Liver fibrosis is the excess of extracellular matrix that cumulate after unyielding ignition and sustained liver damage that direct to an exaggerated tissue hangout process . When hepatic fibrosis is very severe , cirrhosis of the liver develops . In the liver , the most frequent causes that produce fibrosis are chronic viral hepatitis B or C , autoimmune hepatitis , biliary disease , alcoholic , and non - alcoholic steatohepatitis .
Is Fibrosis of the Liver Reversible?
From the clinical point of vista , meek fibrosis is asymptomatic , however the procession to cirrhosis characterized by replacement of the functional parenchyma by scar tissue , twisting and alteration of the vascular architecture with nodule formation of regeneration , clinically may certify itself with alterations in hepatic synthetic occasion with problem in clotting , atomic number 7 management and detoxification system , as well as portal hypertension datum with constitution of ascites and bleeding due to esophageal varix , increased susceptibility to infections and increase risk of hepatocellular carcinoma .
If these problem are notice ab initio before the development of liver cirrhosis , the antiviral treatment could be indicated in the pillowcase of viral hepatitis , intervention with diet and exercise for non - alcohol-dependent steatohepatitis , the discontinuation of intoxicant consumption in case of alcohol-dependent steatohepatitis , thus as the treatment for the residue of the hepatitis , and to keep off that hepatic cirrhosis is reached . However , many patients go to the doctor with innovative fibrosis or cirrhosis of the liver and in this case the process is usually irreversible . For this reason , the development of an anti - fibrotic treatment to foreclose the progression of innovative fibrosis to cirrhosis and to put up regression to avoid complications is very important .
Pathogenic Bases Of The Progression Of Hepatic Fibrosis And Reversibility
There are key chemical mechanism and different cells that check the progression of fibrosis ( fibrogenesis ) and statistical regression ( fibrolysis ) . The extracellular matrix is formed due to ontogenesis factors , cytokines , chemokines and a series of consequence that admit the processes of fibrogenesis and fibrolysis .
Hepatic fibrosis is a dynamic process that result in hepatic remodeling . The liver has a groovy capacity for regeneration . However , this role is lose when there is hepatic damage and results in inadequate regeneration with progressive scarring ( cirrhosis of the liver ) and an increased risk of hepatocellular carcinoma .
Currently there is no effective therapeutic method acting to limit and not even to revoke this appendage , but inquiry in the expanse of cellular pathology and molecular biota have bring out very supporting perspectives about the possibility of find effective treatments for this condition .
The central pathogenic process of cirrhosis of the liver is reform-minded fibrosis . Since decades ago it was suspected that the deposition of connective tissue paper was an unnatural scar response to liver harm due to chemical or infectious agents and that it was the effect of the infiltration of fibroblasts in the liver parenchyma . Therefore , it has been considered an irreversible mental process as with any other scar . Currently there is a more accurate picture of the biomolecular complexity of the fibrogenesis process based on studies of the connective tissue paper of the normal liver as well as the cirrhotic liver . In the normal liver , interstitial collagen ( character I and III ) are chance almost alone around the portal spaces and central veins , while type IV collagen forms very delicate fibers around the place of Disse . In dividing line , in cirrhosis of the liver , collagen I and III are deposited in and through the hepatic lobules , progressively create maverick septum that can become very thick and that geld and inclose portion of the hepatic lobule , forming what is known as regeneration nodules . This distortion of the architecture is the crusade of the serious alteration of arterial and venous intrahepatic circulation . The deposit of collagen type IV in the space of Disse is accompanied by exit of fenestration in the sinusoidal endothelial jail cell , which limits the rally between the hepatocytes and the plasma .
Conclusion
doubtlessly , cellular biota and molecular pathology have notice very promising routes to prevent and reverse liver cirrhosis , at least in data-based modelling .
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