ABSTRACT
La enfermedad celíaca se caracteriza por el daño de la mucosa intestinal y la consiguiente malabsorción de nutrientes en individuos genéticamente predispuestos tras la ingesta de gluten. Es una enfermedad compleja, resultado de la interacción de un componente genético poligénico y varios factores ambientales. Se ha propuesto la teoría de que procesos infecciosos transitorios o aumentos en la permeabilidad de la barrera mucosa podrían facilitar el inicio de la enfermedad por los péptidos del gluten de la luz intestinal. Presentamos el caso de 2 pacientes que presentaron el inicio de la enfermedad tras la curación de una hepatitis aguda por virus de la hepatitis B. Se discute la fisiopatología de la enfermedad y se plantean hipótesis que expliquen esta asociación (AU)
Celiac disease is characterized by small intestinal mucosal injury and nutrient malabsorption in genetically susceptible individuals following dietary ingestion of gluten. The pathogenesis of the disease involves interactions between environmental, genetic, and immunologic factors. Transient infections or increased permeability of the mucosa may facilitate disease onset induced by the uptake of gluten peptides into a microenvironmental milieu in the small intestinal mucosa. We present two patients with onset of celiac disease after resolution of acute hepatitis B virus infection. The physiopathology of celiac disease is discussed and possible explanations for this association are proposed (AU)
Subject(s)
Humans , Male , Middle Aged , Celiac Disease/etiology , Hepatitis B/complications , Acute Disease , Celiac Disease/diagnosisABSTRACT
Celiac disease is characterized by small intestinal mucosal injury and nutrient malabsorption in genetically susceptible individuals following dietary ingestion of gluten. The pathogenesis of the disease involves interactions between environmental, genetic, and immunologic factors. Transient infections or increased permeability of the mucosa may facilitate disease onset induced by the uptake of gluten peptides into a microenvironmental milieu in the small intestinal mucosa. We present two patients with onset of celiac disease after resolution of acute hepatitis B virus infection. The physiopathology of celiac disease is discussed and possible explanations for this association are proposed.
