BACKGROUNDEpidemiologic studies have reported inconsistent results regarding tea consumption and the risk of pancreatic cancer. This study aimed to investigate whether tea consumption is related to the risk of pancreatic cancer.

METHODSWe searched Medline, EMBASE, ISI Web of Science, and the Cochrane library for studies published up to November 2013. We used a meta-analytic approach to estimate overall odds ratio (OR) and 95% confidence interval (CI) for the highest versus the lowest tea consumption categories.

RESULTSThe summary OR for high versus no/almost never tea drinkers was 1.04 (95% CI: 0.91-1.20), with no significant heterogeneity across studies (P = 0.751; I(2) = 0.0%). The OR was 0.99 (95% CI: 0.77-1.28) in males and 1.01 (95% CI: 0.79-1.29) in females. The OR was 1.07 (95% CI: 0.85-1.34) in Asian studies, 1.05 (95% CI: 0.84-1.31) in European studies, and 0.98 (95% CI: 0.72-1.34) in the US studies. The OR was 0.87 (95% CI: 0.69-1.10) without adjustment for a history of diabetes and 1.16 (95% CI: 0.97-0.39) after adjustment for a history of diabetes. The OR was 0.90 (95% CI: 0.72-1.12) without adjustment for alcohol drinking and 1.16 (95% CI: 0.96-1.39) after adjustment for alcohol drinking. The OR was 0.97 (95% CI: 0.76-1.25) without adjustment for BMI and 1.07 (95% CI: 0.87-1.31) after adjustment for BMI.

CONCLUSIONThis systematic meta-analysis of cohort studies dose not provide quantitative evidence that tea consumption is appreciably related to the risk of pancreatic cancer, even at high doses.

Asia ; Humans ; Pancreatic Neoplasms ; epidemiology ; etiology ; Tea ; adverse effects

The prevalence of diabetes mellitus (DM) and associated diseases such as cancers are substantially increasing worldwide. About 80% of the patients with pancreatic cancer have glucose metabolism alterations. This suggests an association between type 2 DM and pancreatic cancer risk and progression. There are hypotheses that show metabolic links between the diseases, due to insulin resistance, hyperglycemia, hyperinsulinemia, low grade chronic inflammation, and alteration in the insulin-insulin-like growth factor axis. The use of diabetes medications can influence the extent of carcinogenesis of the pancreas. This study briefly reviews recent literature on investigation of metabolic link of type 2 DM, risk of carcinogenesis of the pancreas and their association, as well as the current understanding of metabolic pathways implicated in metabolism and cellular growth. The main finding of this review, although there are discrepancies, is that according to most research long-term DM does not raise the risk of pancreatic cancer. The longest duration of DM may reflect hypoinsulinemia due to treatment for hyperglycemia, but recent onset diabetes was associated with increased risk for pancreatic cancer due to hyperinsulinemia and hyperglycemia. In conclusion, the review demonstrates that type 2 DM and the duration of diabetes pose a risk for pancreatic carcinogenesis, and that there is biological link between the diseases.
Diabetes Mellitus, Type 2/complications/epidemiology/metabolism/*pathology ; Humans ; Hyperglycemia/pathology ; Insulin/metabolism ; Insulin Resistance ; Insulin-Like Growth Factor I/metabolism ; Pancreatic Neoplasms/epidemiology/*etiology ; Risk Factors

BACKGROUND/AIMS: An association between past history of hepatitis B virus (HBV) infection and pancreatic cancer (PC) has recently been reported. We investigated whether HBV and hepatitis C virus (HCV) infections are associated with the development of PC in Korea. METHODS: We retrospectively recruited patients with PC and sex- and, age-matched control patients with stomach cancer (SC) during the previous 5 years. Serum HBsAg and anti-HCV were examined, and data on smoking, alcohol intake, diabetes, and the history of chronic pancreatitis (CP) were collected. RESULTS: A total of 506 PC and 1008 SC were enrolled, with respectively 58.1% and 97.3% of these cases being confirmed histologically. The mean age and sex ratio (male:female) were 63.5 years and 1.5:1 in the PC patients and 63.9 years and 1.5:1 in the SC patients respectively (P>0.05). The odds ratios (95% confidence interval, 95% CI) in univariate analysis were 0.90 (0.52-1.56; P=0.70) for HBsAg, 1.87 (0.87-4.01; P=0.11) for anti-HCV, 2.66 (2.04-3.48; P<0.001) for the presence of diabetes, 2.30 (1.83-2.90; P<0.001) for smoking, 1.14 (0.89-1.46; P=0.31) for alcohol intake, and 4.40 (1.66-11.66; P=0.003) for the history of CP. Independent risk factors for PC were presence of diabetes (OR, 2.67; 95% CI, 2.00-3.56; P<0.001), smoking (OR, 2.49; 95% CI, 1.93-3.21; P<0.001) and history of CP (OR, 4.60; 95% CI, 1.56-13.53; P=0.006). CONCLUSIONS: There was no significant association between seropositivity for HBsAg or anti-HCV and PC. Further studies are warranted to clarify the association between HBV infection and PC in regions where HBV is endemic.
Aged ; Case-Control Studies ; Data Interpretation, Statistical ; Female ; Hepatitis B/*complications/diagnosis ; Hepatitis C/complications/diagnosis ; Humans ; Incidence ; Male ; Middle Aged ; Odds Ratio ; Pancreatic Neoplasms/diagnosis/*epidemiology/etiology ; Retrospective Studies ; Risk Factors