RESUMEN
A growing number of studies have shown that exposure to air pollutants such as particulate matter and gases can cause cardiovascular, neurodegenerative and psychiatric diseases. The severity of the changes depends on several factors such as exposure time, age and gender. Inflammation has been considered as one of the main factors associated with the generation of these diseases. Here we present some cellular mechanisms activated by air pollution that may represent risk factors for epilepsy and drug resistance associated to epilepsy.
Asunto(s)
Contaminación del Aire , Epilepsia/etiología , Gases , Exposición por Inhalación , Factores de Edad , Contaminación del Aire/efectos adversos , Contaminación del Aire/estadística & datos numéricos , Epilepsia Refractaria/epidemiología , Epilepsia Refractaria/etiología , Enfermedades Ambientales/epidemiología , Enfermedades Ambientales/etiología , Epilepsia/epidemiología , Epilepsia/patología , Femenino , Gases/administración & dosificación , Gases/efectos adversos , Humanos , Exposición por Inhalación/efectos adversos , Exposición por Inhalación/estadística & datos numéricos , Masculino , Material Particulado/toxicidad , Factores de Riesgo , Factores SexualesRESUMEN
It has been suggested that type 1 (T1D) and type 2 diabetes (T2D) might share some susceptibility risk factors. A higher prevalence of T2D has been reported in families of Caucasian T1D children than in the general population, although data in adults and multiethnic groups is still lacking. Our goal was to compare the prevalence of T2D family history between adults with T1D from a multiethnic population and a non-diabetic control group. We performed a cross-sectional analysis of 145 adults with T1D and 141 healthy adults (control group) that included an interview and a review of the medical charts. Groups were matched for age, sex, ethnicity and body mass index (BMI). We found a higher prevalence of not only T1D but also T2D in first-degree relatives of patients than in controls (p<0.001 and p=0.042, respectively). These differences were not observed for second/third-degree relatives. When subjects were stratified according to their ethnicity, the higher frequency of T2D in FDR of patients than controls became more striking in non-white (p=0.002) and disappeared in white individuals (p=0.85). To conclude, the prevalence of T1D and T2D was higher in first-degree relatives of patients with T1D than of controls. The difference in T2D family history between patients and controls was specially striking among non-whites, which may represent a peculiarity of T1D in this group.