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.
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.
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.
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.
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 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.
Gall bladder polyps, previously called cholesterolosis is being increasing diagnosed on ultrasound scan, quite simply because the scanners today are so much better than they were ten year ago. This is causing increasing and often unnecessary anxiety in patients. The prevalence of Gallbladder polyps (GBPs) is estimated at ~5% in the global adult population,but I suspect it is higher now that better ultrasound scan machines are used.
Your doctor has told you that you have gall bladder polyps:
Should you be worried? No
Can gall bladder polyps become cancerous? Yes they can, but rarely.
So how worried should I be, now that I have gall bladder polyps? Most gall bladder polyps are small and inconsequential and if <4mm in size, they are virtually NEVER malignant.
When do doctors become worried about gall bladder polyps? When they approach or exceed 1cm in size. Gallbladder polyps that are 1cm (10mm) in asymptomatic patients less than 50 years old have a low risk of malignancy, and therefore, a careful “wait and see with follow up by using ultrasonography strategy” might be more appropriate than immediate cholecystectomy. However, at present we just don’t know the risk. The choice is between regular surveillance ultrasound scan or cholecystectomy.
So what do I do? Until we know more about the natural history of gall bladder polyps the current advice is regular imaging by ultrasound, with laparascopic cholecystectomy if needed (gall bladder polyp >1cm in size and age >50 years). If I was in my 40’s (I wish I was) with a 1cm gall bladder polyp what would I do? I think I would opt for a laparascopic cholecystectomy. I say this because we know that up to 5% of such polyps become malignant or are malignant, and monitoring just causes extra stress but no resolution. But the choice is between you and your surgeon/physician.
We see many patients who have had an ultrasound scan which identifies a “lesion” which is probably a haemangioma, but many radiographers (non doctor ultrasonographers) and even radiologists (medically qualified clinicians who undertake ultrasonography) will sit on the fence and be reluctant to say “this is a haemangioma”, mainly because it is hard to be certain. They are 98% certain but not certain. This makes the patient and the GP worried that they may be missing something. In this instance the best test is an MRI scan of the liver. An MRI of the liver generally takes about 30 minutes. It is noisy since the scanner makes a loud noise, and most units provide headphones and horrible piped music (you may like the music, tastes vary!). If you suffer from claustrophobia you may find such a scan difficult, but some units have open scanners which make it easier. If you undertake this privately is needs to be done with contrast, and can be quite expensive (between £500 to £1200 at a guess). If you wish to read about liver haemagioma see the EASL clinical guidelines on benign liver tumours on the link below or just google”EASL benign liver”