Cirrhosis of the liver is a chronic progressive disease involving scarring and destruction of the liver substance and injury to all its structural elements. Depending on the form and stage of the disease, individuals may suffer from weakness, emaciation, jaundice, fever and bleeding. Clubbed fingers, anaemia and leukaemia may also occur, and ultimately, death, which usually results from hepatic coma or haemorrhages from dilated veins of the oesophagus and stomach.
Cirrhosis is characterized anatomically by widespread nodules in the liver combined with fibrosis. It can result from many causes, such as abuse of alcohol, chronic viral hepatitis, metabolic and biliary diseases. The co-existence of another chronic liver disease in a patient who abuses alcohol likely increases the risk of developing cirrhosis (eg. an alcoholic with chronic viral hepatitis C).
Hepatitis C is now the leading cause of cirrhosis worldwide and, consequently, of liver transplant.
In the USA, alcohol abuse is the leading cause of liver cirrhosis. Anatomically, alcoholic cirrhosis is almost always micronodular (i.e. the regenerating liver nodules are small). Alcoholic cirrhosis can occur in patients who have never had evidence of alcoholic hepatitis. Cirrhosis can lead to end-stage liver disease. While, historically, alcohol-related liver cirrhosis has been regarded as a condition that develops after two or three decades of heavy drinking, it’s increasingly showing up in 20- and 30-year-olds. In the 25 to 34 age group, death from cirrhosis more than tripled between 1999 and 2016. The rise in alcohol-related deaths overlapped with a rise in binge drinking in the U.S. that correlates with the 2008 financial crisis.