Long-term remission with rituximab in a patient with severe hepatitis C virus-induced mixed cryoglobulinemia.

Mixed cryoglobulinemia (MC) is a small-vessel systemic vasculitis characterized by the presence of cryoglobulins, immunoglobulin complexes that precipitate at low temperatures ( < 37 ºC) inducing the inflammatory process. The most frequent etiology is hepatitis C infection (HCV) (1). Rituximab (RTX), an anti-CD20 monoclonal antibody, has recently emerged as the treatment of choice for severe MC (2). We present a case of severe hepatitis C virus-induced MC that was controlled and maintained in remission with RTX for 26 months, a remarkable prolonged period of time.

Remisión a largo plazo con rituximab en paciente con crioglobulinemia grave asociada al virus de la hepatitis C / Long-term remission with rituximab in a patient with severe hepatitis C virus-induced mixed cryoglubulinemia

La crioglobulinemia (CG) es una vasculitis sistémica de pequeño vaso caracterizada por la presencia de crioglobulinas, las cuales son inmunocomplejos circulantes que, a bajas temperaturas (< 37 °C), precipitan desencadenando el proceso inflamatorio. La etiología más frecuente es la infección por el virus de la hepatitis C (VHC) (1). En los últimos años el anticuerpo monoclonal anti-CD20 rituximab (RTX) se ha ido posicionando como el tratamiento de primera línea en las CG de presentación agresiva (2). Presentamos el caso de una paciente con brote grave de una CG asociada al VHC que respondió al tratamiento con RTX, manteniéndose posteriormente en remisión de manera inusualmente prolongada durante 26 meses (AU)

Mixed cryoglobulinemia (MC) is a small-vessel systemic vasculitis characterized by the presence of cryoglobulins, immunoglobulin complexes that precipitate at low temperatures (< 37 °C) inducing the inflammatory process. The most frequent etiology is hepatitis C infection (HCV) (1). Rituximab (RTX), an anti-CD20 monoclonal antibody, has recently emerged as the treatment of choice for severe MC (2). We present a case of severe hepatitis C virus-induced MC that was controlled and maintained in remission with RTX for 26 months, a remarkable prolonged period of time (AU)

Inicio de la enfermedad celíaca tras curación de hepatitis aguda por el virus de la hepatitis B / Onset of celiac disease after acute hepatitis B infection

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)

[Onset of celiac disease after acute hepatitis B infection]. / Inicio de la enfermedad celíaca tras curación de hepatitis aguda por el virus de la hepatitis B.

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.