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One of the paramount aspects of treating patients with diabetes mellitus is the association of the disease with chronic complications, which represent a burden not only to public health-care systems but predominantly to individuals who cope with them on a day-to-day basis.
While the exact pathophysiological mechanisms behind both microvascular and macrovascular diabetes complications remain uncertain, oxidative stress appears to play a determining role in their development. An increased mitochondrial superoxide production is the first event that leads to activation of other pathways involved in the pathogenesis of chronic diabetes complications (eg, formation of advanced glycation end products, activation of protein kinase C isoforms, increased polyol pathway flux). Those changes may lead to defective formation of new vessels in response to ischemia and activation of inflammatory processes that may persist after a relative normalization of glucose metabolism.
Chronic complications of diabetes:
1) Microvascular complications:
2) Macrovascular complications, which are mainly related to the accelerated development of atherosclerosis (diabetes is an independent risk factor for atherosclerosis) that is characterized by onset at an early age, disseminated lesions in smaller arteries, impaired development of collateral circulation due to microvascular complications, and a painless course of atherosclerosis-related conditions (eg, myocardial infarction, stroke, death).
3) Diabetic foot syndrome, which is caused by microvascular and macrovascular lesions and neuropathy.
4) Other complications: Skeletal (eg, Dupuytren contracture), joint (eg, Charcot foot), visual impairment (eg, subcapsular cataracts), and cutaneous (eg, necrobiosis lipoidica).