Hepatocellular carcinoma is the 5th most common malignant neoplasm and the second most deadly cancer in oncology.
The disease rarely develops in an intact liver. Predisposing factors are chronic viral hepatitis B and C, alcoholic liver disease, liver steatosis , some metabolic diseases (diabetes, hemochromatosis , Wilson’s disease). In the last stages of the disease, cirrhosis of the liver develops, which is a precancerous condition.
Not every patient with liver cirrhosis develops cancer, but statistics show that more than 60% of patients with hepatocellular carcinoma develop on the background of cirrhotic liver. Liver cirrhosis is the final stop in a long process of organ damage.
As for the risk of cancer, the reason for achieving this degree of damage is not minor. The data show that the risk of developing cancer against the background of alcoholic or metabolic cirrhosis is about 10%, while with cirrhosis, which develops against the background of chronic infection with the hepatitis C virus, the risk of hepatocellular carcinoma is three times higher.
From viral hepatitis at a much greater rate, chronic infection reaches in the case of hepatitis. A chronic infection process changes the structure of the liver, normal liver cells are replaced by non-functional fibrous tissues. Cirrhosis is significantly more common in patients with chronic hepatitis C than in patients with chronic hepatitis B.
The strong association of chronic viral infection with the development of hepatocellular carcinoma initiates a scientific search for pathophysiological mechanisms behind the scenes of this relationship. It has been shown that hepatitis B viral DNA can participate in liver cells at key positions in their hereditary information and stimulate the growth, division and transformation of infected cells.
However, these findings are relevant to only a small proportion of patients with hepatitis B. In most patients with chronic hepatitis B infection, the incorporation of viral hepatitis B DNA appears to be random and does not follow a specific pattern of behavior to be followed to cause the transformation malignant cells.
Many scientists agree that prolonged active inflammation in the liver changes not only the structure and organization of body cells, but also the microenvironment of growth factors and active molecules. In complexity, the presence of viruses intracellularly , activation of the immune system and changes in the environment around liver cells are at the root of the genetic changes that trigger carcinogenesis.
Chronic alcohol abuse, poorly controlled diabetes and metabolic syndrome are other risk factors for impaired liver function and accumulation of simple lipids in liver cells. The condition is known as steatosis and is easily confirmed by ultrasound. The next degrees of damage are steatohepatitis , steatofibrosis and cirrhosis of the liver, in relation to which the risk of developing hepatocellular carcinoma is even greater.
Prevention of hepatocellular carcinoma is not directed at cancer, but at nosological units and bad habits that can lead to liver damage in severe cirrhosis. There is a mandatory vaccine against hepatitis B.
Prevention and adequate treatment of metabolic syndrome, diabetes, and limiting alcohol abuse are also considered. If liver cirrhosis has already developed, patients should have an ultrasound scan every three months. In patients with viral cirrhosis and hemochromatosis, the levels of tumor markers are monitored every 3-6 months, and in cirrhosis of a different etiology – every 6-12 months.