Ileítis en la COVID-19 complicada: ¿causa o efecto?

Felipe Neri Piñol Jiménez, Virginia Capó de la Paz, Teresita Montero González, Julían Francisco Ruíz Torres

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Resumen

Introducción: la comprensión histomorfológica y biomolecular del íleon terminal; sitio clave en el control de la absorción nutricional, del metabolismo, sistema inmunitario, microbiota intestinal, y función de órganos extradigestivos; justifica su participación en los procesos inflamatorios intestinales, como pudiera ser en la infección por el SARS-CoV2.

Objetivos: describir las evidencias biomoleculares de los componentes tisulares del íleon que justifican su función en el eje hepático-intestinal, y citar hallazgos histomorfológicos del íleon en fallecidos de la COVID-19. 

Adquisición de información: se realizó una revisión sistemática, crítica de los estudios biomoleculares sobre los enterocitos, la barrera epitelial intestinal, microbiota y permeabilidad intestinal del íleon que fundamentan su función de barrera epitelial, reportados en sitios Web (PubMed, Scielos, Lilacs, y Elservier), entre 2000 a 2021, y se citan hallazgos preliminares de cortes histomorfológicos del íleon en fallecidos de la COVID-19. 

Desarrollo: se describen las evidencias biomoleculares del íleon normal, y la repercusión de su pérdida, disbiosis e hiperpermeabilidad en los procesos inflamatorios intestinales; también se citan hallazgos histomorfológicos preliminares de ileítis en fallecidos de la COVID-19, que pudiera fundamentar la importancia de la intuición biomolecular del íleon en el equilibrio salud-enfermedad, cuya pérdida justificaría el progreso clínico de la COVID-19.

Conclusiones: la revisión integral del íleon y la cita de los hallazgos histomorfológicos preliminares de ileítis en fallecidos de la COVID-19, motiva realizar estudios amplios, que infieran su papel en el progreso clínico de la COVID-19 y justifique el futuro de nuevas intervenciones terapéuticas para su integridad.

Palabras clave

ileitis 1; COVID-19 2; barrera epitelial intestinal 3; SARS-CoV-2 4.

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