الفهرس 
Review of literatureOnly 14 pages are availabe for public view
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Abstract
Diabetic retinopathy (DR) is one of the commonest and easily demonstrable examples of microvascular damage that diabetes inflicts throughout the body. DR is among the leading causes of blindness in people of working age, affecting both genders equally. Chronic hyperglycemia activates macrophages and stimulates in vivo TNF-α production. Enhanced TNF-α production in a diabetic state may promote the development of diabetic micro- and macroangiopathies through a variety of TNF-α bioactivities. While the pathogenesis of diabetic retinopathy is highly complex and not fully understood, TNF-α is recognised as a major contributor to the development of diabetic retinopathy.Macular oedema, preretinal neovascularisation and neuronal degeneration are primary features of diabetic retinopathy, which result from breakdown of the blood retinal barrier (BRB), angiogenesis or neuronal apoptosis, respectively. TNF-α is a protein manufactured by white blood cells to stimulate and activate the immune system in response to infection or cancer. Overproduction of this compound can lead to disease where the immune system acts against healthy tissues, such as DM, arthritis or psoriasis. Some treatments for these diseases utilize drugs that bind and inactivate TNF-α, thereby reducing unhealthy inflammation. This study was done to evaluate the relation between the stages of diabetic retinopathy & the serum level of tumor necrosis factor-α (TNF- α) in diabetic patients.