Helicobacter pylori and Pancreatic Cancer
Helicobacter pylori and Pancreatic Cancer
ABSTRACT & COMMENTARY
Synopsis: The association of whole-cell H pylori or cytotoxin-associated gene-A-positive (CagA+) strains of H pylori carriage with exocrine pancreatic cancer was investigated in a nested, case-control study within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study cohort of 29,133 male Finnish smokers. The seroprevalence of H pylori was 82% among cases and 73% among control subjects. Two-sided statistical tests demonstrated an elevated risk of pancreatic cancer in subjects seropositive for H pylori or CagA+ strains compared to seronegative controls (odds ratio [OR] = 1.87; 95% confidence interval [CI] = 1.05-3.34); OR = 2.01, 95% CI = 1.09-3.70, respectively). A possible role is suggested for H pylori carriage as a risk factor for pancreatic cancer.
Source: Stolzenberg-Solomon, et al. J Nat Cancer Inst. 2001;93(12):937-941.
Helicobacter pylori carriage is a known risk factor for peptic ulcer disease, gastric cancer, and mucosa-associated lymphoid tissue (MALT) lymphoma.1-3 The CagA+ strains of H pylori have especially been reported to have an association with inflammation, ulceration, and cancer.1 Since the mechanism of H pylori-associated gastric cancer is potentially related to persistent inflammation in the stomach1 and chronic pancreatitis has been associated with pancreatic cancer,4 it was postulated that carriage of H pylori may have an association with inflammation in the pancreas and pancreatic cancer. This possible association of H pylori carriage and pancreatic cancer was also suggested by an earlier case-control study.5 Thus, the potential association of H pylori and pancreatic cancer was evaluated in the current study.
This study by Stolzenberg-Solomon and colleagues was a nested, case-control study of male smokers who previously participated in a double-blind, placebo-controlled, primary prevention trial (ATBC Study) that tested whether alpha-tocopherol or beta-carotene could reduce the incidence of cancer in male smokers.6,7 A total of 29,133 men participated in the original ATBC study from 1985 through 1988, and all cases of pancreatic cancer diagnosed from January 1985 through December 1995 were identified by the Finnish Cancer Registry and death certificates. A total of 130 pancreatic cancer subjects and 260 matched control subjects were identified. Control subjects were selected from ATBC study participants based on being alive at the same time as the pancreatic cancer subjects and were matched by age, month of baseline blood draw, completion of dietary history, study center, and study assignment from the original ATBC study. The final sample size was composed of the 121 case subjects with baseline serum measurements of H pylori whole-cell (WC) and CagA strains and matched control subjects (n = 226). Nonsignificant trends were seen for H pylori seropositivity and a history of ulcer disease. Seropositivity for H pylori WC (82% vs 73%; P = 0.07) and CagA+ strains (60% vs 51%; P = 0.05) was greater in cases than controls. Following adjustment for years of smoking, patients with H pylori carriage with CagA+ strains had a 2-fold increase in likelihood of having pancreatic cancer as those who did not (OR = 2.01; 95% CI = 1.09-3.70). Stolzenberg-Solomon et al conclude that this prospective study demonstrates a significant relationship between H pylori carriage and pancreatic cancer.
Comment by Mark R. Albertini, MD
The association of infection with H pylori and duodenal ulcer has been established.8 This association offers treatment strategies aimed at eradication of the H pylori infection. The role of H pylori as a carcinogenic factor for gastric cancer has also been reported and is thought to result from changes progressing from superficial gastritis to precancerous gastritis to dysplasia.1 An ability to intervene in this process appears possible and requires investigation. The potential mechanisms for H pylori infection and pancreatic cancer remain speculative, and it is unknown whether actual pancreatic colonization with H pylori even occurs. Other factors associated with H pylori infection, including formation of other carcinogenic compounds or associations with other infectious agents, remain possible.
The current study is a relatively large study with prospective blood collection from similar cohorts of individuals. The association of H pylori infection with inflammation provides a possible biological mechanism for H pylori carriage and pancreatic cancer. However, it should be noted that the entire study was based on male smokers. In addition, the association between H pylori carriage and pancreatic cancer in the current study became more significant once the analysis was additionally adjusted for years of cigarettes smoked. While these observations are intriguing, confirmation of the relationship of H pylori infection and pancreatic cancer needs to be evaluated in additional studies. It is hoped that identification of risk factors for pancreatic cancer may help identify pathogenesis of this disease as well as offer insight into treatment and/or prevention strategies.
References
1. Forman D. Br Med Bull. 1998;54:71-78.
2. Blaser MJ, et al. Cancer Res. 1995;55:2111-2115.
3. Go MF, Smoot DT. Semin Gastrointest Dis. 2000;
11:134-141.
4. Lowenfels AB, et al. Gastroenterol Clin North Am. 1999;28:673-685.
5. Raderer M, et al. Oncology. 1998;55:16-19.
6. The ATBC Cancer Prevention Study Group. Ann Epidemiol. 1994;4:1-10.
7. The Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study Group. N Engl J Med. 1994;330:
1029-1035.
8. Parsonnet J. Infect Dis Clin North Am. 1998;12:
185-197.
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