| Autor: |
S.T. Méndez-Morales, J.C. Pérez-De Marcos, O. Rodríguez-Cortés, R. Flores-Mejía, M. Martínez-Venegas, Y. Sánchez-Vera, F. Tamay-Cach, J. Lomeli-Gonzaléz, A. Emilio Reyes, R. Lehman-Mendoza, H.A. Martínez-Arredondo, R.A. Vazquez-Dávila, J.F. Torres-Roldan, J. Correa-Basurto, M.G. Arellano-Mendoza |
| Rok vydání: |
2020 |
| Předmět: |
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| Zdroj: |
Vascular pharmacology. 143 |
| ISSN: |
1879-3649 |
| Popis: |
Diabetic neuropathy (DN) encompasses a group of clinical or subclinical manifestations involving a dysfunction in the peripheral nervous system. The cause of the dysfunction is the development of microvascular complications related to diabetes, a disease that affects about 381 million people worldwide. Approximately 50% of patients currently diagnosed with diabetes are expected to manifest DN in the next 10 years. The diagnosis can be made clinically by establishing a good patient history and delving into the symptoms to rule out other etiologies. Treatment of DN focuses on glycemic control and the use of medications to reduce pain, including NSAIDs, antidepressants and antiepileptic drugs. The pathogenesis is of multifactorial origin, associated with various metabolic, vascular, inflammatory and neurodegenerative disorders. The three fundamental cellular alterations participating in the development of DN are chronic inflammation, endothelial dysfunction and oxidative stress. Since the combination of all three is capable of giving rise to nerve ischemia and direct axonal injury, these factors play a key role in the development of polyneuropathy. However, neuronal and microvascular changes do not occur in the same way in all patients with DN, some of whom have no detectable blood abnormalities. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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Full Text from ScienceDirect