Liver fibrosis is an excessive scarring of a wound, in which connective tissue accumulates within the liver. In this situation, there is excessive production of extracellular matrix, degraded, or both. The trigger for this excessive production or degradation of the extracellular matrix normally is an injury to the liver, more so then there is an inflammatory component present. Fibrosis in it of itself does not cause any symptoms, but it can cause portal hypertension as the excessive scarring disrupts smooth blood flow to the liver or cirrhosis due to scarring causing damage to the liver making it dysfunctional. The diagnosis is normally done by way of a liver biopsy. The treatment consists of treating the underlying cause.
In liver fibrosis, there is accumulation of excessive connective tissues within the liver. This accumulation is due to repetitive chronic liver cell injuries. Frequently, fibrosis progresses and compromises the structure and then the function of the liver, as hepatocytes undergoing regeneration try to repair and replace damaged tissues. Widespread disruption leads to liver cirrhosis.
Several types of chronic liver injuries can result in liver fibrosis. Acute, self-limiting hepatic injury like viral hepatitis A, even if it is fulminating, does not normally damage the basic structure of the liver and, therefore, does not promote the development of fibrosis despite depletion of hepatocytes. In the early stages, liver fibrosis may revert if the cause is reversible. If the patient is exposed to repetitive injuries to the liver spanning over years, fibrosis is more or less permanent. It develops at an even greater rate in the presence of mechanical obstruction of the bile ducts.
What Causes Liver Fibrosis?
The activation of the perivascular stellate liver cells which store lipids promotes development of fibrosis. These and the adjoining cells proliferate and become contractile cells called myofibroblasts, which produce excessive amounts of abnormal matrix and cellular matrix proteins, and with the addition of the Kupffer cells, injured hepatocytes, platelets and leukocytes, reactive O2 species and inflammatory mediators are released. Consequently, the activation of the stellate cells results in development of abnormal extracellular matrix, both in composition and amount causing liver fibrosis.
The myofibroblasts which are stimulated by endothelin-1 promote an increase in resistance in the portal vein and also increase density of abnormal matrix causing portal hypertension. The fibrous tracts are united with branches of the afferent portal and efferent hepatic veins allowing to them to bypass the hepatocytes and limit the blood supply. Therefore, fibrosis is one of the primary causes for both hepatocyte ischemia along with hepatocellular dysfunction and also portal hypertension. The magnitude of ischemia and portal hypertension gives an overview of the status of the liver and how much has it been affected by fibrosis. For example, congenital hepatic fibrosis affects the branches of the portal vein but spares the parenchyma with resultant portal vein hypertension albeit with normal hepatocellular function.
What are the Signs and Symptoms of Liver Fibrosis?
Hepatic fibrosis by itself does not result in any noticeable symptoms. The main symptoms are usually from the underlying cause of liver fibrosis or when the fibrosis advances to liver damage or cirrhosis due to portal hypertension arising out of liver fibrosis. The patient may experience bleeding from varicose veins and ascites (accumulation of fluid in the abdominal cavity). Cirrhosis can be catastrophic for the patient and cause complete liver failure.
How is Liver Fibrosis Diagnosed?
- Clinical evaluation
- Blood draws with radiologic studies
- Liver biopsy
Liver fibrosis will be in the reckoning if the patient has a known history of chronic liver disease, abuses alcohol, has hepatitis. The functionality of the liver can be determined by liver function tests and in cases of a liver dysfunction these tests will be abnormal. Once liver fibrosis is suspected, further investigations will be done and once confirmed its extent will be determined. The knowledge of extent of fibrosis can help physicians formulate an effective treatment plan for the patient.
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