Neuropatía Diabética: Una revisión narrativa de fisiopatología, diagnóstico y tratamiento

La neuropatía diabética se presenta hasta en el 60 % de los pacientes diabéticos. La neuropatía diabética periférica es la causa más común de neuropatía en el mundo. La fisiopatología de la neuropatía diabética involucra daño periférico nervioso por acumulación de productos tóxicos derivados de la hiperglicemia. El sistema nervioso central se ve posteriormente involucrado a través de sensibilización, disminución de la función del sistema inhibitorio y aumento en la excitabilidad del sistema de facilitación. La clínica más común se manifiesta de manera simétrica afectando fibras sensitivas pequeñas y grandes, aunque se han encontrado formas atípicas de presentación. Las pruebas diagnósticas confirmatorias se reservan para la duda diagnóstica, casos de síntomas atípicos o investigación. El consenso en cuanto a tratamiento es el uso de gabapentinoides, antidepresivos tricíclicos e inhibidores de recaptura de serotonina y noradrenalina. Estas tres familias se consideran como primera línea de tratamiento.

Diabetic neuropathy occurs in up to 60% of diabetic patients. Diabetic peripheral neuropathy is the most common cause of neuropathy in the world. The pathophysiology of diabetic neuropathy involves peripheral nerve damage due to the accumulation of toxic products derived from hyperglycemia. The central nervous system is subsequently involved through sensitization, decreased function of the inhibitory system, and increased excitability of the facilitative system. The most common symptoms manifest symmetrically, affecting small and large sensory fibers, although atypical forms of presentation have been found. Confirmatory diagnostic tests are reserved for diagnostic doubt, atypical symptoms, or research. The consensus regarding treatment is the prescription of gabapentinoids, tricyclic antidepressants, and serotonin and norepinephrine reuptake inhibitors. These three families are considered the first line.

Association of vitamin d with mild cognitive impairment and alzheimer's dementia in older mexican adults

ABSTRACT Background It has been proposed that Vitamin D helps reduce the accumulation of cerebral β-amyloid-42 by innate immune stimulation and phagocytosis activation. An association between low Vitamin D levels and Alzheimer’s dementia (AD) has been established. We determined the association between Vitamin D, mild cognitive impairment (MCI), and AD in older Mexican adults (> 65 years) Methods Cross-sectional study conducted at the memory clinic in a tertiary-level hospital in Mexico City. We evaluated subjects with MCI, AD, and normal cognition (NC) with available serum Vitamin D [25(OH)D] levels (past 6 months). Three categories were assigned according to 25(OH)D levels: sufficiency (> 30 ng/mL), insufficiency (21-29 ng/mL), and deficiency (≤ 20 ng/mL). Descriptive statistics, means and standard deviations were used. Logistic regression analyses adjusted by age, sex, and educational level were performed Results We evaluated 208 patients. Mean age was 79 ± 1 year, 65% (n = 136) were female; and mean educational level was 6.7 ± 2.3 years. Thirty-one subjects (14%) had NC; 42% (n = 88) had MCI; and 43% (n = 89) had AD. Prevalence of Vitamin D deficiency was 54%, more frequent in the AD group (64%) followed by the MCI (59%) and NC (13%) (p < 0.001) groups. In the multivariate logistic regression analysis, Vitamin D deficiency was associated with MCI (HR 25.02 [confidence interval 95% 4.48-139]; p < 0.001) and AD (HR 41.7 [5.76-301]; p < 0.001) after adjusting for confounders Conclusions Serum Vitamin D deficiency was associated with MCI and dementia; low levels produced a greater effect over executive functions.