Although much progress has been made in the prevention and treatment of chronic viral hepatitis in recent decades, this disease remains burdened by a significant complication rate, including liver cirrhosis and hepatocellular carcinoma.
Despite the preventive measures introduced, the incidence of cirrhosis and hepatocellular carcinoma has increased in recent years in both the United States and Europe.
Hepatic infections linked to the two main etiological agents of the disease, the hepatitis C and B viruses, cause over one million deaths every year and it is expected that by 2040, deaths from chronic hepatitis will exceed those combined of HIV, tuberculosis and malaria.
Most hepatitis C virus infections are generally caused by contact with contaminated blood. It is believed that actions such as the repeated use of a non-sterilized syringe or needle are among the main causes that lead to a type C virus infection.
On the contrary, infection with hepatitis B virus is mainly linked to a transmission from mother to child. In fact, only 5% of people become infected in adulthood.
A new Swedish study, recently published in The New England Journal of Medicine, assessed whether low-dose aspirin could reduce the risk of developing hepatocellular carcinoma in patients with chronic viral hepatitis.
For this purpose, the researchers used the data collected in nationwide Swedish health registries, identifying a first group of over 50,000 subjects diagnosed with chronic hepatitis B or C who did not have a history of aspirin use.
This group was compared to a second group of patients who were starting to take low-dose aspirin.
The two main endpoints of the study were the diagnosis of hepatocellular carcinoma and liver-related mortality. The incidence of gastrointestinal bleeding was also assessed.
The results of the study showed that the estimated incidence of hepatocellular carcinoma was 4% among patients treated with aspirin, while it rose to 8.3% among patients who did not use this drug.
The analysis of the data also revealed that the risk of developing liver cancer was increasingly reduced if the aspirin treatment was prolonged over time, reaching a risk ratio of 0.57 when the drug was taken for 5 or more years.
Liver-related ten-year mortality was also positively influenced by aspirin intake, resulting in 11% among users and 17.9% among non-users.
Concerning safety, results are completely reassuring. In fact, the ten-years risk of gastrointestinal bleeding did not differ significantly between the two groups of patients.
This research, therefore, seems to confirm the protective effect induced by aspirin against the development of liver cancer in patients with chronic viral hepatitis. An advantage obtained without increasing simultaneously the risk of gastrointestinal bleeding.
The mechanisms by which aspirin exerts its protective effect on liver cells have not yet been defined, but among these, the prevention of platelet degranulation, the modulation of bioactive lipids and the inhibition of cyclooxygenase-2, a proinflammatory enzyme, have been proposed.
Hepatocellular carcinoma mortality has recently been increasing faster than that from any other cancer. Having simple and safe treatments, already available on the market, could help counteract this trend.
On the other hand, as the authors admit, to confirm these results conclusively, additional randomized clinical trials will be needed, designed to evaluate the benefits of aspirin in the prevention of hepatocellular carcinoma.
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