Abstract
Gastric bypass is a clinical option for obesity surgery. An increased susceptibility to Helicobacter pylori infection in the bypassed stomach has been speculated. The aim of the present study was to examine the susceptibility of the bypassed stomach to H. pylori infection in rats and mice. Adult Sprague-Dawley and Wistar rats and NMRI mice were subjected to either gastric bypass or laparotomy only as control. The animals were inoculated with the CagA- and VacA-positive H. pylori strain 67/21 (not mouse-adapted) in the first experiment and with 9 additional isolates in the second, by injection into the bypassed stomach or the control stomach during surgery. The stomach of each animal was collected for H. pylori culture 2–3 weeks later. While all the rats were H. pylori negative, 54% of gastric bypassed mice and 75% of controls were positive (P = 0.4). We conclude that susceptibility to H. pylori infection in the stomach is not increased by gastric bypass surgery.
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References
Blaser, M. J. (1998). Helicobacter pylori and gastric diseases, Br. Med. J. 316, 1507–1510.
Caterson, I. D. and Gill, T. P. (2002). Obesity: epidemiology and possible prevention, Clin. Endocrinol. Metabol. 16, 595–610.
Colquitt, J., Clegg, A., Sidhu, M., et al. (2003). Surgery for morbid obesity, Cochrane Database Syst. Rev. 2, CD003641.
Hedley, A. A., Ogden, C. L., Johnson, C. L., et al. (2004). Prevalence of overweight and obesity among US children, adolescents, and adults, 1999–2002, J. Am. Med. Ass. 291, 2847–2850.
Li, H., Kalies, I., Mellgård, B. and Helander, H. F. (1998). A rat model of chronic Helicobacter pylori infection. Studies of epithelial cell turnover and gastric ulcer healing, Scand. J. Gastroenterol. 33, 370–378.
Lindström, E., Chen, D., Norlén, P., et al. (2001). Control of gastric acid secretion:the gastrin-ECL cell-parietal cell axis, Comp. Biochem. Physiol. Mol. Integr. Physiol. 128, 505–514.
Mina, W. C., Burns, R. W. and Terry, B. E. (2003). The treatment of obesity, Missouri Med. 100, 248–255.
Nilsson, C., Sillén, A., Eriksson, L., et al. (2003). Correlation between cag pathogenicity island composition and Helicobacter pylori-associated gastroduodenal disease, Infect. Immun. 71, 6573–6581.
Ramaswamy, A., Lin, E., Ramshaw, B. J., et al. (2004). Early effects of Helicobacter pylori infection in patients undergoing bariatric surgery, Arch. Surg. 139, 1094–1096.
Soltesz, V., Schalén, C. and Mårdh, P. A. (1988). New selective medium for Campylobacter pylori, in: Proceedings of the Fourth International Workshop on Campylobacter Infections, Gothenburg, Sweden, pp. 433–436.
Sundbom, M., Nyman, R., Hedenström, H., et al. (2001). Investigation of the excluded stomach after Roux-en-Y gastric bypass, Obes. Surg. 11, 25–27.
Uemura, N., Okamoto, S., Yamamoto, S., et al. (2001). Helicobacter pylori infection and the development of gastric cancer, N. Engl. J. Med. 345, 784–789.
Young, E. A., Taylor, M. M., Taylor, M. K., et al. (1984). Gastric stapling for morbid obesity: gastrointestinal response in a rat model, Am. J. Clin. Nutr. 40, 293–302.
Zivny, J., Wang, T. C., Yantiss, R., et al. (2003). Role of therapy or monitoring in preventing progression to gastric cancer, J. Clin. Gastroenterol. 36(Suppl. 5), S50–S60.
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Stenström, B., Løseth, K., Bevanger, L. et al. Gastric bypass surgery does not increase susceptibility to Helicobacter pylori infection in the stomach of rat or mouse. Inflammopharmacol 13, 229–234 (2005). https://doi.org/10.1163/156856005774423791
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DOI: https://doi.org/10.1163/156856005774423791