Hepatocellular carcinoma in young, mentally retarded HBsAg carriers without cirrhosis

Lohiya, Ghan-Shyam; Pirkle, Hubert; Hoefs, John C.; Lohiya, Sunita; Ngo, Vinh Trong

doi:10.1002/hep.1840050519

“…We have observed a very high HCC incidence (246 times greater than United States males) in institutionalized mentally retarded HBsAg carriers (7). This finding was contrary to the previously assumed rarity of HCC in such populations (5).…”

Section: Introductioncontrasting

confidence: 76%

Serum alpha fetoprotein in 714 mentally retarded carriers of hepatitis B surface antigen

Lohiya¹,

Lohiya²,

Fischer³

et al. 1988

Eur J Epidemiol

1

0

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Sera from 714 mentally retarded carriers of hepatitis B surface antigen were screened for alpha fetoprotein (AFP) by monoclonal radioimmunoassay. Serum AFP levels were less than 20 mcg/L in 708 (99.2%) carriers. One 29-year-old carrier with normal liver function had serum AFP level of 1500 mcg/L, which increased to 12,500 mcg/L after 72 days. She died of multifocal hepatocellular carcinoma (HCC) with cirrhosis. Five other carriers with serum AFP levels between 20 and 165 mcg/L are alive without clinical HCC. No correlation was found between serum AFP level and race, age, sex, Down's syndrome, serum alanine aminotransferase level, and hepatitis B e antigen positivity. Single cross-sectional serum AFP screening by itself is not sufficient for early diagnosis of HCC.

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“…Although HCC is thought to be multifactorial in aetiology, some evidence indicates that HBV can act alone as a risk factor for the tumour (Lohiya et al 1985). HBsAg-positive mentally handicapped children, growing up in an environment thought to be free of aflatoxin B 1 and other known chemical carcinogens, had a relative risk for developing HCC of 246.…”

Section: Introductionmentioning

confidence: 99%

Hepatitis B virus and hepatocellular carcinoma

Arbuthnot¹,

Kew²

2001

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Chronic hepatitis B virus (HBV) infection is a major global cause of hepatocellular carcinoma (HCC). Individuals who are chronic carriers have a greater than 100-fold increased relative risk of developing the tumour. Several mechanisms of HBV-induced HCC have been proposed. Integration of HBV DNA into the genome of hepatocytes occurs commonly, although integration at cellular sites that are important for regulation of hepatocyte proliferation appears to be a rare event. Functions of the HBx protein are also potentially oncogenic. These include transcriptional activation of cellular growth regulatory genes, modulation of apoptosis and inhibition of nucleotide excision repair of damaged cellular DNA. The effects of HBx are mediated by interaction with cellular proteins and activation of cell signalling pathways. Variations in HBV genome sequences may be important in hepatocarcinogenesis, although their significance has not yet been completely elucidated. Necroinflammatory hepatic disease, which often accompanies chronic HBV infection, may contribute indirectly to hepatocyte transformation in a number of ways, including by facilitating HBV DNA integration, predisposing to the acquisition of cellular mutations and generating mutagenic oxygen reactive species. Although HCC is a malignancy with a poor prognosis, the availability of an effective vaccine against HBV infection, and its inclusion in the Expanded Programme of Immunization of many countries, augurs well for the eventual elimination of HBV-associated HCC.

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“…Although HCC is thought to be multifactorial in aetiology, some evidence indicates that HBV can act alone as a risk factor for the tumour (Lohiya et al . 1985).…”

Section: Introductionmentioning

confidence: 99%

Hepatitis B virus and hepatocellular carcinoma

Arbuthnot

¹

,

Kew

²

2001

Int J Experimental Path

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Chronic hepatitis B virus (HBV) infection is a major global cause of hepatocellular carcinoma (HCC). Individuals who are chronic carriers have a greater than 100-fold increased relative risk of developing the tumour. Several mechanisms of HBV-induced HCC have been proposed. Integration of HBV DNA into the genome of hepatocytes occurs commonly, although integration at cellular sites that are important for regulation of hepatocyte proliferation appears to be a rare event. Functions of the HBx protein are also potentially oncogenic. These include transcriptional activation of cellular growth regulatory genes, modulation of apoptosis and inhibition of nucleotide excision repair of damaged cellular DNA. The effects of HBx are mediated by interaction with cellular proteins and activation of cell signalling pathways. Variations in HBV genome sequences may be important in hepatocarcinogenesis, although their significance has not yet been completely elucidated. Necroinflammatory hepatic disease, which often accompanies chronic HBV infection, may contribute indirectly to hepatocyte transformation in a number of ways, including by facilitating HBV DNA integration, predisposing to the acquisition of cellular mutations and generating mutagenic oxygen reactive species. Although HCC is a malignancy with a poor prognosis, the availability of an effective vaccine against HBV infection, and its inclusion in the Expanded Programme of Immunization of many countries, augurs well for the eventual elimination of HBV-associated HCC.

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Hepatocellular carcinoma in young, mentally retarded HBsAg carriers without cirrhosis

Cited by 15 publications

References 7 publications

Serum alpha fetoprotein in 714 mentally retarded carriers of hepatitis B surface antigen

Serum alpha fetoprotein in 714 mentally retarded carriers of hepatitis B surface antigen

Hepatitis B virus and hepatocellular carcinoma

Hepatitis B virus and hepatocellular carcinoma

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