scholarly journals Ap53genetic polymorphism as a modulator of hepatocellular carcinoma risk in relation to chronic liver disease, familial tendency, and cigarette smoking in hepatitis B carriers

Hepatology ◽  
1999 ◽  
Vol 29 (3) ◽  
pp. 697-702 ◽  
Author(s):  
Ming-Whei Yu ◽  
Shi-Yi Yang ◽  
Yueh-Hsia Chiu ◽  
Yi-Ching Chiang ◽  
Yun-Fan Liaw ◽  
...  
PEDIATRICS ◽  
1992 ◽  
Vol 89 (4) ◽  
pp. 795-800 ◽  
Author(s):  

HEPATITIS B DISEASE AND EPIDEMIOLOGY In the United States 200 000 to 300 000 acute infections with hepatitis B virus (HBV) occur each year.1,2 More than one million persons in the United States have chronic HBV infection, and approximately 4000 to 5000 persons die each year from HBV-induced chronic liver disease and hepatocellular carcinoma. Although HBV infections occur during childhood and adolescence, the full impact of these infections is not recognized until many years later when chronic liver disease and hepatocellular carcinoma may develop. The incidence of HBV infection increases rapidly during adolescence, with higher rates among blacks than among whites (Fig 1).3 Although rates vary by region, sex, and race, between 3.3% and 25% of all persons have had HBV infection by 25 to 34 years of age. The likelihood of becoming chronically infected with HBV varies inversely with the age at which infection occurs. HBV transmitted from hepatitis B surface antigen (HBsAg)-positive mothers to their newborns results in HBV carriage for up to 90% of infants. Between 25% and 50% of children infected before 5 years of age become carriers, whereas only 6% to 10% of acutely infected adults become carriers. It is estimated that more than 25% of carrier infants will die from primary hepatocellular carcinoma or cirrhosis of the liver, with most of these deaths occurring during adult life. HBV infection occurs more commonly in certain populations, including Pacific Islanders, Alaskan Natives, immigrants from countries in which infection is highly endemic, persons who require multiple transfusions of blood or blood products, and persons with high-risk lifestyles, including intravenous drug abuse and contact with multiple sexual partners.


2008 ◽  
Vol 6 (4) ◽  
pp. 189-198 ◽  
Author(s):  
Hajime Hada ◽  
Terukatsu Arima ◽  
Kazumi Togawa ◽  
Yoshio Okada ◽  
Shigeru Morichika ◽  
...  

The Lancet ◽  
1973 ◽  
Vol 302 (7831) ◽  
pp. 690-694 ◽  
Author(s):  
W.D. Reed ◽  
A.L.W.F. Eddleston ◽  
R.B. Stern ◽  
Roger Williams ◽  
A.J. Zuckerman ◽  
...  

1981 ◽  
Vol 305 (18) ◽  
pp. 1067-1073 ◽  
Author(s):  
David A. Shafritz ◽  
Daniel Shouval ◽  
Howard I. Sherman ◽  
Stefanos J. Hadziyannis ◽  
Michael C. Kew

Gut ◽  
1998 ◽  
Vol 42 (1) ◽  
pp. 107-111 ◽  
Author(s):  
M Guilera ◽  
J C Sáiz ◽  
F X López-Labrador ◽  
E Olmedo ◽  
S Ampurdanés ◽  
...  

Background—The hepatitis G virus (HGV), a recently identified member of the Flaviviridae family, can cause chronic infection in man but the role of this agent in chronic liver disease is poorly understood.Aims—To evaluate the prevalence and meaning of HGV infection in a large series of patients with chronic liver disease.Subjects—Two hundred volunteer blood donors, 179 patients with chronic hepatitis C, 111 with chronic hepatitis B, 104 with alcoholic liver disease, 136 with hepatocellular carcinoma, and 24 with cryptogenic chronic liver disease were studied.Methods—HGV RNA was investigated in serum samples by reverse transcription and polymerase chain reaction amplification of the 5′ non-coding region of HCV and hybridisation to a specific probe. The main features of HGV RNA seropositive and seronegative patients were compared.Results—The prevalence of HGV infection was 3% in blood donors, 7% in chronic hepatitis C, 8% in chronic hepatitis B, 2% in alcoholic liver disease, 4% in hepatocellular carcinoma, and 8% in cryptogenic chronic liver disease. HGV infected patients tended to be younger than non-infected patients but no differences concerning sex, possible source of infection, clinical manifestations, biochemical and virological parameters, or severity of liver lesions were found.Conclusions—The prevalence of HGV infection in chronic liver disease seems to be relatively low in our area. Infection with HGV does not seem to play a significant pathogenic role in patients with chronic liver disease related to chronic HBV or HCV infection or to increased alcohol consumption, or in those with cryptogenic chronic liver disease.


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