Obesity as a cause of hepatocellular carcinoma.

During recent years the incidence of obesity has increased significantly, and in some instances rapidly, in many resource-rich countries. Paralleling this increase has been an increase in the incidence of hepatocellular carcinoma. It has been estimated that as many as 90% of obese adults will develop the metabolic syndrome. The worldwide incidence of this syndrome in adults at this time ranges from 9 to 34%. Furthermore, obesity in childhood increases the risk of obesity in adulthood, and hence the development of the metabolic syndrome and hepatocellular carcinoma. Ten to 20% of patients with non-alcoholic fatty liver disease progress to non-alcoholic steatohepatitis, and 8.3% of the latter develop cirrhosis. Up to 50% of these patients with cirrhosis, and a significant proportion of those without cirrhosis, progress to hepatocellular carcinoma. Much remains to be learnt about the mechanisms by which obesity and the metabolic syndrome cause hepatocellular carcinoma, although insulin resistance, increased tissue necrosis factor activity, alterations in serum lipids, non-alcoholic fatty liver disease and non-alcoholic steatosis play important roles. There is also increasing evidence that gut microbiota play a role in the development of the metabolic syndrome and hence of hepatocellular carcinoma.

Epidemiology of hepatocellular carcinoma in sub-Saharan Africa.

Published incidences of hepatocellular carcinoma in the Black population of sub-Saharan Africa underestimate the true incidence of the tumor because of the many instances in which hepatocellular carcinoma is either not definitively diagnosed or is not recorded in a cancer registry. Despite this, it is manifestly evident that the tumor occurs commonly and is a major cause of cancer deaths in Black African peoples living in the sub-continent, particularly in those living in rural areas. 46,000 new cases of hepatocellular carcinoma have been recorded to be diagnosed in sub-Saharan Africa each year, and age-standardized incidences of the tumor as high as 41.2/100,000 persons/year have been documented. The highest incidence of hepatocellular carcinoma has been recorded in Mozambique. The tumor occurs at a young age in rural dwelling and, to a lesser extent, urban dwelling Black Africans. It is also more common in men than women, particularly in the younger patients. Cirrhosis co-exists with hepatocellular carcinoma in about 60% of patients and is equally common in the two sexes. The tumor is not only common in the Black African population, it also carries an especially grave prognosis, with about 93% of the patients dying within 12 months of the onset of symptoms. Caucasians living in the sub-continent have a low incidence of hepatocellular carcinoma and it occurs at an older age.

Prevention of hepatocellular carcinoma.

Because of its frequency and grave prognosis, preventing hepatocellular carcinoma is an urgent priority. Prevention should be possible because environmental carcinogens-chronic hepatitis B and C virus infections, dietary exposure to aflatoxins, and iron overload-cause the great majority of these tumors. Chronic hepatitis B virus infection accounts for 55% of global hepatocellular carcinomas and 80% of those in the high-incidence Asia Pacific and sub-Saharan African regions. In these regions the infection that becomes chronic is predominantly acquired very early in life. A safe and effective vaccine against this virus is available and its universal inclusion in the immunization of infants has already resulted in a marked reduction of chronic infection and a 70% decrease in the occurrence of hepatocellular carcinoma in those immunized. Chronic hepatitis C virus infection is the major cause of hepatocellular carcinoma in industrialized countries. The infection is mainly acquired in adulthood and, until a vaccine becomes available, prevention will consist mainly of identifying, counselling, and treating chronically infected individuals, preventing spread of the virus by the use of safe injection practices (particularly in intravenous drug abusers), and screening all donated blood for the presence of the virus. 4.5 billion of the world.s population are exposed to dietary aflatoxins. Prevention involves treating susceptible crops to prevent fungal contamination, and handling the foodstuffs in such a way as to prevent contamination during storage. Iron overload in hereditary hemochromatosis can be prevented by repeated venesection and in African dietary iron overload by fermenting the home-brewed beer in iron-free containers.