الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Diabetes Mellitus (DM) is a syndrome of disturbed metabolism involving carbohydrate, protein and fat which results from the degree of insulin deficiency (absolute or relative) and tissue sensitivity to its actions.
Chronic elevation of blood glucose results in a wide range of complications most notably microvascular and macrovascular complications. The microvascular complications include retinopathy, nephropathy and neuropathy.
Diabetes mellitus causes a broad array of neuropathic complications affecting the peripheral nerves at different locations from the root to the distal axon. It involves sensory, motor and autonomic nerves. Distal symmetric polyneuropathy is recognized as the most common form with pain reported as the chief symptom. So far, tight glycemic control is the only approved treatment that halts progression of neuropathy.
The mechanism of nerve injury in diabetes mellitus is believed to be accounted for by multiple factors including metabolic aberrations and vascular compromise. Increase in polyol flux, accumulation of advanced glycation end-products, oxidative stress and activation of protein kinase C are thought to be the key drivers in the pathophysiology of neuropathy. Recent studies have attempted to study the role of depletion of neurotrophic factors such as VEGF in the development of DPN. Study of these pathophysiologic changes is vital in the quest to find treatment.
Vascular endothelial growth factor (VEGF) is a potent cytokine for endothelial cells and is usually released in response to hypoxia. It promotes angiogenesis and development of collateral vessels in tissues undergoing ischemic changes. It has been strongly implicated in the development of diabetic retinopathy and has been associated with glomerular changes in diabetic nephropathy. Very little information is available regarding the role of VEGF in diabetic neuropathy. Studies have shown that it can be both a pathogenic factor and also a protective factor in diabetic neuropathy.
The aim of the present study was to demonstrate the relationship between serum VEGF levels and the severity of DPN. A cross-sectional study was conducted on 81 patients with diabetes mellitus. All participants were subjected to full history and physical examination. Electromyography was used to diagnose and stage neuropathy. 14 patients had no neuropathy, 24 had mild neuropathy, 33 had moderate neuropathy and 10 patients were classified as having severe neuropathy. Glycemic control, blood pressure, total cholesterol and BMI were some recorded parameters.
Our study showed a significant negative correlation between the severity of neuropathy and serum VEGF levels. Additionally, we found that glycemic control, creatinine levels and total cholesterol negatively correlated with the serum levels of VEGF.