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RISK FACTORS

Hepatocellular carcinoma (HCC or liver cancer) is a major health problem. Worldwide, it is responsible for 500 000 deaths annually. A number of risk factors are associated with either the induction of the disease or its progression; these include infection with hepatitis B (HBV) or hepatitis C (HCV) virus, alcohol consumption, non-alcoholic steatohepatitis and certain congenital disorders. In approximately 80% of the cases, liver cancer is associated with cirrhosis or advanced fibrosis and with inflammation and oxidative stress.

Hepatitis B
Chronic hepatitis B is the most frequent cause of liver cancer in countries with few medical resources. In fact, more than half of all liver cancer incidence in the world can be attributed to chronic hepatitis B. The risk and development of liver cancer in hepatitis B carriers appears to depend largely on ethnicity. Caucasian hepatitis B carriers tend to develop liver cancer at an advanced age after a period of progressive liver cirrhosis, whereas Asian and African individuals tend to develop liver cancer in young adulthood and middle age and might exhibit fewer signs of cirrhotic liver disease than white hepatitis B carriers. Genetic variation might underlie the differences between these ethnic groups. Alternatively, this difference might be explained by variations in the age at which HBV infection is acquired in different populations: vertical transmission is the major route of HBV acquisition in Asia, whereas horizontal transmission in early life is the predominant route of transmission in Africa. By contrast, in Western countries HBV is mostly transmitted in adolescence and adulthood through high-risk behaviors, such as intravenous drug use, sexual exposure or iatrogenic causes including blood transfusion, unsafe needle practices, invasive procedures, hemodialysis or organ transplantation.

Hepatitis C
Hepatitis C is the leading cause of both chronic liver disease and liver cancer in most Western countries, including the United States. HCV is usually transmitted through direct exposure to blood, such as intravenous drug use or high-risk sexual behavior involving multiple sexual contacts Iatrogenic transmission of HCV via contaminated needles, syringes and other medical instruments and procedures is also common. Since the implementation of HCV screening programs for donated blood in 1992 in the majority of developed countries the risk of HCV transmission from a blood transfusion is now less than 0.03% per unit transfused.Other potential routes of transmission include intranasal cocaine use, scarification, cupping, tattooing, and body piercing. Concurrent heavy alcohol use, diabetes mellitus, latent HBV infection, increasing age, belonging to a black ethnic group, a low platelet count, high levels of alkaline phosphatase, presence of varices and smoking seem to increase the risk of liver cancer in patients with HCV

Comorbidities and Environmental Factors
Alcoholic liver disease is the second most common risk factor for liver cancer in the United States, after hepatitis C. Women are more susceptible than men to liver injury from alcohol intake�women are more likely than men to develop cirrhosis at equivalent alcohol intakes�owing to sex differences in alcohol metabolism.Coexisting viral hepatitis increases the effect of excessive alcohol intake on the risk of liver cancer.

Non Alcoholic Steatohepatitis (NASH) is also emerging as a risk factor for liver cancer in many developed countries.Obesity, a major risk factor for NASH, has increased in the United States; contemporary survey data suggest that one-third of American adults are obese.[48,49] Although the increased number of people with NASH (as a result of increases in the prevalence of both obesity and the metabolic syndrome) is believed to contribute to the rising incidence of liver cancer, few population-based data support this assumption, as the loss of liver steatosis with the development of cirrhosis makes it difficult to prove a history of NASH at the time of liver cancer diagnosis.

Finally, Aflatoxin B is a mycotoxin that acts synergistically with HBV in the development of liver cancer. Aflatoxin causes DNA mutations, particularly of the TP53 gene, that attenuate the tumor suppressor function of p53. This mycotoxin frequently contaminates food in regions with low medical resources, such as sub-Saharan Africa and eastern Asia. Efforts to eliminate aflatoxin B exposure are ongoing in regions with particularly high exposure to this mycotoxin, including China and West Africa

REFERENCES

Bosch, F. X., Ribes, J., Diaz, M. & Cleries, R. Primary liver cancer: worldwide incidence and trends. Gastroenterology 127 (Suppl. 1), S5-S16 (2004).
Chen, C. L. et al. Metabolic factors and risk of hepatocellular carcinoma by chronic hepatitis B/C infection: a follow-up study in Taiwan. Gastroenterology 135, 111-121 (2008).
Flegal, K. M., Carroll, M. D., Ogden, C. L. & Curtin, L. R. Prevalence and trends in obesity among US adults, 1999-2008. JAMA 303, 235-241 (2010). 
Hassan, M. M. et al. Risk factors for hepatocellular carcinoma: synergism of alcohol with viral hepatitis and diabetes mellitus. Hepatology 36, 1206-1213 (2002).
Ikeda, K. et al. Antibody to hepatitis B core antigen and risk for hepatitis C-related hepatocellular carcinoma: a prospective study. Ann. Intern. Med. 146, 649-656 (2007). Lok, A. S. et al. Incidence of hepatocellular carcinoma and associated risk factors in hepatitis C-related advanced liver disease. Gastroenterology 136, 138-148 (2009).
Ohki, T. et al. Obesity is an independent risk factor for hepatocellular carcinoma development in chronic hepatitis C patients. Clin. Gastroenterol. Hepatol. 6, 459-464 (2008).
Parkin, D. M. The global health burden of infection-associated cancers in the year 2002. Int. J. Cancer 118, 3030-3044 (2006).

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