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. Author manuscript; available in PMC: 2018 May 2.
Published in final edited form as: Int J Cancer. 2017 Apr 15;140(8):1727–1735. doi: 10.1002/ijc.30590

Table 3.

Association between serologically determined chronic corpus atrophic gastritis and risk of pancreatic cancer: a case-control study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort.

Control subjects Cases Crude model1 Adjusted model2

N, % N, % OR 95% CI OR 95% CI
Chronic corpus atrophic gastritis3
No 415 (94.1) 407 (92.1) 1.00 1.00
Yes 26 (5.9) 35 (7.9) 1.39 0.81, 2.38 1.35 0.77, 2.37
Stratifying by H. pylori and CagA serostatus
H. pylori+ or CagA+
Chronic corpus atrophic gastritis (no) 204 (46.5) 202 (46.1) 1.00 1.00
Chronic corpus atrophic gastritis (yes) 22 (5.0) 18 (4.1) 0.88 0.45, 1.72 0.85 0.42, 1.72
H. pylori− and CagA−
Chronic corpus atrophic gastritis (no) 210 (47.8) 202 (46.1) 1.00 1.00
Chronic corpus atrophic gastritis (yes) 3 (0.7) 16 (3.7) 5.29 1.53, 18.23 5.66 1.59, 20.19
1

Crude conditional logistic regression model was inherently adjusted for the matching factors, including study center, sex, age at blood collection (±3 years), date of blood donation (±3 months), time of blood donation (±2 h), and fasting status (<3h, 3–6h or >6 after the last meal).

2

Adjusted conditional logistic regression model was inherently controlled for the matching factors, and was further adjusted for height, waist-to-hip ratio, smoking status (never, former or current) and diabetes mellitus status (no or yes).

3

Chronic corpus atrophic gastritis was defined as pepsinogen I <25 µl/l or pepsinogen I/II<3.