Page 173 - ebook HCC

170 PROGRAMME AND ABSTRACTS GENEVA, SWITZERLAND EASL HCC SUMMIT 171
FEBRUARY 13 - 16, 2014

HEPATOCELLULAR CARCINOMA:
EPIDEMIOLOGY AND GLOBAL BURDEN

1
1
Shiv Kumar Sarin , A Jindal , AS Bhadoria 1
1 Department of Hepatology, Institute of Liver and Biliary Sciences, New Delhi, India
Corresponding author’s e-mail: shivsarin@gmail.com

Hepatocellular carcinoma (HCC) is one of the major causes of liver related mortality HCV infection is associated with a 15- 20 fold increase in risk for HCC compared with
in cirrhosis. It is the sixth most common cancer worldwide and the third leading cause HCV-negative subjects; nearly two times more with genotype 1b. Successful HCV cure
of cancer mortality. There is significant geographic and racial disparity in the incidence substantially reduces (57-75%) the risk. Predicting role of HCV viral load and genotype is
and risk for development of HCC. Majority of all liver cancers occur in high-rate areas still controversial.
(>20 HCC /100,000 persons) mainly in Asia (China, Japan and Korea) and Sub-Sahara For the past century, the global risk of HCC has been largely driven by HBV and HCV
Africa (Zimbabwe and Egypt), where chronic Hepatitis B Virus (HBV) infection and/or infection. This is rapidly changing. Common risk factors relevant to HCC risk include
Aflatoxin B1 exposure are common. However, among low-rate areas (<10 HCC /100,000 chronic alcohol intake (> 50 g/day), presence of diabetes (OR-2.5), obesity (OR-
persons) which includes northern Europe as well as North and South America, Hepatitis 1.5), chronic smoking and co-infections (HBV/HCV, HIV/HCV and HBV/HDV). Alcohol
C Virus (HCV) infection, alcohol and metabolic syndrome play more important roles. The might induce HCC risk by the production of acetaldehyde and free radicals during its
length of time these factors have been present determine the risk of HCC development. metabolism, cytochrome P4502E1 induction, modulation of cell regeneration, promotion
Environmental, host genetic, and viral factors can also affect the risk of HCC. Often or exacerbation of nutritional deficiencies, and alterations of the immune system. It is still
patients with HCC presents late and only in less than a third of patients it is curable at uncertain whether alcohol is related to HCC independently of cirrhosis. Non-alcoholic fatty
presentation, rest have 1-year survival of less than 50% and the 5-year survival < 10%. liver disease/Non-alcoholic Steatohepatitis (NASH) with or without metabolic syndrome
CLINICAL SPEAKERS ABSTRACTS Hepatitis B/C and decompensated cirrhosis. At least 80% of HCC have positive serology HCC. A fair proportion of HCC developing in NASH patients occurs in non-cirrhotic livers, CLINICAL SPEAKERS ABSTRACTS
is already emerging as the one of the commonest risk factor of HCC and intrahepatic
More than 80% of HCC patients are cirrhotic. The 5-year cumulative risk of developing
choalngiocarcinoma. The later is gradually becoming an important differential diagnosis of
HCC in cirrhosis ranges between 5% and 30%, more in Asians and in the presence of
elderly subjects and with metabolic syndrome. Small amount of alcohol consumption,
for hepatitis B and/or hepatitis C viruses, with male predominance. Contrary to west, it
NASH and obesity individually add to the risk of developing HCC. Insulin resistance
is not unusual to have HCC before fourth decade in areas where HBV is hyperendemic
increases the risk of HCC substantially. From nearly 60% of all HCC due to HBV, there is a
(e.g, East Asia), as the infection acquired is largely perinatal. There are several known
change in the trend with rise in the HCC due to alcohol and NASH in the past two decades
risk factors for HCC, such as advanced age, male gender, high viral load, raised ALT,
HBeAg positive status cirrhosis, and some of these form the basis of HCC risk scores
with alcohol or obesity and no underlying viral infections. Coffee consumption has been
such as GAG-HCC, CU-HCC and REACH-B. Suppression of HBV viral replication through
shown in several studies and meta-analysis to reduce the risk of cirrhosis and HCC. The
effective use of antiviral therapy or Interferon therapy has been shown to reduce but not in our country. Of the 468 HCC recently analyzed by us, about 18% have association
eliminate the risk of HCC. A 5-fold higher risk to develop HCC among non-cirrhotic chronic relative risk for coffee drinkers vs non-coffee drinkers was 0.54 from case-control studies
HBV infected subjects is documented in comparison to healthy cohorts. A study conducted and 0.64 from cohort studies in development of HCC. Early assessment of hepatic fibrosis
by us also revealed that HBsAg-negative and antibody positive (anti-HBe and/or total anti- using non-invasive tests such as fibroscan, reduction in alcohol consumption, large scale
HBc) have 12.34 times higher risk for HCC, irrespective of presence of cirrhosis. Finally, surveillance programs and universal vaccination against hepatitis B would help reduce the
other factors such as HBV genotype D (vs. A, in India) and genotype C (vs. A/B, except growing burden and late detection of HCC.
Taiwan where B <50 yrs is more often associated with HCC), presence of basal core
promoter mutations, such as T1762 and A1764, mutations in Pre-S, positive family history
of HBV also play an important role.