The EPIC-Norfolk Study
Helicobacter pylori infection, chronic corpus atrophic gastritis and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort: A nested case-control study.
International journal of cancer 2016 ; 140: 1727-1735.
Huang J, Zagai U, Hallmans G, Nyrén O, Engstrand L, Stolzenberg-Solomon R, Duell EJ, Overvad K, Katzke VA, Kaaks R, Jenab M, Park JY, Murillo R, Trichopoulou A, Lagiou P, Bamia C, Bradbury KE, Riboli E, Aune D, Tsilidis KK, Capella G, Agudo A, Krogh V, Palli D, Panico S, Weiderpass E, Tjønneland A, Olsen A, Martínez B, Redondo-Sánchez D, Chirlaque MD, Hm Peeters P, Regnér S, Lindkvist B, Naccarati A, Ardanaz E, Larrañaga N, Boutron-Ruault MC, Rebours V, Barré A, Bueno-de-Mesquita HB, and Ye W
DOI : 10.1002/ijc.30590
PubMed ID : 28032715
PMCID : PMC5930360
URL : https://onlinelibrary.wiley.com/doi/10.1002/ijc.30590
Abstract
The association between H. pylori infection and pancreatic cancer risk remains controversial. We conducted a nested case-control study with 448 pancreatic cancer cases and their individually matched control subjects, based on the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, to determine whether there was an altered pancreatic cancer risk associated with H. pylori infection and chronic corpus atrophic gastritis. Conditional logistic regression models were applied to calculate odds ratios (ORs) and corresponding 95% confidence intervals (CIs), adjusted for matching factors and other potential confounders. Our results showed that pancreatic cancer risk was neither associated with H. pylori seropositivity (OR = 0.96; 95% CI: 0.70, 1.31) nor CagA seropositivity (OR = 1.07; 95% CI: 0.77, 1.48). We also did not find any excess risk among individuals seropositive for H. pylori but seronegative for CagA, compared with the group seronegative for both antibodies (OR = 0.94; 95% CI: 0.63, 1.38). However, we found that chronic corpus atrophic gastritis was non-significantly associated with an increased pancreatic cancer risk (OR = 1.35; 95% CI: 0.77, 2.37), and although based on small numbers, the excess risk was particularly marked among individuals seronegative for both H. pylori and CagA (OR = 5.66; 95% CI: 1.59, 20.19, p value for interaction < 0.01). Our findings provided evidence supporting the null association between H. pylori infection and pancreatic cancer risk in western European populations. However, the suggested association between chronic corpus atrophic gastritis and pancreatic cancer risk warrants independent verification in future studies, and, if confirmed, further studies on the underlying mechanisms.