Helicobacter pylori in colorectal neoplasms: Is there an aetiological relationship?

被引：63
作者：
Jones M. [1 ]
Helliwell P. [1 ]
Pritchard C. [2 ]
Tharakan J. [3 ]
Mathew J. [1 ]
机构：
[1] Department of Histopathology, Royal Cornwall Hospital
[2] Department of Research and Development, Royal Cornwall Hospital
[3] Department of Medicine, Princess Alexandra Hospital, Harlow, Essex
来源：
World Journal of Surgical Oncology | / 5卷 / 1期
关键词：
Adenoma; Colorectal Adenocarcinoma; Aberrant Crypt Focus; Colorectal Neoplasia; Villous Adenoma;
D O I：
10.1186/1477-7819-5-51
中图分类号：
学科分类号：
摘要：
Background: This pilot study was carried out to determine whether Helicobacter pylori can be detected in normal colon or in association with colorectal neoplasia. Methods: Paraffin processed colonic tissue blocks of normal colonic mucosa (n = 60), and patients diagnosed as adenoma (n = 60), and adenocarcinoma (n = 60) were retrieved from our archive; the adenoma group included tubular (n = 20), tubulovillous (n = 20) and villous adenomas (n = 20). 4 μm sections were stained by immunohistochemical methods using anti-Helicobacter pylori antibodies (polyclonal NCL-HPp and monoclonal NCL-C-jejuni). Results: Significant numbers of Helicobacter pylori were identified in tubular adenomas (OR = 11.13; 95%CI = 1.62-76.70), tubulovillous adenomas (OR = 10.45; 95%CI = 1.52-71.52) and adenocarcinomas (OR = 8.13; 95%CI = 1.40-46.99) compared to controls: there was no association in numbers of Helicobacter pylori and villous adenomas (OR = 2.95; 95%CI = 0.29-9.96). Conclusion: We conclude that although, in this pilot study, there appears to be an association in the prevalence of Helicobacter pylori with some, but not all, colorectal neoplasms, we can not infer causality from these results. These findings need to be further substantiated with a prospective study and the use of molecular biological techniques to determine a causal association. © 2007 Jones et al; licensee BioMed Central Ltd.
引用
收藏
相关论文
共 54 条
  • [1] Cummings O.W., Pathology of the adenoma-carcinoma sequence: From aberrant crypt focus to invasive carcinoma, Semin Gastrointest Dis, 11, pp. 229-237, (2000)
  • [2] Hardy R.G., Meltzer S.J., Jankowski J.A., ABC of colorectal cancer: Molecular basis for risk factors, BMJ, 321, pp. 886-889, (2000)
  • [3] Day D.W., Jass J.R., Price A.B., Shepherd N.A., Sloan J.M., Talbot I.C., Warren B.F., Williams G.T., Morson and Dawson's Gastrointestinal Pathology, (2003)
  • [4] Gryfe R., Swallow C., Bapat B., Redston M., Gallinger S., Couture J., Molecular biology of colorectal cancer, Curr Probl Cancer, 21, pp. 233-300, (1997)
  • [5] Liu C., Crawford J.M., The gastrointestinal tract, Robbins and Cotran Pathologic Basis of Disease, pp. 797-875, (2005)
  • [6] Midgley R., Kerr D., Colorectal cancer, Lancet, 353, pp. 391-399, (1999)
  • [7] Vogelstein B., Fearon E.R., Hamilton S.R., Kern S.E., Preisinger A.C., Leppert M., Nakamura Y., White R., Smits A.M., Bos J.L., Genetic alterations during colorectal-tumor development, N Engl J Med, 319, pp. 525-532, (1988)
  • [8] Konturek S.J., Konturek P.C., Hartwich A., Hahn E.G., Helicobacter pylori infection and gastrin and cyclooxygenase expression in gastric and colorectal malignancies, Regul Pept, 93, pp. 13-19, (2000)
  • [9] Meucci G., Tatarella M., Vecchi M., Ranzi M.L., Biguzzi E., Beccari G., Clerici E., de Franchis R., High prevalence of Helicobacter pylori infection in patients with colonic adenomas and carcinomas, J Clin Gastroenterol, 25, pp. 605-607, (1997)
  • [10] Calam J., Clinician's Guide to Helicobacter Pylori, (1996)
123456