Publication: Importancia de la elastografía de transición y de los polimorfismos de un solo nucleótido (SNPs) en la evolución de la enfermedad hepática de pacientes con hepatitis crónica C
Loading...
Files
Official URL
Full text at PDC
Publication Date
2019-02-01
Authors
Advisors (or tutors)
Editors
Journal Title
Journal ISSN
Volume Title
Publisher
Universidad Complutense de Madrid
Citations
Exportar
Abstract
Se calcula que entre 0,6% y 1% de la población española se encuentra infectada por el virus de la hepatitis C (VHC). La historia natural de la infección por VHC se caracteriza por la cronificación de la infección en más de un 80% de los individuos, con el consiguiente desarrollo de fibrosis hepática y progresión a cirrosis. La fibrosis hepática es el resultado del proceso de respuesta biológica ante el daño crónico y la posterior remodelación hepática. Tras una hepatitis aguda se produce una rápida respuesta de los hepatocitos que sustituyen el tejido necrótico restableciendo la arquitectura hepática normal. Durante este proceso de reparación, existe una reacción inflamatoria junto a un depósito de matriz extracelular que servirá de tejido de sostén para los hepatocitos regenerados. Cuando se mantiene la necrosis, este proceso reparativo se perpetúa y aumenta la producción de la matriz extracelular que se deposita de manera desorganizada en el lobulillo hepático sustituyendo a la población normal de hepatocitos, comenzando así el desarrollo de fibrosis hepática. Sin embargo, la tasa de progresión de fibrosis hepática es muy variable y difícil de predecir. Algunos individuos experimentan progresión rápida de fibrosis con una evolución precoz hacia la enfermedad hepática terminal, mientras que otras personas experimentan una progresión lenta, lo que hace menos probable la descompensación hepática. Esta variabilidad en la progresión de la fibrosis, así como el desarrollo de carcinoma hepatocelular, descompensación hepática y muerte es debido a interacciones multifactoriales entre factores virales y del huésped. A pesar de los conocimientos sobre la historia natural de la hepatitis crónica C, los métodos actuales para predecir la progresión de la fibrosis no son lo suficientemente precisos como para identificar qué pacientes evolucionarán a fibrosis avanzada, cirrosis o descompensación hepática...
It is estimated that between 0.6% and 1% of the Spanish population is infected with the hepatitis C virus (HCV). The natural history of HCV infection is characterized by the chronification of the infection in more than 80% of individuals, with the consequent development of liver fibrosis and progression to cirrhosis. Liver fibrosis is the result of the biological response process to chronic damage and subsequent liver remodeling. After acute hepatitis C, there is a rapid response of the hepatocytes that replace the necrotic tissue, restoring the normal hepatic architecture. During this repair process, there is an inflammatory reaction together with an extracellular matrix deposit that will serve as a supporting tissue for the regenerated hepatocytes. When necrosis is maintained, this reparative process is perpetuated and increases the production of the extracellular matrix that is deposited in a disorganized manner in the hepatic lobule, replacing the normal population of hepatocytes, thus beginning the development of liver fibrosis. However, the rate of progression of liver fibrosis is very variable and difficult to predict. Some individuals experience rapid progression of fibrosis with an early progression towards terminal liver disease, while others experience a slow progression, which makes liver decompensation less likely. This variability in the progression of fibrosis, as well as the development of hepatocellular carcinoma, hepatic decompensation and death is due to multifactorial interactions between viral and host factors. Despite knowledge of the natural history of chronic hepatitis C, current methods for predicting the progression of fibrosis are not accurate enough to identify which patients will progress to advanced fibrosis, cirrhosis, or liver decompensation...
It is estimated that between 0.6% and 1% of the Spanish population is infected with the hepatitis C virus (HCV). The natural history of HCV infection is characterized by the chronification of the infection in more than 80% of individuals, with the consequent development of liver fibrosis and progression to cirrhosis. Liver fibrosis is the result of the biological response process to chronic damage and subsequent liver remodeling. After acute hepatitis C, there is a rapid response of the hepatocytes that replace the necrotic tissue, restoring the normal hepatic architecture. During this repair process, there is an inflammatory reaction together with an extracellular matrix deposit that will serve as a supporting tissue for the regenerated hepatocytes. When necrosis is maintained, this reparative process is perpetuated and increases the production of the extracellular matrix that is deposited in a disorganized manner in the hepatic lobule, replacing the normal population of hepatocytes, thus beginning the development of liver fibrosis. However, the rate of progression of liver fibrosis is very variable and difficult to predict. Some individuals experience rapid progression of fibrosis with an early progression towards terminal liver disease, while others experience a slow progression, which makes liver decompensation less likely. This variability in the progression of fibrosis, as well as the development of hepatocellular carcinoma, hepatic decompensation and death is due to multifactorial interactions between viral and host factors. Despite knowledge of the natural history of chronic hepatitis C, current methods for predicting the progression of fibrosis are not accurate enough to identify which patients will progress to advanced fibrosis, cirrhosis, or liver decompensation...
Description
Tesis de la Universidad Complutense de Madrid, Facultad de Medicina, Departamento de Microbiología I (Inmunología), leída el 12-07-2017. Tesis formato europeo (compendio de artículos)