Aim. The aim of this study was to investigate the prevalence and risk factors of H. pylori infection in areas with high prevalence of gastric cancer in Jiangsu Province, China. Methods. A prospective epidemiologic survey of H. pylori infection was accomplished in a natural population of 5417 individuals in Yangzhong city. Questionnaires and 13C-urea breath test for H. pylori infection were performed. Results. Among 5417 subjects who completed questionnaires and 13C-urea breath test, 3435 (63.41%) were H. pylori positive. The prevalence reached a peak at the age of 30–39 years (90.82%). There was significant difference between sexes and women had a higher infection rate than men. The prevalence of H. pylori infection was also associated with eating kipper food and fried food. No association between H. pylori prevalence and smoking or drinking was found. Compared to healthy individuals, people with dyspeptic diseases (peptic ulcer, gastroenteritis) presented a high prevalence of H. pylori infection. Using multivariate logistic regression analysis, age and history of peptic ulcer and gastroenteritis were the independent predictors for H. pylori infection. Conclusions. Yangzhong city had a high prevalence of H. pylori infection and was related to several risk factors. The underlying mechanisms are needed to be further investigated. 1. Introduction Helicobacter pylori is a microaerophilic Gram-negative spiral bacterium [1]. Its helix shape is thought to have evolved to penetrate the mucoid lining of the stomach [2]. It is linked to the development of chronic gastritis, gastric ulcers, duodenal ulcers, and stomach mucosal atrophy. Moreover, Helicobacter pylori is well recognized as a class I carcinogen because chronic inflammation and atrophy can further lead to malignant transformation [3, 4]. At least half the world’s population is infected by this bacterium, making it the most widespread infection in the world, especially in the developing world where rates are estimated to be around 80% [5]. H. pylori is contagious, although the exact route of transmission is not known [6, 7]. Person-to-person transmission by either the oral-oral or fecal-oral route is most likely. H. pylori may also be transmitted orally by means of fecal matter through the ingestion of waste-tainted water [2]. Many of the reported factors for H. pylori infection included poor hygiene, deficient sanitation, and crowded living conditions [8]. However, the roles of many other factors associated have not been elucidated. The aim of the current study was to determine the prevalence of
References
[1]
K. W. Tsang, W. K. Lam, K. N. Chan et al., “Helicobacter pylori sero-prevalence in asthma,” Respiratory Medicine, vol. 94, no. 8, pp. 756–759, 2000.
[2]
L. M. Brown, “Helicobacter pylori: epidemiology and routes of transmission,” Epidemiologic Reviews, vol. 22, no. 2, pp. 283–297, 2000.
[3]
P. Correa, “Human gastric carcinogenesis: a multistep and multifactorial process—first American Cancer Society Award lecture on cancer epidemiology and prevention,” Cancer Research, vol. 52, no. 24, pp. 6735–6740, 1992.
[4]
J. G. Fox and T. C. Wang, “Inflammation, atrophy, and gastric cancer,” Journal of Clinical Investigation, vol. 117, no. 1, pp. 60–69, 2007.
[5]
J. Torres, Y. Leal-Herrera, G. Perez-Perez et al., “A community-based seroepidemiologic study of Helicobacter pylori infection in Mexico,” Journal of Infectious Diseases, vol. 178, no. 4, pp. 1089–1094, 1998.
[6]
F. Megraud, “Transmission of Helicobacter pylori: faecal-oral versus oral-oral route,” Alimentary Pharmacology and Therapeutics, vol. 9, supplement 2, pp. 85–91, 1995.
[7]
D. R. Cave, “Transmission and epidemiology of Helicobacter pylori,” American Journal of Medicine, vol. 100, pp. 12S–17S, 1996.
[8]
V. C. C. Dattoli, R. V. Veiga, S. S. Da Cunha, L. C. Pontes-De-Carvalho, M. L. Barreto, and N. M. Alcantara-Neves, “Seroprevalence and potential risk factors for Helicobacter pylori infection in Brazilian children,” Helicobacter, vol. 15, no. 4, pp. 273–278, 2010.
[9]
R. Shi, S. Xu, H. Zhang et al., “Prevalence and risk factors for Helicobacter pylori infection in chinese populations,” Helicobacter, vol. 13, no. 2, pp. 157–165, 2008.
[10]
L. Zhang, W. J. Blot, W.-C. You et al., “Helicobacter pylori antibodies in relation to precancerous gastric lesions in a high-risk Chinese population,” Cancer Epidemiology Biomarkers and Prevention, vol. 5, no. 8, pp. 627–630, 1996.
[11]
T. De Sablet, M. B. Piazuelo, C. L. Shaffer et al., “Phylogeographic origin of Helicobacter pylori is a determinant of gastric cancer risk,” Gut, vol. 60, no. 9, pp. 1189–1195, 2011.
[12]
N. Kim, R. Y. Park, S.-I. Cho et al., “Helicobacter pylori infection and development of gastric cancer in Korea: long-term follow-up,” Journal of Clinical Gastroenterology, vol. 42, no. 5, pp. 448–454, 2008.
[13]
A. Kurzeja-Miros？aw, K. Celiński, M. S？omka, A. Madro, and H. Cichoz-Lach, “The effects of environmental factors on the incidence of Helicobacter pylori infection in the adult population of the Lublin region,” Annales Universitatis Mariae Curie-Sklodowska. Sectio D, vol. 59, no. 2, pp. 247–253, 2004.
[14]
G. I. Perez-Perez, D. Rothenbacher, and H. Brenner, “Epidemiology of Helicobacter pylori infection,” Helicobacter, vol. 9, supplement 1, pp. 1–6, 2004.
[15]
C. A. Malcolm, W. G. MacKay, A. Shepherd, and L. T. Weaver, “Helicobacter pylori in children is strongly associated with poverty,” Scottish Medical Journal, vol. 49, no. 4, pp. 136–138, 2004.
[16]
K. Ariizumi, T. Koike, S. Ohara et al., “Incidence of reflux esophagitis and Helicobacter pylori infection in diabetic patients,” World Journal of Gastroenterology, vol. 14, no. 20, pp. 3212–3217, 2008.
[17]
M. P. Dore, M. Bilotta, H. M. Malaty et al., “Diabetes mellitus and Helicobacter pylori infection,” Nutrition, vol. 16, no. 6, pp. 407–410, 2000.
[18]
J. Borg, O. Melander, L. Johansson, K. Uvn？s-Moberg, J. F. Rehfeld, and B. Ohlsson, “Gastroparesis is associated with oxytocin deficiency, oesophageal dysmotility with hyperCCKemia, and autonomic neuropathy with hypergastrinemia,” BMC Gastroenterology, vol. 9, article 17, 2009.
[19]
R. E. Pounder and D. Ng, “The prevalence of Helicobacter pylori infection in different countries,” Alimentary Pharmacology and Therapeutics, vol. 9, supplement 2, pp. 33–39, 1995.
[20]
C. Bodner, W. J. Andersen, T. S. Reid, and D. J. Godden, “Childhood exposure to infection and risk of adult onset wheeze and atopy,” Thorax, vol. 55, no. 5, pp. 383–387, 2000.
[21]
B. D. Aguemon, M. J. Struelens, A. Massougbodji, and E. M. Ouendo, “Prevalence and risk-factors for Helicobacter pylori infection in urban and rural Beninese populations,” Clinical Microbiology and Infection, vol. 11, no. 8, pp. 611–617, 2005.
[22]
S. Tsugane, “Salt, salted food intake, and risk of gastric cancer: epidemiologic evidence,” Cancer Science, vol. 96, no. 1, pp. 1–6, 2005.
[23]
S. Kikuchi, M. Kurosawa, and T. Sakiyama, “Helicobacter pylori risk associated with sibship size and family history of gastric diseases in Japanese adults,” Japanese Journal of Cancer Research, vol. 89, no. 11, pp. 1109–1112, 1998.
[24]
A. Ogihara, S. Kikuchi, A. Hasegawa et al., “Relationship between Helicobacter pylori infection and smoking and drinking habits,” Journal of Gastroenterology and Hepatology, vol. 15, no. 3, pp. 271–276, 2000.
[25]
L. J. Murray, E. E. McCrum, A. E. Evans, and K. B. Bamford, “Epidemiology of Helicobacter pylori infection among 4742 randomly selected subjects from Northern Ireland,” International Journal of Epidemiology, vol. 26, no. 4, pp. 880–887, 1997.
[26]
S. Tsugane, Y. Tei, T. Takahashi, S. Watanabe, and K. Sugano, “Salty food intake and risk of Helicobacter pylori infection,” Japanese Journal of Cancer Research, vol. 85, no. 5, pp. 474–478, 1994.
[27]
K. Shinchi, H. Ishii, K. Imanishi, and S. Kono, “Relationship of cigarette smoking, alcohol use, and dietary habits with Helicobacter priori infection in japanese men,” Scandinavian Journal of Gastroenterology, vol. 32, no. 7, pp. 651–655, 1997.
[28]
G. Battaglia, F. Di Mario, M. Pasini et al., “Helicobacter pylori infection, cigarette smoking and alcohol consumption. a histological and clinical study on 286 subjects,” Italian Journal of Gastroenterology, vol. 25, no. 8, pp. 419–424, 1993.
[29]
C. Zhong, K.-N. Li, J.-W. Bi, and B.-C. Wang, “Sodium intake, salt taste and gastric cancer risk according to Helicobacter pylori infection, smoking, histological type and tumor site in China,” Asian Pacific Journal of Cancer Prevention, vol. 13, no. 6, pp. 2481–2484, 2012.
[30]
K. Endoh and F. W. Leung, “Effects of smoking and nicotine on the gastric mucosa: a review of clinical and experimental evidence,” Gastroenterology, vol. 107, no. 3, pp. 864–878, 1994.
[31]
D. Forman, M. Coleman, G. De Backer et al., “Epidemiology of, and risk factors for, Helicobacter pylori infection among 3194 asymptomatic subjects in 17 populations,” Gut, vol. 34, no. 12, pp. 1672–1676, 1993.
[32]
D. Y. Graham, H. M. Malaty, D. G. Evans, D. J. Evans Jr., P. D. Klein, and E. Adam, “Epidemiology of Helicobacter pylori in an asymptomatic population in the United States: effect of age, race, and socioeconomic status,” Gastroenterology, vol. 100, no. 6, pp. 1495–1501, 1991.
[33]
M. Paunio, J. Hook-Nikanne, T. U. Kosunen et al., “Association of alcohol consumption and Helicobacter pylori infection in young adulthood and early middle age among patients with gastric complaints. a case-control study on Finnish conscripts, officers and other military personnel,” European Journal of Epidemiology, vol. 10, no. 2, pp. 205–209, 1994.
[34]
E. T. H. Fontham, B. Ruiz, A. Perez, F. Hunter, and P. Correa, “Determinants of Helicobacter pylori infection and chronic gastritis,” American Journal of Gastroenterology, vol. 90, no. 7, pp. 1094–1101, 1995.
[35]
T. Rokkas, C. Pursey, E. Uzoechina et al., “Campylobacter pylori and non-ulcer dyspepsia,” American Journal of Gastroenterology, vol. 82, no. 11, pp. 1149–1152, 1987.
[36]
H. Brenner, D. Rothenbacher, G. Bode, and G. Adler, “Relation of smoking and alcohol and coffee consumption to active Helicobacter pyloli infection: cross sectional study,” British Medical Journal, vol. 315, no. 7121, pp. 1489–1492, 1997.
[37]
A. Franke, H. Harder, A. K. Orth, S. Zitzmann, and M. V. Singer, “Postprandial walking but not consumption of alcoholic digestifs or espresso accelerates gastric emptying in healthy volunteers,” Journal of Gastrointestinal and Liver Diseases, vol. 17, no. 1, pp. 27–31, 2008.
[38]
M. V. Singer, C. Leffmann, V. E. Eysselein, H. Calden, and H. Goebell, “Action of ethanol and some alcoholic beverages on gastric acid secretion and release of gastrin in humans,” Gastroenterology, vol. 93, no. 6, pp. 1247–1254, 1987.
[39]
A. Robert, J. E. Nezamis, C. Lancaster, J. P. Davis, S. O. Field, and A. J. Hanchar, “Mild irritants prevent gastric necrosis through “adaptive cytoprotection” mediated by prostaglandins,” The American Journal of Physiology, vol. 245, no. 1, pp. G113–G121, 1983.
[40]
L. O. Ingram and T. M. Buttke, “Effects of alcohols on micro-organisms,” Advances in Microbial Physiology, vol. 25, pp. 253–300, 1985.
[41]
W. L. Peterson, P. A. Mackowiak, C. C. Barnett, M. Marling-Cason, and M. L. Haley, “The human gastric bactericidal barrier: mechanisms of action, relative antibacterial activity, and dietary influences,” Journal of Infectious Diseases, vol. 159, no. 5, pp. 979–983, 1989.
[42]
M. E. Weisse, B. Eberly, and D. A. Person, “Wine as a digestive aid: comparative antimicrobial effects of bismuth salicylate and red and white wine,” British Medical Journal, vol. 311, no. 7021, pp. 1657–1660, 1995.
