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Diabetic foot disorder (abnormalities) is clearly one of the most important complications of diabetes mellitus (DM) and is the leading cause of hospitalization with substantial morbidity , impairment of quality of life and engender high treatment costs.
The term diabetic foot disorders DFDs refers to a group of disorders which clinically present with one or more of the following clinical manifestations: foot ulceration, infection, neuropathy, deformity, gangrene and/or ischemia. Due to the impaired metabolic mechanisms in DM, there is an increased risk of infection and poor wound healing due to a series of mechanisms which include decreased cell and growth factor response, diminished peripheral blood flow and decreased local angiogenesis . Thus, the feet are predisposed to peripheral vascular disease, damage of peripheral nerves, deformities, ulcerations and gangrene .
Many factors contribute to the pathogenesis of foot ulceration ,including loss of protective sensation due to peripheral neuropathy where the feet become numb and the injury goes unnoticed. Also, arterial insufficiency complicates the neuropathic ulcer which leads to poor wound healing. Approximately 45%-60% of all diabetic foot ulcerations are purely neuropathic, whereas 45% have both neuropathic and ischemic components . In this review we are trying to explain the important points in pathogenesis of diabetic foot disorders that may lead dramatically to foot amputation . In 2005 the International Diabetes Fed¬eration (IDF) published a position statement about common diabetes complications, data from epidemiological studies have indicated that between 40 – 70% of all lower extremity amputations are related to diabetes. Eighty five percent of all amputations related to diabetes are preceded by foot ulcers. Researchers established that between 49-85% of all amputations can be prevented .
The mechanism of neuropathy development include that the increased level of glucose in blood leads to increased enzyme production such as aldose reductase and sorbitol dehydrogenase. These enzymes convert glucose into sorbitol and fructose. As these sugar products accumulate, the synthesis of nerve cell myoinositol is decreased, affecting nerve conduction. Moreover , hyperglycaemia induced microangiopathy leads to reversible metabolic, immunologic and ischemic injury of autonomic, motor and sensory nerves [6,7].
Sensory neuropathy is a major component leading to the develop¬ment of diabetic foot ulceration. Motor neuropathy leads to atrophy of the small muscles of the foot and this will lead to foot deformities. Development of foot deformities with lack of foot care awareness and lack of proper foot wear in Arabian patients significantly contrib¬utes to the increasing problems of foot complica¬tions in our diabetic patients. High levels of glucose in the blood provide an excellent breeding ground for bacteria and fungi, and can reduce the bod