[Fibrotic diseases in the gastrointestinal tract : Liver fibrosis and more].

Abstract

Chronic liver damage, such as metabolic dysfunction-associated steatotic liver disease (MASLD), viral hepatitis B or C, cholestatic hepatitis (PBC, PSC), toxic damage (alcohol) or genetic alterations (hemochromatosis, Wilson's disease, etc.) usually cause a chronic inflammatory response in liver cells or bile duct epithelial cells. In the long term this chronic inflammatory response can lead to scarring of the liver, a condition known as fibrosis. The development of liver fibrosis is largely independent of the causative agent, although the pattern of initial fibrosis (periportal, pericentral or sinusoidal) can vary. Untreated and progressive fibrosis can sometimes lead to complete architectural deconstruction and deposition of connective tissue in the liver, intestines and other parenchymal organs, with a gradual loss of function. In the end stage of liver cirrhosis, portal hypertension, encephalopathy, bleeding or carcinomas, e.g., hepatocellular carcinoma (HCC) and intrahepatic cholangiocellular carcinoma (iCCCa), can occur. Intestinal fibrosis is one of the most devastating complications of Crohn's disease. With novel and consistent therapeutic interventions, fibrotic processes can be stopped and reversed. New research technologies have substantially improved our knowledge of liver fibrogenesis and intestinal fibrosis. The focus of this review article is on MASLD and Crohn's disease, chronic inflammatory diseases of the liver and intestines with increasing prevalence and a major impact on the general population. The current principles and potential possibilities of preventive and therapeutic antifibrotic interventions are illustrated.