Hepatic fibrosis is overly exuberant wound healing in which excessive connective tissue builds up in the liver. The extracellular matrix is either overproduced, degraded deficiently, or both. The trigger is chronic injury, especially if there is an inflammatory component. Fibrosis itself causes no symptoms but can lead to portal hypertension (the scarring distorts blood flow through the liver) or cirrhosis (the failure to properly replace destroyed liver cells results in liver dysfunction). Diagnosis is based on liver biopsy. Treatment involves correcting the underlying condition when possible.
Hepatic fibrosis itself does not cause symptoms. Symptoms may develop secondary to the primary disorder or to portal hypertension. Portal hypertension with splenomegaly is often asymptomatic unless complications develop, such as variceal GI bleeding, ascites, or portal-systemic encephalopathy. Eventually, cirrhosis supervenes.
Hepatic fibrosis is suspected in patients who have an underlying disorder or take a drug that could cause fibrosis or who have unexplained abnormalities in liver function or enzymes. Noninvasive tests (eg, serologic markers) are under study but are not yet ready for routine clinical use. Imaging tests such as ultrasonography, CT, and MRI may detect findings associated with fibrosis (eg, portal hypertension, splenomegaly, cirrhosis) but are not sensitive to parenchymal fibrosis itself. Liver biopsy is currently the only means of detecting hepatic fibrosis. Biopsy is indicated to clarify the diagnosis (eg, nonalcoholic steatohepatitis, primary biliary cirrhosis) and stage its progress (eg, in chronic hepatitis C, whether fibrosis is present or whether it has progressed to cirrhosis).