Brief Article
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World J Gastroenterol. May 7, 2014; 20(17): 5060-5065
Published online May 7, 2014. doi: 10.3748/wjg.v20.i17.5060
Hepatitis B and C viruses are not risks for pancreatic adenocarcinoma
Ming-Chu Chang, Chien-Hung Chen, Ja-Der Liang, Yu-Wen Tien, Chiun Hsu, Jau-Min Wong, Yu-Ting Chang
Ming-Chu Chang, Chien-Hung Chen, Ja-Der Liang, Jau-Min Wong, Yu-Ting Chang, Department of Internal Medicine, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei 101, Taiwan
Yu-Wen Tien, Department of Surgery, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei 101, Taiwan
Chiun Hsu, Graduate Institute of Oncology, College of Medicine, National Taiwan University, Taipei 101, Taiwan
Author contributions: Chang MC, Chen CH and Chang YT contributed to the study concept and design; all the authors contributed to the acquisition of data; Chang MC, Chen CH, Liang JD, Chang YT contributed to analysis and interpretation of data; Chang MC, and Chang YT contributed to drafting of the manuscript and statistical analysis; Chang MC contributed to administrative, technical, and material support; Chang YT contributed to the study supervision.
Supported by National Science Council, Taiwan, NSC94-2314-B002-272, NSC94-3112-B-002-017, NSC95-3112-B-002-001, and NSC95-2314-B-002-244-M Y3, NSC98-2314-B-002, NSC99-2314-B-002-096, NSC102-2321-B-002-083; National Taiwan University Hospital, and Liver Disease prevention and Treatment Research Foundation, NTUH 95M022, NTUH 98M 1227
Correspondence to: Yu-Ting Chang, MD, MS, PhD, Department of Internal Medicine, National Taiwan University Hospital, College of Medicine, National Taiwan University, Chung Shan South Road 7, Taipei 101, Taiwan. yutingchang@ntu.edu.tw
Telephone: +886-2-23123456-65768 Fax: +886-2-23633658
Received: November 11, 2013
Revised: January 5, 2014
Accepted: January 19, 2014
Published online: May 7, 2014
Processing time: 176 Days and 15.1 Hours
Abstract

AIM: To investigate whether hepatitis B virus (HBV) and hepatitis C virus (HCV) increase risk of pancreatic ductal adenocarcinoma (PDAC).

METHODS: We recruited 585 patients with cytological and/or pathologically confirmed PDAC in National Taiwan University Hospital from September 2000 to September 2013, and 1716 age-, sex-, and race-matched controls who received a screening program in a community located in Northern Taiwan. Blood samples were tested for the presence of HCV antibodies (anti-HCV), HBV surface antigen (HBsAg), antibodies against HBsAg (anti-HBs), and hepatitis B core antigen (anti-HBc) in all cases and controls. The odds ratio (OR) of PDAC was estimated by logistic regression analysis with adjustment diabetes mellitus (DM) and smoking.

RESULTS: HBsAg was positive in 73 cases (12.5%) and 213 controls (12.4%). Anti-HCV was positive in 22 cases (3.8%) and 45 controls (2.6%). Anti-HBs was positive in 338 cases (57.8%) and 1047 controls (61.0%). The estimated ORs of PDAC in multivariate analysis were as follows: DM, 2.08 (95%CI: 1.56-2.76, P < 0.001), smoking, 1.36 (95%CI: 1.02-1.80, P = 0.035), HBsAg+/anti-HBc+/anti-HBs-, 0.89 (95%CI: 0.89-1.68, P = 0.219), HBsAg-/anti-HBc+/anti-HBs+, 1.03 (95%CI: 0.84-1.25, P = 0.802).

CONCLUSION: HBV and HCV infection are not associated with risk of PDCA after adjustment for age, sex, DM and smoking, which were independent risk factors of PDAC.

Keywords: Hepatitis B virus, Hepatitis C virus, Pancreatic ductal adenocarcinoma, Risk, Endemic disease, Diabetes mellitus

Core tip: Previous studies on hepatitis B virus (HBV) status and pancreatic cancer risk have produced conflicting results. This study is the first study to use controls from the general population compared to previous hospital-based case-controls studies with age- and sex-matched controls. HBV infection was determined by measuring antibodies against hepatitis B core antigen and HBV surface antigen. The risk of HBV/hepatitis C virus infection was evaluated after adjustment for important risk factors such as age, sex, diabetes mellitus and smoking in a high-endemic HBV area.