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ABSTRACT: This study was to assess the role of hepatitis B virus (HBV) infection in pancreatic ductal adenocarcinoma (PDAC) risk using a hospital-based case-control design.
Patients with pathologically confirmed PDAC (943) and 1128 matched controls were recruited from 2 hospitals. We evaluated the associations between risk of PDAC and age, sex, history of diabetes mellitus (DM), etc. In addition, we examined the interactive effects of HBV status and known risk factors for pancreatic cancer.
Chronic hepatitis B and inactive hepatitis B surface antigen (HBsAg) carrier state (HBsAg positive) had a significantly increased risk of pancreatic cancer, with an adjusted odds ratio of 1.60 (95% confidence interval [CI], 1.15-2.24). Furthermore, significant interactions were detected between a history of DM and chronic hepatitis B and inactive HBsAg positive, but not with antibodies to hepatitis B core antigen (anti-HBc) positive/antibodies to HBsAg (anti-HBs) negative, with an adjusted odds ratio of 5.42 (95% CI, 2.76-10.64), compared with those who were HBsAg negative/anti-HBc negative without a history of DM.
These results suggest that HBsAg-positive or anti-HBc-positive/anti-HBs-negative patients have an increased risk for PDAC independent of other risk factors. Significant interactions were found between a history of DM and chronic HBV infection for PDAC risk.
Pancreas 04/2012; 41(3):435-40. · 2.39 Impact Factor
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ABSTRACT: Inconsistent results regarding the association between abdominal obesity and the risk of colorectal adenoma (CRA), the precursor of colorectal cancer (CRC), have been reported. To provide a quantitative assessment of this relationship, we summarized the evidence from observational studies in categorical, linear dose-response meta-analyses. We searched MEDLINE and EMBASE for studies of waist circumference (WC) and/or waist-hip ratio (WHR) and CRA risk published until the end of October 2011. Summary relative risks (SRRs) with 95% confidence intervals (CIs) were summarized using a random-effects model. Between-study heterogeneity was assessed using the Cochran's Q and I statistics. A total of 21 studies (four case-control studies, 12 cross-sectional studies, and five cohort studies) were included in this meta-analysis. Overall, the SRRs of CRA were 1.39 (95% CI: 1.24-1.56) for the highest versus the lowest level of WC and 1.22 (95% CI: 1.10-1.35) for WHR (P-value for heterogeneity 0.013 and 0.458, respectively). In linear dose-response analysis, a 10-cm increase in WC was related to an increased risk of CRA (SRR, 1.19; 95% CI, 1.13-1.26) and a 0.1-unit increment in WHR gave 1.16 (95% CI: 1.06-1.26). Subgroup analyses revealed that the increased risk of CRA in abdominally obese individuals was independent of geographic location, design, sex, and confounders: alcohol use, smoking status, and family history of colorectal cancer. However, BMI may be a confounder for the association between WC and CRA risk. These results suggest that abdominally obese individuals, both men and women, may have an increased risk of CRA.
European journal of cancer prevention: the official journal of the European Cancer Prevention Organisation (ECP) 02/2012; 21(6):523-31. · 2.21 Impact Factor
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ABSTRACT: Inconsistent findings from observational studies have prolonged the controversy over the effects of history of diabetes mellitus (DM) on the risk of esophageal cancer (EC). We conducted a meta-analysis of epidemiologic studies to evaluate the association of a history of DM with the risk of EC.
We identified studies by a literature search of MEDLINE (from 1 January 1966) and EMBASE (from 1 January 1974), through 28 Feburary 2011, and by searching the reference lists of pertinent articles. Summary relative risks (SRRs) with 95% confidence intervals (CIs) were calculated with a random-effects model. All statistical tests were two-sided.
A total of 17 studies (6 case-control studies and 11 cohort studies) fulfilled the inclusion and exclusion criteria. Compared with non-diabetic individuals, diabetic individuals had a modestly increased risk of EC (SRRs 1.30, 95% CI: 1.12-1.50), with significant heterogeneity among studies (p = 0.042). In stratified analysis, the SRRs of EC were 1.28 (1.10-1.49) for diabetic men and 1.07 (95% CI, 0.71-1.62) for diabetic women, respectively. In addition, DM was associated with an increased risk of esophageal adenocarcinoma (SRR 2.12, 95% CI 1.01-4.46). There was no significant publication bias (p = 0.127 for Begg's adjusted rank correlation test and p = 0.629 for Egger's regression test).
These findings support the hypothesis that men with diabetes may have a modestly increased risk of EC, while diabetic women were not the case.
Cancer Causes and Control 11/2011; 23(2):263-72. · 2.88 Impact Factor
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ABSTRACT: Diabetes mellitus (DM) is widely considered to be associated with pancreatic cancer, however, whether DM is a cause or consequence of pancreatic cancer is controversial. In the present study, 1458 patients with pancreatic ductal adenocarcinoma (PDAC) and 1528 age-, sex- and sociodemographic variables-matched controls were recruited in two university-affiliated hospitals from 1st January 2000 to 31st December 2009. DM was defined as fasting blood glucose (FBG) level of 7.0 mmol/L or greater. An unconditional multivariable logistic regression analysis was used to estimate adjusted odds ratios (AORs) and 95% confidence interval (CI). Compared with controls, a moderate increased risk of PDAC was observed among cases with long-standing diabetes (≥ 2-year duration), with an AOR (95% CI) of 2.11 (1.51-2.94). Interestingly, a significant higher risk was observed among cases with new-onset DM (<2-year duration), with an AOR of 4.43 (3.44-5.72) compared to controls without DM. In addition, we found a synergistic interaction between cigarette smoking and DM on modifying the risk of pancreatic cancer development (AOR=6.17, 95% CI 3.82-9.94). Similarly, a synergistic interaction between new-onset DM and family history of pancreatic cancer was found for pancreatic cancer risk, with an AOR (95% CI) of 11.04 (2.51-48.53). This study suggested that DM could be both an early manifestation of pancreatic cancer and an aetiologic factor. Possible effect modification on DM by family history of pancreatic cancer and smoking status should be further explored in future aetiologic studies.
European journal of cancer (Oxford, England: 1990) 01/2011; 47(2):248-54. · 4.12 Impact Factor
