Cirrhosis is primarily a histological diagnosis defined by diffuse, liver-wide fibrosis separating regenerating nodules of hepatic parenchyma. It is a result of chronic hepatotoxic processes (see below for causes). It is generally regarded as irreversible, although it is now recognised that a degree of fibrosis may resolve if the original insult is removed.
The pathogenesis involves stellate cells (also known as Ito cells) that reside in the the perisinusoidal spaces, i.e. the space between the hepatocytes and the sinusoids. They respond to chronic inflammation by depositing type 1 and 3 collagen which is normally only found within the portal tracts. A process of capillarisation and venulisation also occurs.
The main sequelae of cirrhosis are:
- Reduction in the functional capacity of the liver, in particular synthesis and elimination. Severe cirrhosis may result in hepato-renal syndrome and hepatic encephalopathy.
- Disruption of the architecture and microvasculature may lead to portal hypertension with resulting ascites and porto-systemic varices.
- In the longer term, cirrhosis predisposes to hepatocellular carcinoma.
10% of cases are cryptogenic. The other causes, which may co-exist, include:
- Chronic viral hepatitides - B (+/- D) and C
- Important because it is common world wide and specific treatments for the viral infection may be indicated to prevent
- Alcohol hepatitis causing alcoholic liver cirrhosis
- Non-alcoholic steatohepatitis (causing non-alcoholic fatty liver disease - NAFLD)
- Autoimmune hepatitis
Biliary Tract Diseases
- ↑ Duffin JM. Why does cirrhosis belong to Laennec? CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne. 1987 Sep 1; 137(5):393-6.
- ↑ Moreau R. Acute-on-chronic liver failure: a new syndrome in cirrhosis. Clinical and molecular hepatology. 2016 Mar; 22(1):1-6.(Link to article – subscription may be required.)
- ↑ Sanchez-Pareja A, Clément S, Peyrou M, Spahr L, Negro F, Rubbia-Brandt L, Foti M. Phosphatase and tensin homolog is a differential diagnostic marker between nonalcoholic and alcoholic fatty liver disease. World journal of gastroenterology. 2016 Apr 14; 22(14):3735-45.(Link to article – subscription may be required.)