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Papel del ácido úrico en pacientes con enfermedad cerebrovascular isquémica

  • Autores: Jose Carlos Arévalo Lorido
  • Directores de la Tesis: Nicolás Roberto Robles Pérez-Monteoliva (dir. tes.)
  • Lectura: En la Universidad de Extremadura ( España ) en 2019
  • Idioma: español
  • Programa de doctorado: Programa de Doctorado en Investigación Biomédica Aplicada por la Universidad de Extremadura
  • Materias:
  • Enlaces
    • Tesis en acceso abierto en: Dehesa
  • Resumen
    • español

      El papel del ácido úrico (AU) es controvertido en pacientes con ictus isquémico. Nuestro objetivo es comprobar si los niveles de AU medidos en las primeras 24 horas tras un ictus isquémico determinan el pronóstico funcional en la fase aguda, y si están relacionados con el daño y el pronóstico cardiovascular. Metodología: estudio de cohortes retrospectivo de pacientes ingresados por ictus isquémico. Se obtienen datos epidemiológicos, analíticos, y funcionales y se realiza seguimiento durante un año. Resultados: se realizan tres análisis. El primero, relaciona la distribución de AU con el deterioro neurológico y funcional de los pacientes durante el ingreso, demostrándose que los pacientes con niveles elevados de AU tienen un menor daño neurológico y una mejoría funcional. En el segundo se relaciona la distribución de AU con el daño endotelial carotídeo mediante ecografía, siendo un predictor independiente para presentar un grosor íntima-media mayor o igual a 1mm (OR de 1.26, IC95% 1.04-1.52, p=0.01). Finalmente, en el tercer análisis, se correlacionan los niveles de AU separados en grupos en función de la existencia o no de enfermedad renal y el pronóstico cardiovascular a un año (ictus e infarto agudo de miocardio fatal y no fatal más hospitalizaciones por angina inestable, e insuficiencia cardíaca). Los niveles elevados de AU determinan un peor pronóstico cardiovascular (HR 1.45, IC95% 1.17-1.81, p=0.006), en pacientes con y sin enfermedad renal.

      Conclusiones: Como conclusiones finales de la presente tesis podemos deducir: 1. Que los niveles elevados de ácido úrico medidos en la fase aguda de un ictus isquémico determinan un mejor pronóstico desde el punto de vista de déficit neurológico y funcional de los pacientes en ese momento agudo.

      2. Que ese mejor pronóstico es independiente de la presencia o no de enfermedad renal, beneficiándose este último grupo igualmente de esos efectos beneficiosos.

      3. Que sobre el lecho vascular, esos mismos niveles de ácido úrico al aumentar se correlacionan con un mayor daño endotelial determinado por el incremento del grosor íntima media y con la formación de la placa de ateroma determinado por el grado de estenosis que esta produce a nivel carotídeo.

      4. Que como consecuencia de ese efecto a nivel vascular, pero también a nivel metabólico, los niveles de ácido úrico medidos en el momento de un ictus, determinan un peor pronóstico cardiovascular (aumento de mortalidad e ingresos por causa cardiovascular) a lo largo del año siguiente a haber sufrido el ictus, a pesar de presentar inicialmente una mejor capacidad funcional y menor daño neurológico.

      5. Que ese incremento del riesgo vascular se produce tanto en enfermos sin afectación de la función renal, como en aquellos que tienen enfermedad renal definida por la fórmula HUGE, población esta última que conlleva el mayor riesgo cardiovascular.

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    • English

      The role of serum uric acid (SUA) is controversial in patients with ischemic stroke. Our aim is to know if SUA determined at admission after a stroke are related to the functional outcome and similarly if SUA has a relationship with a negative vascular damage and outcome. METHODS: Retrospective cohort study of patients admitted by ischemic stroke. Upon admission, we got a comprehensive medical history and took on a complete physical and functional examination. Patients then were followed-up for one year. RESULTS: Three analysis were performed. The first-one relates the distribution of UA with the neurological and functional status of patients during admission, demonstrating that patients with high SUA levels have less neurological damage and better functional improvement. The second relates the distribution of UA with carotid endothelial damage by ultrasound, being an independent predictor to have an intima-media thickness greater than or equal to 1mm (OR of 1.26, 95% CI 1.04-1.52, p=0.01). Finally, in the third analysis, the levels of SUA separated in groups according to the existence or not of renal disease were correlated with cardiovascular outcome (stroke and acute myocardial infarction both, fatal and nonfatal plus hospitalizations for unstable angina, and heart failure). Higher SUA levels determine a worse cardiovascular prognosis (HR 1.45, 95% CI 1.17-1.81, p=0.006), in patients with and without kidney disease. CONCLUSIONS: SUA levels have a neuroprotectant role in acute phase of ischemic stroke, though are deleterious both in vascular system as in cardiovascular outcome.


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