Armando el Rompecabezas Fisiopatológico del COVID-19
DOI:
https://doi.org/10.18004/anales/2020.053.02.105Palabras clave:
Infecciones por Coronavirus (Coronavirus Infections), SARS-CoV2, Angiotensinas (Angiotensins), ParaguayResumen
Un nuevo coronavirus hace su aparición en China a fines del año 2019, produciendo infección respiratoria aguda y falla respiratoria. Debido a su similitud clínica y microbiológica con el agente del síndrome respiratorio agudo grave (SARS por sus siglas en inglés), el SARS-CoV1, que afecto a China en el año 2003, fue bautizado como SARS-CoV2, y la enfermedad que produce como COVID-19 (COronaVIrus Disease 2019). Desde su identificación el mundo médico se vio inundado de reportes estadísticos, tablas y cifras que hacen al comportamiento epidemiológico del SARSCoV2, pero pocos autores han focalizado su investigación en los mecanismos patogénicos y si lo han hecho sus artículos han sido diluidos por la vorágine de datos estadísticos. El objetivo del presente trabajo es profundizar en los aspectos fisiopatológicos de la infección por SARS-CoV2 para lo cual realicé una revisión de la literatura desde el inicio de la actual pandemia hasta el mes de junio de 2020, utilizando para la búsqueda Mendeley y PubMed, centrado sobre todo en la capacidad del virus de alterar el delicado balance entre la angiotensina II y sus antagonistas, analizar las posibles razones de la peor evolución en un subgrupo de pacientes y proponer medidas terapéuticas enfocadas en estos hallazgos. El SARS-CoV2 infecta células que expresan el receptor primario para el virus, la enzima ACE2, presente en epitelio intestinal y respiratorio, así como en endotelio. Genera inicialmente hipoxia por lesión alveolar para luego generar disfunción endotelial por lesión directa, lesión mediada por anticuerpos, tormenta de citoquinas y alteración del balance entre la angiotensina II y sus antagonistas funcionales, con eventual trombosis en territorio pulmonar y sistémico, así como hemólisis angiopática y por hiperactividad macrofágica. La retroalimentación positiva entre hipoxia, inflamación y angiotensina II potencian el desarrollo de un síndrome de distrés y fallo multiorgánico, con escalada de la mortalidad. El análisis de la fisiopatología probable en la infección por SARS-CoV2 permite sacar algunas conclusiones siendo las centrales que el endotelio es uno de los actores centrales en la patogenia de la enfermedad y que los pacientes con mayor riesgo de complicaciones son aquellos con disfunción endotelial previa debida a la presencia de obesidad, diabetes mellitus o hipertensión, así como que existen diferentes fases o estadios, cada uno con una posible intervención terapéutica particular, es decir, que la COVID-19 es diferente entre pacientes y en el mismo paciente es diferente en el tiempo, con cada momento requiriendo una intervención terapéutica particular.
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