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Title: Hepatitis B antigenemia, specific immune deficiency and hepatocellular carcinoma
Authors: Simons, M.J.
Yu, M.
Shanmugaratnam, K. 
Issue Date: 1973
Citation: Simons, M.J., Yu, M., Shanmugaratnam, K. (1973). Hepatitis B antigenemia, specific immune deficiency and hepatocellular carcinoma. Tumor Research Vol. 8 : 120-126. ScholarBank@NUS Repository.
Abstract: One of the major objectives of studies involving Hepatitis B antigen (HB Ag) is to determine whether HB antigenemia following exposure to the HB agent is a risk factor in the development of hepatocellular carcinoma (HCC). An increased frequency of HB Ag was demonstrated in the sera of patients with HCC and those with other chronic liver diseases. It has been claimed that these findings provide circumstantial evidence in support of the view that persistent HB antigenemia (the 'carrier state') predisposes to the development of HCC. There appear to be 2 main modes of immune responsiveness on exposure to the HB agent; development either of immunity with the production of antibody to HB Ag in the absence of detectable antigen, or of HB antigenemia with or without specific antibody (HB Ab). In the former situation, immune mechanisms appear to be effective in eliminating the HB agent. By contrast, the carrier state of HB antigenemia probably reflects an ineffective immune response and consequent persisting infection. Based on the foregoing, it is postulated that exposure to the HB agent, a precondition for the development of HB antigenemia may cause HCC either directly or indirectly through one of the types of post hepatitic pathology. Evidence relating to this proposition may be obtained by answering the following questions. Do HCC patients differ from suitable ethnic, sex and age matched normal subjects and patients with a variety of liver diseases in HB agent exposure rate, or in the proportion of antigenemic persons in the exposed population (HB antigenemic rate)? Do individuals who are infected by the HB agent, and in particular those who become HB Ag 'carriers', develop HCC more frequently than individuals who are not exposed? Could the incidence of HCC be decreased by the introduction of measures directed towards reducing the risk of exposure and in particular of developing HB antigenemia (eg. vaccination of the population at risk, elimination of the HB agent)? The present status of some studies in progress in Singapore relating to the first of these questions is summarised in this paper.
Source Title: Tumor Research
ISSN: 00414093
Appears in Collections:Staff Publications

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