytokines may be released from damaged endothelium, macrophages, and smooth muscle cells. Platelets may adhere to the site of macrophage attachment and release thromboxane and growth factors. Smooth muscle cells may proliferate and migrate, accompanied by thrombus formation, vascular encroachment, and occlusion. On the other hand, many unexplained issues remain. As already noted, the pathogenesis of accelerated atherosclerosis in diabetes is incredibly complicated, and it is probably simplistic to speculate that an imbalance in one system, such as the fibrinolytic system, is the major contributor. Further, many conditions are associated with hyperinsulinism, such as obesity, certain forms of type II diabetes, acromegaly, and insulinoma, that do not appear to have accelerated atherosclerosis