Family history of liver cancer may modify the association between HBV infection and liver cancer in a Chinese population.


Journal

Liver international : official journal of the International Association for the Study of the Liver
ISSN: 1478-3231
Titre abrégé: Liver Int
Pays: United States
ID NLM: 101160857

Informations de publication

Date de publication:
08 2019
Historique:
received: 12 04 2019
revised: 07 06 2019
accepted: 08 06 2019
pubmed: 23 6 2019
medline: 18 9 2020
entrez: 23 6 2019
Statut: ppublish

Résumé

The potential interaction between family history of liver cancer and HBV infection on liver cancer has not been fully examined. We conducted a population-based case-control study composed of 2011 liver cancer cases and 7933 controls in Jiangsu province, China from 2003 to 2010. Data on major risk or protective factors were collected and HBV/HCV sero-markers were assayed using blood samples. Semi-Bayes (SB) adjustments were applied to provide posterior estimates. Both family history of liver cancer (adjusted odds ratios [OR]: 4.32, 95% confidence intervals [CI]: 3.25-5.73) and hepatitis B surface antigen (HBsAg) positivity (adjusted OR: 9.94, 95% CI: 8.33-11.87) were strongly associated with liver cancer development. For individuals with different combinations of serological markers, the adjusted ORs were 8.45 (95% CI: 5.16-13.82) for HBsAg- and HBcAb-positive; 7.57 (95% CI: 4.87-11.77) for HBsAg-, HBeAg- and HBcAb-positive; and 3.62 (95% CI: 2.47-5.31) for HBsAg-, HBeAb- and HBcAb-positive, compared to all negatives in HBV serological markers. One log increase in HBV DNA level was associated with 17% increased risk (adjusted OR: 1.17, 95% CI: 1.03-1.32). The SB-adjusted OR of HBV-positive individuals with family history of liver cancer was 41.34 (95% posterior interval [PI]: 23.69-72.12) compared with those HBV-negative without family history. Relative excess risk due to additive interaction, the attributable proportion and synergy index were 73.13, 0.87 and 8.04 respectively. Adjusted ratio of OR for multiplicative interaction was 2.84 (95% CI: 1.41-5.75). Super-additive and super-multiplicative interactions may exist between family history of liver cancer and HBV infection on the development of liver cancer.

Sections du résumé

BACKGROUND & AIMS
The potential interaction between family history of liver cancer and HBV infection on liver cancer has not been fully examined.
METHODS
We conducted a population-based case-control study composed of 2011 liver cancer cases and 7933 controls in Jiangsu province, China from 2003 to 2010. Data on major risk or protective factors were collected and HBV/HCV sero-markers were assayed using blood samples. Semi-Bayes (SB) adjustments were applied to provide posterior estimates.
RESULTS
Both family history of liver cancer (adjusted odds ratios [OR]: 4.32, 95% confidence intervals [CI]: 3.25-5.73) and hepatitis B surface antigen (HBsAg) positivity (adjusted OR: 9.94, 95% CI: 8.33-11.87) were strongly associated with liver cancer development. For individuals with different combinations of serological markers, the adjusted ORs were 8.45 (95% CI: 5.16-13.82) for HBsAg- and HBcAb-positive; 7.57 (95% CI: 4.87-11.77) for HBsAg-, HBeAg- and HBcAb-positive; and 3.62 (95% CI: 2.47-5.31) for HBsAg-, HBeAb- and HBcAb-positive, compared to all negatives in HBV serological markers. One log increase in HBV DNA level was associated with 17% increased risk (adjusted OR: 1.17, 95% CI: 1.03-1.32). The SB-adjusted OR of HBV-positive individuals with family history of liver cancer was 41.34 (95% posterior interval [PI]: 23.69-72.12) compared with those HBV-negative without family history. Relative excess risk due to additive interaction, the attributable proportion and synergy index were 73.13, 0.87 and 8.04 respectively. Adjusted ratio of OR for multiplicative interaction was 2.84 (95% CI: 1.41-5.75).
CONCLUSIONS
Super-additive and super-multiplicative interactions may exist between family history of liver cancer and HBV infection on the development of liver cancer.

Identifiants

pubmed: 31228882
doi: 10.1111/liv.14182
pmc: PMC6705127
mid: NIHMS1045272
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1490-1503

Subventions

Organisme : NCI NIH HHS
ID : T32 CA009142
Pays : United States
Organisme : NIEHS NIH HHS
ID : R21 ES011667
Pays : United States
Organisme : NINR NIH HHS
ID : K01 NR017852
Pays : United States
Organisme : NIAID NIH HHS
ID : U01 AI035040
Pays : United States
Organisme : FIC NIH HHS
ID : D43 TW000013
Pays : United States

Informations de copyright

© 2019 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

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Auteurs

Xing Liu (X)

Department of Epidemiology, Fielding School of Public Health, University of California, Los Angeles, California.
Department of Epidemiology, School of Public Health, Fudan University, Shanghai, China.

Aileen Baecker (A)

Department of Epidemiology, Fielding School of Public Health, University of California, Los Angeles, California.

Ming Wu (M)

Jiangsu Provincial Center for Disease Control and Prevention, Nanjing, Jiangsu, China.

Jin-Yi Zhou (JY)

Jiangsu Provincial Center for Disease Control and Prevention, Nanjing, Jiangsu, China.

Jie Yang (J)

Jiangsu Provincial Center for Disease Control and Prevention, Nanjing, Jiangsu, China.

Ren-Qiang Han (RQ)

Jiangsu Provincial Center for Disease Control and Prevention, Nanjing, Jiangsu, China.

Pei-Hua Wang (PH)

Jiangsu Provincial Center for Disease Control and Prevention, Nanjing, Jiangsu, China.

Zi-Yi Jin (ZY)

Department of Epidemiology, School of Public Health, Fudan University, Shanghai, China.

Ai-Min Liu (AM)

Dafeng Center for Disease Control and Prevention, Dafeng, Jiangsu, China.

Xiaoping Gu (X)

Dafeng Center for Disease Control and Prevention, Dafeng, Jiangsu, China.

Xiao-Feng Zhang (XF)

Ganyu Center for Disease Control and Prevention, Ganyu, Jiangsu, China.

Xu-Shan Wang (XS)

Ganyu Center for Disease Control and Prevention, Ganyu, Jiangsu, China.

Ming Su (M)

Chuzhou County Center for Disease Control and Prevention, Chuzhou, Jiangsu, China.

Xu Hu (X)

Chuzhou County Center for Disease Control and Prevention, Chuzhou, Jiangsu, China.

Zheng Sun (Z)

Tongshan County Center for Disease control and Prevention, Tongshan, Jiangsu, China.

Gang Li (G)

Tongshan County Center for Disease control and Prevention, Tongshan, Jiangsu, China.

Alan Fu (A)

Department of Epidemiology, Fielding School of Public Health, University of California, Los Angeles, California.

Su Yon Jung (SY)

Jonsson Comprehensive Cancer Center, UCLA, Los Angeles, California.
School of Nursing, UCLA, Los Angeles, California.

Lina Mu (L)

Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, University at Buffalo, The State University of New York, Buffalo, New York.

Na He (N)

Department of Epidemiology, School of Public Health, Fudan University, Shanghai, China.

Liming Li (L)

Department of Epidemiology, School of Public Health, Peking University, Beijing, China.

Jin-Kou Zhao (JK)

Jiangsu Provincial Center for Disease Control and Prevention, Nanjing, Jiangsu, China.

Zuo-Feng Zhang (ZF)

Department of Epidemiology, Fielding School of Public Health, University of California, Los Angeles, California.
Jonsson Comprehensive Cancer Center, UCLA, Los Angeles, California.
Center for Human Nutrition, David Geffen School of Medicine, UCLA, Los Angeles, California.

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