Article

Chronic Hepatitis B Virus Infection and Pancreatic Cancer: A Case-control Study in Southern China

Department of Gastrointestinal and Pancreatic Surgery, the First Affiliated Hospital, Sun Yat-Sen University, China.
Asian Pacific journal of cancer prevention: APJCP (Impact Factor: 2.51). 01/2011; 12(6):1405-8.
Source: PubMed

ABSTRACT

The association of hepatitis B virus (HBV) infection and pancreatic cancer is still controversial. The purpose of this study is to determine whether chronic HBV infection increases the risk.
In this case-control study, there were 1,066 patients recruited, with 533 in the study group and 533 controls, frequency-matched for age and sex. Blood samples were collected to detect hepatitis viral infection.
Compared to 77 patients (14.4%) in the control group, 80 pancreatic cancer patients (15.0%) were seropositive for HBV surface antigen (not statistically significant, P=0.8). The prevalence of HBV e antigen was higher in study group than that of control group (P=0.03). Further analysis indicated that HBeAg was a risk factor for pancreatic cancer (OR=2.935, 95% CI: 1.048-8.220).
In HBV endemic area of China, there appears to be no significant association between chronic HBV infection and pancreatic cancer, but the role of HBeAg needs further exploration.

Full-text

Available from: Haoran Li, Jan 06, 2014
Asian Pacic Journal of Cancer Prevention, Vol 12, 2011
1405
Chronic Hepatitis B Virus Infection and Pancreatic Cancer in Southern China
Asian Pacic J Cancer Prev, 12, 1405-1408
Introduction
Hepatitis B virus (HBV) has caused worldwide public
health problems, especially in China. It is estimated that
more than 2 billion people in the world were previously
exposed to HBV, and more than 350 million of them are
chronic carriers (WHO, 2008). As a result, 600,000 deaths
approximately can be attributed to HBV associated disease
such as hepatocellular cancer and liver cirrhosis by annual
incidence (Shepard et al., 2006; Caldwell and Park, 2009).
e prevalence of HBV infection in China is up to 7.18%,
which means more than 90 million Chinese are infected.
HBV has a strong preference for liver cells and is
interrelated to hepatocellular cancer consequently.
Although the virus can be found in some extrahepatic
organs such as kidney and pancreas, it was not originally
considered that the virus contributed to carcinogenesis
of these ones (Ganem and Prince, 2004). However, some
recent studies reported that there was relationship between
pancreatic cancer and infection with HBV (Hassan et al.,
2008; Iloeje et al., 2009).
Provided their intimate relationship in anatomy and
common blood supply shared by liver and pancreas,
its reasonable to presume that HBV could mislocate in
pancreas. In fact, HBsAg and HBV DNA were detected in
pancreatic juice and tissue several decades ago (Hoefs et
al., 1980; Yoshimura et al., 1981; Dejean et al., 1984). Viral
penetration and multiplication in pancreatic cells might
lead to further injuries. Some studies demonstrated that
1
Department of Gastrointestinal and Pancreatic Surgery, the First Aliated Hospital, Sun Yat-Sen University,
2
Department of Medical
Oncology, Cancer Centre, Sun Yat-Sen University,
3
Department of Colorectoanal Surgery, NanHai Hospital,Nanfang Medical University,
China *For correspondence: caishr@mail.sysu.edu.cn
Abstract
Background: e association of hepatitis B virus (HBV) infection and pancreatic cancer is still controversial.
e purpose of this study is to determine whether chronic HBV infection increases the risk. Methods: In this case-
control study, there were 1,066 patients recruited, with 533 in the study group and 533 controls, frequency-matched
for age and sex. Blood samples were collected to detect hepatitis viral infection. Results: Compared to 77 patients
(14.4%) in the control group, 80 pancreatic cancer patients (15.0%) were seropositive for HBV surface antigen (not
statistically signicant, P=0.8). e prevalence of HBV e antigen was higher in study group than that of control
group ( P=0.03). Further analysis indicated that HBeAg was a risk factor for pancreatic cancer (OR=2.935, 95% CI:
1.048-8.220). Conclusions: In HBV endemic area of China, there appears to be no signicant association between
chronic HBV infection and pancreatic cancer, but the role of HBeAg needs further exploration.
Keywords: Hepatitis B Virus - pancreatic cancer - hepatitis C virus - case-control study - HBeAg
RESEARCH COMMUNICATION
Chronic Hepatitis B Virus Infection and Pancreatic Cancer: A
Case-control Study in Southern China
Fang Zhu
1
, Hao-Ran Li
2
, Guo-Neng Du
3
, Jian-Hui Chen
1
, Shi-Rong Cai
1
*
pancreatic enzyme elevated in chronic hepatitis patients
(Katakura et al., 2005). Moreover, higher level of HBsAg
was detected in tissue specimens of pancreatic carcinoma
and chronic pancreatitis (Hohenberger, 1985).
Although these previous studies suggested that HBV
might play a role in the development of pancreatic cancer,
the information we can refer to is limited currently. e
purpose of this study is to explore whether chronic HBV
infection would increase the risk of pancreatic cancer.
Materials and Methods
Patients
is study is a multi-centre, case-control study. From
January 1997 to September 2008, patients treated in two
hospitals in Southern China (the First Aliated Hospital
of Sun Yat-sen University and Cancer Center of Sun Yat-
sen University) were screened to recruit. e inclusion
criteria of study group were as follows: pancreatic cancer
conrmed by histology or diagnosed by symptoms, signs
and more than two types of imaging tools; age of 16 years
or older; no other malignancy coexisted. Patients in the
control group were chosen randomly in the patients from
orthopedics department and neurology department in the
same hospitals. Patients in case and control groups were
frequency-matched by age (±5 years) and sex. e study
was conducted in accordance with the ethics principles
of the Declaration of Helsinki. Written informed consent
was obtained from all patients.
Page 1
Fang Zhu et al
Asian Pacic Journal of Cancer Prevention, Vol 12, 2011
1406
Viral infection testing
Blood samples were collected from patients before
treatment. Enzyme-linked immunosorbent assay was used
to test for the presence of HBsAg, hepatitis B antibody
(anti-HBs), anti-HBc, hepatitis B e antigen (HBeAg),
hepatitis B e antibody (anti-HBe), hepatitis A antibody
(anti-HAV), hepatitis C antibody (anti-HCV), hepatitis
D antibody (anti-HDV), hepatitis E antibody (anti-HEV).
The researchers running these assays were blinded for the
subjects. Uncertain results should be reconrmed at an
outside laboratory (Kingmed Diagnostics, Guangzhou,
China).
Chronic HBV infection was dened by the presence of
HBsAg, and appearance of anti-HBs signies the recovery
of HBV infection or immunized with vaccine (Lee, 1997).
HBeAg was considered as an indication of high titers of
HBV in the blood, and seroconversion to anti-HBe was
a marker of circulating viral load reduction (Ganem and
Prince, 2004). Detection of anti-HBc but negative for
HBsAg and anti-HBs was a evidence of past exposure to
HBV (Lee, 1997). Chronic HCV infection was dened by
the presence of anti-HCV (Pawlotsky et al., 1998).
Statistical analysis
Sample size was estimated under the presumption that
infection rates in control and study group are 10% and 16%
respectively according to prior studies, and the power to
detect this dierence is 80% with 5% level of signicance.
According to these parameters, 1000 patients were needed
at least. Student’s t-test was used to compare means of age
and Chi-square tests were used to compare proportions
between the two groups. Unconditional logistic regression
was conducted to explore potential risk factors. SPSS 16.0
for Windows (SPSS Inc., Chicago, IL) was used for all
statistical analysis.
Results
At last, there were 1,066 patients recruited, with 533 in
study group and 533 in control group. e study:control
ratio is 1:1. ere were no signicant dierences in age and
sex between the study and control groups (Table 1). e
proportion of diabetes in pancreatic cancer patients (n=86,
16.1%) was higher than that in the control group (n=62,
11.6%) with statistically signicant dierence (P=0.03).
HBsAg was seropositive in 80 cases (15.0%) in
the study group and 77 cases (14.4%) in the control
group (Table 2). e between-group dierence was not
statistically signicant (P=0.8). e prevalence of HBeAg
was signicantly higher in the study group (2.6% vs. 0.9%,
P=0.03), while the prevalences of anti-HBs (38.1% vs.
61.7%, P<0.0001), anti-HBc (35% vs. 45.2%, P=0.04) and
anti-HBe (20.1% vs. 31.5%, P<0.0001) were lower in study
group than those in the control group.
The prevalences of anti-HCV and anti-HEV were
higher in pancreatic cancer patients than that in the control
group, but neither has statistically signicant dierences
(P=0.4, P=0.3). Besides, the prevalences of anti-HAV and
anti-HDV had no signicant dierences between the study
and control groups.
To evaluate the risk factors associated with pancreatic
cancer further, we employed logistic regression to analyze
the data. As shown in Table 1, it was indicated that diabetes
(OR=1.464, 95% CI: 1.029-2.083) and HBeAg (OR=2.935,
95% CI: 1.048-8.220) were risk factors for pancreatic
cancer. HCV (OR=1.1.592, 95% CI: 0.562-4.512) and HEV
(OR=1.814, 95% CI: 0.584-5.322) didnt increase the risk
of pancreatic cancer statistically.
Discussion
Chronic HBV infection was dened by the presence
of HBsAg (Lee, 1997), and its prevalence in both groups
were almost the same in our study. e major nding of
this study was that there was no signicant dierence
in chronic HBV infection between pancreatic cancer
patients and other patients in hepatitis B endemic area of
China. is is in accordance with some studies in Korea.
A prospective research recruited 201,975 HBsAg positive
individuals to follow up for a median of 12 years. As a
result, the adjusted relative risk of pancreatic cancer for
HBsAg positivity was 1.13 (95% CI: 0.84-1.52), suggesting
no association between pancreatic cancer and hepatitis B
infection (de Gonzalez et al., 2009). Additionally, a recent
case-control study between pancreatic cancer and stomach
cancer patients among Koreans also reported a negative
result. e odds ratio of HBsAg is 0.90 (95% CI: 0.52-1.56)
(Hong et al., 2010).
But some studies reported dierent conclusions. A
prospective cohort study conducted in Taiwan reported
that chronic carriers of HBsAg had a signicantly high
risk of pancreatic cancer, with the HR of 1.95 (95% CI:
1.01-3.78) (Iloeje et al., 2009). ere are also some studies
which didn’t reach clear conclusions. In a retrospective
cohort study conducted in the United States, researchers
compared the risk of pancreatic cancer development in
28,719 HBV-negative patients, 5,141 previous exposed
patients and 404 active infected patients. Univariate
analysis showed that prior HBV infection was associated
with pancreatic cancer, with a hazard ratio of 1.827 (95%
CI: 1.154-2.891). However, in a multivariate analysis
that included race, sex, and age, the result was no longer
statistically signicant (Gordon et al., 2009). Besides, a
case-control study in the United States indicated that there
was a relationship between the presence of hepatitis B
core antibody (anti-HBc) and pancreatic cancer patients
showing a hazard ratio of 2.5 (95% CI: 1.5-4.2). But the
role of HBsAg was hard to evaluate, because the cases with
positive HBsAg was few in this study (Hassan et al., 2008).
e truth is that pancreatic cancer related deaths rank
fourth in the United States while the incidence is much
lower in China (Hidalgo, 2010; Jemal et al., 2008). Given
that HBV infection did contribute to the development
of pancreatic cancer, it would be very confusing that the
Table 1. Risk Factors for Pancreatic Cancer and
Association with Hepatitis Virus Infection (OR(95%CI)
Variable Univariable Multiple
HBeAg Positive 2.849 (1.019-7.965) 2.935 (1.048-8.220)
Anti-HCV positive 1.509 (0.533-4.268) 1.592 (0.562-4.512)
Anti-HEV positive 1.814 (0.604-5.448) 1.764 (0.584-5.322)
Diabetes 1.462 (1.029-2.077) 1.464 (1.029-2.083)
Page 2
Asian Pacic Journal of Cancer Prevention, Vol 12, 2011
1407
Chronic Hepatitis B Virus Infection and Pancreatic Cancer in Southern China
0
25.0
50.0
75.0
100.0
Newly diagnosed without treatment
Newly diagnosed with treatment
Persistence or recurrence
Remission
None
Chemotherapy
Radiotherapy
Concurrent chemoradiation
10.3
0
12.8
30.0
25.0
20.3
6.3
51.7
75.0
51.1
30.0
31.3
54.2
56.3
27.6
25.0
33.1
30.0
31.3
23.7
31.3
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HBV epidemic countries such as China and Korea have a
relatively lower incidence of pancreatic cancer. erefore,
the result of our study is reasonable from this perspective.
Interestingly, we found the prevalence of HBeAg was
signicantly higher in pancreatic cancer patients, (2.6%
vs. 0.9%, P=0.03). Further analysis indicated that HBeAg
was a risk factor for pancreatic cancers (OR=2.935, 95%
CI: 1.048-8.220). HBeAg is a marker of HBV replication,
and the seroconversion from HBeAg to anti-HBe is
considered as a sign of disease recovery. Some studies
have demonstrated that continuous HBeAg detection
increases the risk of hepatocellular carcinoma (Yang
et al., 2002; Yang et al, 2010). e possible association
between HBeAg and pancreatic cancer may lie in similar
mechanism: high-titer HBV replication stimulates
continuous inammatory response, which could be a
pivotal step of tumor progression (Coussens and Werb,
2002). Nevertheless, the study was not designed for
HBeAg and the patients who are seropositive of HBeAg
is quite few in both groups of our study especially in the
control group, so it is not proper to make conclusions.
Moreover, there might be another explanation that HBV
reactivation was secondary to oncogenesis considering
frequent suppression of immunity function in cancer
patient (Oksuzoglu et al., 2002). We also found that the
prevalences of anti-HBs, anti-HBe and anti-HBc were
even higher in the control group. e reason may lie in
suppression of immunity function, either (Oksuzoglu et
al., 2002). We will do further research to make it clear.
In this study, we also found that diabetes mellitus was
associated with pancreatic cancer signicantly with the
OR of 1.462(95% CI: 1.029-2.077) which coincided with
the reported risk association between pancreatic cancer
and diabetes mellitus (Everhart and Wright, 1995). In
addition, there have been reports of high frequency of
HCV infection in pancreatic patients (Hassan et al.,
2008; El-Serag et al., 2009). Similarly, we found that the
prevalence of anti-HCV and Anti-HEV was higher in
pancreatic cancer patients than that in control group.
However, logistic regression didn’t identify them as risk
factors, and we will increase the sample size to conrm
the conclusion in further study.
Our study has some limitations. As a case-control
study, the control group came from other patients but
not the healthy individuals, allowing the possibility of
admission bias. However, the prevalence of HBV in our
study was similar with previous report in the same area
(Wang et al., 2007), suggesting that control group is
qualied to represent the general population of the area.
Furthermore, all patients were from HBV endemic district,
with the infection prevalence much higher than other
district of China, so the result can’t represent the situation
of the whole country. is problem will be solved in the
upcoming prospective study.
In summary, current evidence indicated that there was
no signicant association between chronic HBV infection
and pancreatic cancer. However, the data provided some
hints that HBeAg may play a role in the development of
pancreatic cancer. is study is the rst one to report the
relationship between HBV infection and pancreatic cancer
in Mainland China and further studies are expected to
conrm our conclusion.
Page 3
Fang Zhu et al
Asian Pacic Journal of Cancer Prevention, Vol 12, 2011
1408
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Page 4
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    • "References Country or area Age (years) Study period Study design Control type PaC ascertainment Number of cases Number of control participants a HBV markers HBV detection NOS score Berrington de Gonzalez et al. (2008) Korea 45 + 1992–2005 Cohort NA Cancer registry; death certificates 2194 b 631 172 b HBsAg NS 6 Hassan et al. (2008) USA NS 2000–2007 Case–control P Pathologically 476 879 HBsAg, anti-HBs, anti-HBc ELISA 9 Iloeje et al. (2009) Taiwan 30–65 1991–2007 Cohort NA Cancer registry; death certification; national health insurance profiles 48 22 471 HBsAg, HBeAg c , HBV DNA Radioimmunoassay 9 Tang et al. (2009) USA 18 + 1995–2008 Retrospective cohort NA Cancer registry 101 74 851 HBsAg, anti-HBs, anti-HBc, HBeAg, HBV DNA NS 9 Chang et al. (2009) Taiwan NA NA Case–control P Cytological pathologically 147 1716 HBsAg, anti-HBs, anti-HBc — d — d Hong et al. (2010) Korea NS 2003–2008 Case–control H Histologically (58.1%) 506 1008 HBsAg anti-HBs, HBV DNA ARCHITECT assay 8 Wang et al. (2011) Mainland China NS 1999–2010 Case–control H Discharge diagnoses (histologically) 645 711 HBsAg, anti-HBs, anti-HBc, HBeAg, anti-HBe ELISA 8 Zhu et al. (2011) "
    [Show abstract] [Hide abstract] ABSTRACT: Objective: Whether hepatitis B virus (HBV) infection increases the risk of pancreatic cancer (PaC) is controversial. We carried out a meta-analysis to evaluate the association between HBV status and the risk of PaC. Methods: PubMed, Embase, and the China National Knowledge Infrastructure were searched from their inception through April 2012 for case-control and cohort studies that have reported an association between HBV status and the risk of PaC. The reference lists of pertinent publications were also reviewed for potential studies. Methodological quality was assessed using the Newcastle-Ottawa Quality Assessment Scale. A random-effects model was used to summarize odd ratios (ORs) and 95% confidence intervals (CIs). Results: We included seven case-control studies and three cohort studies, involving 5883 PaC cases. The summary OR of developing PaC was 1.22 (95% CI: 0.90-1.67) for individuals who were HBV surface antigen (HBsAg)-positive. Compared with the individuals who were never exposed to HBV infection, the summary OR of the risk of PaC was 1.60 (95% CI: 1.26-2.05) for chronic or inactive HBsAg carriers (HBsAg-positive) and 1.76 (95% CI: 1.05-2.93) for anti-HBc-positive but anti-HBs-negative individuals. Conclusion: Inactive HBsAg carrier status and possible occult HBV infection may increase the risk of PaC. Large population-based multicenter prospective studies are required to further confirm this finding.
    Full-text · Article · Nov 2012 · European journal of cancer prevention: the official journal of the European Cancer Prevention Organisation (ECP)
  • [Show abstract] [Hide abstract] ABSTRACT: Background: Hepatitis B virus (HBV) infection is reported to be associated with an increased risk of pancreatic cancer (PaC), but it remains controversial whether this is a causal relationship. In addition, it is unclear whether the status of HBV infection also affects PaC risk. Therefore, we conducted a meta-analysis to more closely examine the association between HBV infection and PaC. Method: The studies included in the meta-analysis were identified and retrieved from PubMed and several other databases. The literature search was conducted up until August 2012. We adopted the Cochrane Collaboration's RevMan 5.1 in a combined analysis of pooled relative risk (RR) with their corresponding 95 % confidence intervals (CIs) using a random-effects and a fixed-effects model. Results: Nine studies including 6 case-control and 3 cohort studies met eligibility criteria. The meta-analysis showed that the PaC risk was positively correlated with HBV infection when comparing with 'never exposed to HBV' subgroup, the pooled RR was 1.39 (95 % CI 1.22-1.59, p < 0.00001) in chronic HBV carriers, 1.41 (95 % CI 1.06-1.87, p = 0.02) in past exposure to HBV, and 3.83 (95 % CI 1.76-8.36, p = 0.0007) in active HBV infection. Using a stratified analysis, we also found that the risk of PaC was independent of smoking, alcohol drinking, and diabetes. Conclusion: Findings from this meta-analysis strongly support that HBV infection is associated with an increased risk of PaC.
    No preview · Article · Jan 2013 · Cancer Causes and Control
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    [Show abstract] [Hide abstract] ABSTRACT: Several studies have reported that ABO blood group, hepatitis B virus (HBV) and hepatitis C virus (HCV) infection contribute to the development of pancreatic cancer. The aim of this study was to evaluate the association between these factors and pancreatic cancer in the Korean population. We retrospectively recruited 753 patients with pancreatic cancer and 3,012 healthy controls, matched 4 to 1 with cancer patients for age and sex, between 2001 and 2011, at the National Cancer Center, Korea. A multivariate logistic regression analysis was employed to estimate adjusted odds ratios (AORs). The AOR for pancreatic cancer in subjects with non-O blood types (A, AB, and B), compared to blood type O, was 1.29 (95% CI, 1.05-1.58; P = 0.01). Seropositivity for hepatitis B virus surface antigen was not significantly related to pancreatic cancer, either in univariate (odds ratio 1.03; 95% CI, 0.69-1.53; P = 0.91) or multivariate analysis (AOR, 1.02; 95% CI, 0.67-1.56; P = 0.93). The AOR for pancreatic cancer in subjects displaying seropositivity for anti-HCV was 2.30 (95% CI, 1.30-4.08; P < 0.01). Our results suggest that the non-O blood types and anti-HCV seropositivity, but not HBV infection, may increase the risk of developing pancreatic cancer in Korea, where HBV is endemic.
    Full-text · Article · Feb 2013 · Journal of Korean medical science
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