Cirrhosis refers to the development of irreversible scarring and damage to the liver through chronic repetitive injury. As the liver tries to regenerate itself it develops regenerative nodules of liver tissue surrounded by scar tissue or fibrosis. Repetitive liver injury can be caused by chronic viral infection (HCV or HBV), repetitive alcohol misuse, fatty liver and steatohepatitis (NASH, non-alcoholic steatohepatitis), autoimmune liver disease (antibodies against the liver), iron overload (haemochromatosis or hemochromatosis) or various cholestatic disease such as primary biliary cirrhosis (biliary cholangiopathy) or sclerosing cholangitis. There are other rarer causes of cirrhosis.
The dogma has always been that once cirrhosis develops it never reverses to normal, but we know that this is not strictly true and removal of a repetitive insult can lead to reversal of cirrhosis (e.g. the alcoholic who stops drinking) but the vast majority of cases do NOT revert to normal.
Liver cancer or hepatocellular carcinoma:
The risk of liver cancer for patients with cirrhosis is between 2-5% per annum, hence why it is recommended that all patients with cirrhosis undergo regular surveillance by ultrasound examination of the liver for liver cancer every 6 months. Early diagnosis can lead to a cure. I am not an expert in the treatment of liver cancer and if detected you would be referred to a specialist.
Portal Hypertension, Ascites, Hepatorenal Syndrome, and encephalopathy
I have considerable experience in the management of complications of cirrhosis. The development of cirrhosis leads to portal hypertension which causes the development of dilated veins in the oesophagus or stomach (oesophageal or gastric varices), the development of fluid in the peritoneal cavity (ascites which can become infected), hepatorenal syndrome (acute kidney failure) or hepatic encephalopathy (mental confusion, slowing and sleep disturbance). Treatment of these complications is straightforward although some patients respond poorly to treatment or develop lots of side effects.
Alcohol Misuse and Alcoholic Liver Disease
It is estimated that 25% of the adult population regularly drink more than the recommended limits for alcohol (14 units/week in women, and now 14 units/week in men).
In general you need to consume >100 units/week for more than ten years to develop cirrhosis but there are many exceptions. Thus, we see young women who have developed cirrhosis more rapidly whilst consuming 50 units/week. There is wide genetic variability and only 20-25% of subjects who drink excessive alcohol develop liver disease.
However, alcohol misuse causes significantly increases mortality from cardiac disease, stroke, various cancers or pancreatic disease. Thus, alcohol misuse is associated with a much lower survival than normal, but mainly through other causes of death rather than liver disease per se.
As Clinical Lead for the Alcohol Care Team at the Royal Free London Foundation Trust, which now includes Barnet and Chase Farm Hospitals we see a lot of patients with alcohol misuse or alcohol related liver disease. We provide a caring non-judgemental environment for the care of our patients. People drink for many reasons such as anxiety, social, or because of past trauma. Some have established habits that are triggered by certain situations. Clearly to overcome addictive behaviour these issues have to be dealt with, and to this end we have also established a transpersonal integrative psychotherapeutic counselling service for our patients who would benefit from such treatments. I have good links with a number of psychotherapists who could offer counselling to overcome such barriers to recovery.
DVLA, driving and Screening for chronic alcohol misuse
The classic tests that doctors have used historically for screening for alcohol misuse namely the Gamma GT and MCV measurement are useless, being normal in 50% of subjects with alcohol used disorders. The DVLA have adopted measurement of carbohydrate deficient transferrin (CDT) in drivers who have lost their licence in the UK. CDT gives a time integrated index of alcohol consumption over the previous ten days or so, and has a specificity and sensitivity of 90% and 60%. In Germany they use measurement of urinary ethyl glucuronide/ethyl sulphate, which has a very high sensitivity (90%) and specificity (95%) and can detect alcohol consumption in the previous 72 hours. There are other tests such as fatty acid ethyl esters, hair ethyl glucuronide which I can discuss with you. If you have lost your licence and need to prove continued abstinence from alcohol there are a number of approaches that I employ, including remote monitoring by breathalyser as well as CDT and urinary ethyl glucuronide testing.
Drug-Induced Liver Injury or drug hepatotoxicity
Drug-induced liver injury is one of the commonest causes for a drug to be withdrawn from the market. In general most drug reactions involving the liver are idiosyncratic and take between 3-8 weeks to develop. Paracetamol is an exception, since it is directly hepatotoxic in overdose, with liver injury being maximal at 3-4 days post ingestion. Paracetamol hepatoxicity may be enhanced by alcohol or anti-epileptic drugs or St John’s Wort. Paracetamol is the commonest cause of acute liver failure in the UK, accounting for >200 cases per year.
Other dugs commonly associated with severe hepatotoxicity include the anti-tuberculous drugs isoniazid and pyrazinamide, as well as co-amoxiclav, NSAIDs, Chinese herbal medicines, and various anti-depressants.