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Published Online First: 27 September 2006. doi:10.1136/gut.2006.109082
Gut 2007;56:464-468
Copyright © 2007 BMJ Publishing Group Ltd & British Society of Gastroenterology.

OESOPHAGEAL CANCER

Risk of oesophageal cancer by histology among patients hospitalised for gastroduodenal ulcers

Shahram Bahmanyar1,2, Kazem Zendehdel1,3, Olof Nyrén1, Weimin Ye1

1 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
2 Faculty of Medicine, Golestan University of Medical Sciences, Gorgan, Iran
3 Cancer Institute Research Centre, Tehran University of Medical Sciences, Tehran, Iran

Correspondence to:
Shahram Bahmanyar
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Box 281, SE 171 77, Stockholm, Sweden; Shahram.bahmanyar{at}ki.se

ABSTRACT

Objective: The mechanism behind the epidemiologically evident inverse relation between Helicobacter pylori seropositivity and risk of oesophageal adenocarcinoma (OAC) remains obscure. Severe corpus gastritis is unlikely to be in the causal pathway. With the hypothesis of a uniformly low risk, the associations of OAC with duodenal ulcer and gastric ulcer were explored, both linked to H pylori infection but with different patterns of bacterial colonisation and intragastric acidity. Possible associations of oesophageal squamous cell carcinoma (OSCC) with these ulcer types were also addressed.

Design and patients: Retrospective cohorts of 61 548 and 81 379 unoperated patients with duodenal ulcer and gastric ulcer, respectively, recorded in the Swedish Inpatient Register since 1965, were followed from the first hospitalisation until the date of any cancer, death, emigration, definitive surgery, or 31 December 2003. Standardised incidence ratios (SIRs), with 95% CIs, expressed relative risk of oesophageal cancer, compared with the Swedish population matched for age, sex and calendar period.

Results: Contrary to expectation, patients with duodenal ulcer had a significant 70% excess risk of OAC (SIR 1.7, 95% CI 1.1 to 2.5). Gastric ulcer was unrelated to OAC (SIR 1.1, 95% CI 0.6 to 1.7). Although duodenal ulcer was non-significantly associated with a small excess of OSCC (SIR 1.3, 95% CI 0.96 to 1.8), gastric ulcer was linked to 80% increased risk (SIR 1.8, 95% CI 1.4 to 2.3).

Conclusion: The inverse association between H pylori and OAC does not pertain to all infections. The pattern of gastric colonisation and/or impact on acidity may be important. With the reservation for the possibility of confounding, this study also provides some support for the importance of intragastric environment in the aetiology of OSCC.

Abbreviations: CagA, cytotoxin-associated gene A; CI, confidence interval; H pylori, Helicobacter pylori; NRN, national registration number; OAC, oesophageal adenocarcinoma; OSCC, oesophageal squamous cell carcinoma; SIR, standardised incidence ratio

Keywords: oesophageal cancer; oesophageal adenocarcinoma; oesophageal squamous cell carcinoma; duodenal ulcer; gastric ulcer


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