THE RELATIONSHIP BETWEEN VASCULAR ENDOTHELIAL GROWTH FACTOR-A SERUM LEVEL AND THE SEVERITY OF DIABETIC PERIPHERAL NEUROPATHY

Abstract

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 diabetic peripheral neuropathy (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.