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Introduction and objective: Diabetic patients are at high risk for peripheral arterial disease (PAD) characterized by symptoms of intermittent claudication or critical limb ischemia. Measurement of ankle-brachial index (ABI) has emerged as the diagnostic tool of choice, because it is relatively simple, non-invasive and inexpensive. It is also an independent marker of increased morbidity and mortality from cardiovascular diseases. The aim of the presented study was to assess the relationship between current glycemic control defined by glycated hemoglobin (HbA1c) level, and quantitative changes in the arteries of the lower limbs in patients with type 2 diabetes. Materials and methods: 175 patients with type 2 diabetes hospitalized in the Diabetology Ward were studied. VENO Doppler and a sphygmomanometer were used to assess blood flow. Results: The average level of HbA1c was assessed at 8.48%. Although the average level of ABI indicator was 1.20 (normal), only 45% of evaluated patients had their individual index within the normal range. Signs of ischemia were found in 17.7% of examined subjects. There was no conclusive correlation between ABI and HbA1c levels. Conclusions: The current level of glycemic control evaluated as HbA1c has no direct impact on the advancement of diabetic angiopathy evaluated as ABI.
 Diabetes is one of the major challenges of modern medicine, as it is considered a global epidemic of the XXI century. The disease often leads to the development of serious, health threatening complications. Diabetic foot syndrome is a characteristic set of anatomical and molecular changes. At the macroscopic level, major symptoms are neuropathy, ischemia and chronic ulceration of the lower limb. In every third patient, the neuropathy develops into Charcot neuroarthropathy characterized by bone and joints deformation. Interestingly, all these complications are a result of impaired healing processes and are characteristic for diabetes. The specificity of these symptoms comes from impaired molecular mechanisms observed in type 1 and type 2 diabetes. Decreased wound and fracture healing reflect gene expression, cellular response, cell functioning and general metabolism. Here we present a comprehensive literature update on the molecular factors contributing to diabetic foot syndrome.
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