Objective: To determine the relationship between clinical parameters (HbA1c) whit metabolic control and deterioration of peripheral arterial perfusion in diabetic patients. Methodology: 108 medical records of patients...Objective: To determine the relationship between clinical parameters (HbA1c) whit metabolic control and deterioration of peripheral arterial perfusion in diabetic patients. Methodology: 108 medical records of patients with type 2 diabetes mellitus were evaluated. We obtained averages of: blood glucose (162.3 ± 73.10 mg/dl), glycated hemoglobin (HbA1c = 7.64% ± 1.77%), cholesterol (189.28 ± 35.25 mg/dl), triglycerides (189.11 ± 87.76 mg/dl), Systolic Blood Pressure (SBP = 119.69 ± 14.95 mmHg), Diastolic Blood Pressure (DBP = 77.15 ± 9.55 mmHg) and Media Blood Pressure (MBP = 91.36 ± 9.89 mmHg). We correlated variable HbA1c with vascular injury symptomatology. Results: Correlation was found between sensitivity dysfunction and HbA1c with a statistical significance of p = 0.01, and a correlation Kendal coefficient w = 0.01, any other parameter of metabolic control was not correlated with symptoms of vascular injury. Conclusion: It is remarkable that the sensitivity dysfunction is a symptom of poorly vascularized lower extremities caused for both functional impairment and structural changes in diabetic patients’ peripheral nerves, even in the preclinical stage of vascular disease. The HbA1c could also be investigated as a likely sensitivity dysfunction biomarker in DM due to the correlation presented in this study but more studies must be realized.展开更多
文摘Objective: To determine the relationship between clinical parameters (HbA1c) whit metabolic control and deterioration of peripheral arterial perfusion in diabetic patients. Methodology: 108 medical records of patients with type 2 diabetes mellitus were evaluated. We obtained averages of: blood glucose (162.3 ± 73.10 mg/dl), glycated hemoglobin (HbA1c = 7.64% ± 1.77%), cholesterol (189.28 ± 35.25 mg/dl), triglycerides (189.11 ± 87.76 mg/dl), Systolic Blood Pressure (SBP = 119.69 ± 14.95 mmHg), Diastolic Blood Pressure (DBP = 77.15 ± 9.55 mmHg) and Media Blood Pressure (MBP = 91.36 ± 9.89 mmHg). We correlated variable HbA1c with vascular injury symptomatology. Results: Correlation was found between sensitivity dysfunction and HbA1c with a statistical significance of p = 0.01, and a correlation Kendal coefficient w = 0.01, any other parameter of metabolic control was not correlated with symptoms of vascular injury. Conclusion: It is remarkable that the sensitivity dysfunction is a symptom of poorly vascularized lower extremities caused for both functional impairment and structural changes in diabetic patients’ peripheral nerves, even in the preclinical stage of vascular disease. The HbA1c could also be investigated as a likely sensitivity dysfunction biomarker in DM due to the correlation presented in this study but more studies must be realized.
