The recommendations from the specialist groups are based on the common belief that alcoholic cirrhosis patients have a liver cancer risk that tops 1.5 percent per year. (That’s the level at which screening is considered cost-effective.)
But Jepsen’s team says the risk may actually be much lower - a 1 percent chance over five years, based on their findings.
What’s more, the researchers found, less than 2 percent of deaths in their study group were due to liver cancer.
Some past studies in various countries have suggested that liver cancer is a bigger risk for alcoholic cirrhosis patients than the current study implies. (A study in France, for example, found that cirrhosis patients developed cancer at a rate of over 5 percent per year.)
Hepatitis means inflammation of the liver. The inflammation can range from mild to severe.
- Mild hepatitis may not cause any symptoms. The only indication of inflammation may be an abnormal level of liver enzymes in the blood, which can be detected by a blood test. However, in some cases the hepatitis becomes persistent (chronic), which can gradually damage the liver and eventually cause cirrhosis.
- A more severe hepatitis tends to cause symptoms such as feeling sick, jaundice (yellowing of the skin, caused by a high level of bilirubin - a chemical normally metabolised in the liver), generally feeling unwell and, sometimes, pain over the liver.
- A very severe bout of alcoholic hepatitis can quickly lead to liver failure. This can cause deep jaundice, blood clotting problems, confusion, coma, and bleeding into the guts, and is often fatal.
- The main treatment for alcoholic hepatitis is to provide adequate nutrition (this sometimes involves passing liquid feeds through a tube in the stomach) and steroids.
Cirrhosis is a condition where normal liver tissue is replaced by scar tissue (fibrosis). The scarring tends to be a gradual process. The scar tissue affects the normal structure and regrowth of liver cells. Liver cells become damaged and die as scar tissue gradually develops. So, the liver gradually loses its ability to function well. The scar tissue can also affect the blood flow through the liver which can cause back pressure in the blood vessels which bring blood to the liver.
About 1 in 10 heavy drinkers will eventually develop cirrhosis. It tends to occur after 10 or more years of heavy drinking. Note: cirrhosis can develop in people who have never had alcoholic hepatitis.
Cirrhosis can happen from many causes other than alcohol - for example, persistent viral hepatitis and some hereditary and metabolic diseases. If you have another persistent liver disease, and drink heavily, you are likely to increase your risk of developing cirrhosis.
Cirrhosis can lead to end-stage liver disease (liver failure). However, in the early stages of the condition, often there are no symptoms. You can get by with a reduced number of working liver cells. But, as more and more liver cells die, and more and more scar tissue builds up, symptoms start to appear. The eventual symptoms and complications are similar to a severe episode of hepatitis (listed above). However, unlike a bout of severe hepatitis, the symptoms and complications tend to develop slowly.
But Jepsen said the bigger numbers are based on “clinic-based” studies, which look at select groups of patients being treated at medical centers.
His team’s study, in contrast, was population-based. They had information on all 8,482 Danish citizens who had a first-time hospitalization for alcoholic cirrhosis between 1993 and 2005.
Population-based studies give a clearer idea of the liver cancer risk for the typical alcoholic cirrhosis patient.
Jepsen said he thinks his team’s findings are likely to be relevant to countries other than Denmark. The higher rates that have been in some other countries, he noted, are probably because of study design, rather than actual geographic variation.
SOURCE: Annals of Internal Medicine, June 19, 2012
Risk for Hepatocellular Carcinoma in Patients With Alcoholic Cirrhosis: A Danish Nationwide Cohort Study
Results: Among 8482 patients, 169 developed HCC. A total of 5734 patients died, 151 of whom had developed HCC. Five-year cumulative HCC risk was 1.0% (95% CI, 0.8% to 1.3%), and 5-year cumulative mortality was 43.7% (CI, 42.6% to 44.7%). Only 1.8% of all deaths were HCC-related. In sensitivity analyses that included all possible HCC diagnoses and a subpopulation of patients who were followed by hepatologists, the highest 5-year HCC risk was 1.9% (CI, 0.8% to 3.9%). These patients did not have higher mortality than patients in the nationwide cohort.
Limitation: Cirrhosis and HCC diagnoses were made by hospital physicians without uniform clinical criteria, and use of registry data precluded detailed information on clinical care of patients, including HCC surveillance.
Conclusion: Danish patients with alcoholic cirrhosis have a low risk for HCC, and HCC contributes little to their high mortality. On the basis of these data, HCC surveillance would be expected to have a minimal effect on mortality and is unlikely to be cost-effective.
Peter Jepsen, MD, PhD; Peter Ott, MD, DMSc; Per Kragh Andersen, PhD, DMSc; Henrik Toft S?rensen, MD, PhD, DMSc; and Hendrik Vilstrup, MD, DSc