The Impact of Type 2 Diabetes on the Development of Hepatocellular Carcinoma in Different Viral Hepatitis Statuses

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http://cebp.aacrjournals.org/cgi/content/abstract/18/7/2054

Cancer Epidemiology Biomarkers & Prevention 18, 2054, July 1, 2009. Published

Online First June 23, 2009;

doi: 10.1158/1055-9965.EPI-08-1131

The Impact of Type 2 Diabetes on the Development of Hepatocellular Carcinoma in

Different Viral Hepatitis Statuses

Chong-Shan Wang1,2, Wei-Jen Yao3, Ting-Tsung Chang4, Shan-Tair Wang5 and Pesus

Chou1

1 Community Medicine Research Center and Institute of Public Health, National

Yang-Ming University, Taipei, Taiwan; 2 A-Lein Community Health Center,

Kaohsiung County, Taiwan; 3 Department of Radiology, Division of

Gastroenterology, 4 Department of Internal Medicine and Institute of Clinical

Medicine, and 5 Institute of Public Health, College of Medicine, National Cheng

Kung University, Tainan, Taiwan

Requests for reprints: Pesus Chou, Community Medicine Research Center and

Institute of Public Health, National Yang Ming University, Shih-Pai, Taipei 112,

Taiwan. Phone: 886-2-2822-9695; Fax: 886-2-2820-1461. E-mail: pschou@...

Background: The risk of type 2 diabetes on the development of hepatocellular

carcinoma remains inconclusive in different hepatitis statuses.

Methods: We prospectively followed a community-based cohort with 5,929 persons

in southern Taiwan from January 1997 through December 2004, made up of 4,117

seronegative, 982 anti–hepatitis C virus–positive [HCV(+)], 696 hepatitis B

surface antigen–positive [HBsAg(+)], and 134 coinfected persons. Before the

study, 546 participants had developed diabetes. Hepatocellular carcinoma

diagnoses were from the National Cancer Registry.

Results: After 50,899 person-years of follow-up, 111 individuals had developed

hepatocellular carcinoma. The highest risk of hepatocellular carcinoma, compared

with seronegative individuals without diabetes, was in anti-HCV(+) individuals

with diabetes [incidence rate ratio (IRR), 76.0], then coinfected (IRR, 46.0),

anti-HCV(+) without diabetes (IRR, 26.1), HBsAg(+) with diabetes (IRR, 21.4),

and seronegative with diabetes (IRR, 7.2; P < 0.001). Anti-HCV(+) (n = 132) and

seronegative individuals (n = 352) with diabetes had a higher cumulative

incidence rate of hepatocellular carcinoma than those without diabetes (log-rank

test, P < 0.001). Multivariate proportional hazards analysis showed that

gender, age, body mass index 30, HBsAg(+) [hazards ratio (HR), 12.6],

anti-HCV(+) (HR, 18.8), coinfection (HR, 25.9), and diabetes [hr, 2.7; 95%

confidence interval (95% CI), 1.7-4.3] were independent predictors of

hepatocellular carcinoma (P < 0.05). After stratifying hepatitis status in

multivariate analysis, diabetes was significant for seronegative (HR, 5.4;

95% CI, 1.7-17.1) and anti-HCV(+) individuals (HR, 3.1; 95% CI, 1.7-5.4). Body

mass index 30 was significant for HBsAg(+) individuals (HR, 3.3; 95% CI,

1.3-8.1).

Conclusion: Type 2 diabetes is a strong independent predictor of hepatocellular

carcinoma in anti-HCV(+) and seronegative individuals but not in HBsAg(+)

individuals. (Cancer Epidemiol Biomarkers Prev 2009;18(7):2054–60)