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Association of Helicobacter Pylori Infection and Colon Cancer

BACKGROUND: Gastrin has been shown to exert carcinogenic effect to the epithelium of the colon. This study examines whether hypergastrinemia and H. pylori infection -especially infection by the CagA+ strain- are statistically associated with colorectal cancer and examine possible correlations with t...

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Detalles Bibliográficos
Autores principales: Strofilas, Alexandros, Lagoudianakis, Emmanuel E, Seretis, Charalambos, Pappas, Apostolos, Koronakis, Nikolaos, Keramidaris, Dimitrios, Koukoutsis, Ilias, Chrysikos, Ioannis, Manouras, Ioannis, Manouras, Andreas
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elmer Press 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3376875/
https://www.ncbi.nlm.nih.gov/pubmed/22719803
http://dx.doi.org/10.4021/jocmr880w
Descripción
Sumario:BACKGROUND: Gastrin has been shown to exert carcinogenic effect to the epithelium of the colon. This study examines whether hypergastrinemia and H. pylori infection -especially infection by the CagA+ strain- are statistically associated with colorectal cancer and examine possible correlations with the colorectal cancer stage and lymph node metastasis. METHODS: In this prospective case-control study, fasting serum samples from 93 consecutive patients with colorectal cancer treated in a university surgical clinic were preoperatively collected and serum levels of gastrin were measured. A group of 20 age matched hernia patients were used as controls. The pathology report of the specimens was documented and statistical analysis of the data where performed with the spss 17 statistical suite. RESULTS: H. pylori IgG antibodies was reported in 66/93 (71%) in the colorectal cancer group and 13/20 patients in the control group (65%), the difference having non-statistical significance (P = n.s). The prevalence of cagA protein expression in the anti- H. pylori IgG+ patients were higher in the colorectal cancer group (56% positivity), when compared to the control group (38,4% positivity) but the difference was not of statistical significance (P = n.s). The mean levels of serum gastrin levels in the two groups did not significantly differ (Ca group 51.1 ± 36.6 pg/mL vs Control 49.8 ± 17.6 P = n.s.). Patients with lymph node metastasis had higher serum gastrin levels than patients without metastasis and this difference was statistically significant. (53.6 vs 41.06 pg/mL P = 0.025). CONCLUSIONS: Although the serum gastrin levels were not statistically different between the TNM stages of our patient cohort, our data found that serum gastrin levels were significantly higher in patients with lymph node metastasis. Whether gastrin is implicated in the ability of cancer cells to metastasize to the lymph nodes merits further research.