Journal of Emergency Health Care
Formerly known as: International Journal of Medical Investigation
Volume 8, Issue 2 (5-2019)
J Emerg Health Care 2019, 8(2): 23-30 |
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Rastgoo A, Jooya A. Association between Helicobacter Pylori Infection in the Gastric Mucosa and Severity of Gastric Inflammation in Children and Teenagers. J Emerg Health Care 2019; 8 (2) :23-30
URL: http://intjmi.com/article-1-396-en.html
URL: http://intjmi.com/article-1-396-en.html
Student Research Committee, Hamedan University of Medical Sciences, Hamedan, Iran
Abstract: (6246 Views)
Background and aim: Helicobacter pylori (H. pylori) is a bacterial infection which is highly likely to be developed during childhood. The present study was conducted aiming to examine the degree of H. pylori colonization in gastric mucosa and its association with the severity of gastritis in children and adolescents.
Method: The present study examined 1006 biopsy samples of children and adolescents under the age of 18 who visited Hamedan Be’sat Hospital from 2011 to the end of 2018 while showing chronic gastrointestinal symptoms such as abdominal pain, nausea and vomiting as well as weak responses to medications regarding presence and severity of H. pylori, histological findings of gastritis severity, active and non-active gastritis types as well as atrophy and metaplasia.
Results: Out of 1006 biopsies, it was found that 766 samples (76.1%) had different degrees of H. pylori colonization. Moreover, it was revealed that the highest degree of H. pylori was moderate (49.9%) in the group with mean age of 8.94, and, moreover, the lowest degree of H. pylori belonged to the rare (1.9%) and severe (2.5%) categories in the mean age groups of 7 and 10.48, respectively. Also, it was found that the highest and lowest gastritis degrees were non-atrophic (46.7%) and atrophic (0.2%). Other gastritis types were respectively erosive gastritis (0.4%), lymphocytic (0.4%), ulcer (0.4%), hemorrhagic (0.4%) and reactive gastritis (1.7%). According to findings, as age increases, so does the prevalence of H. pylori colonization and active inflammation. A significant relationship was reported to be between severity of H. pylori and gastritis. It was, moreover, indicated that moderate and severe gastritis occurred more in moderate and severe colonization of H. pylori (p<0.001). The prevalence of atrophy and metaplasia were 0.2 and 0.1, respectively.
Conclusion: H. pylori colonization is followed by severity of gastritis, activity as well as chronic abdominal and intestinal complications. Given the high prevalence of this infection in the developing countries and high risks of its acquisition in childhood, it can impose a higher economic and medical burden on the society.
Method: The present study examined 1006 biopsy samples of children and adolescents under the age of 18 who visited Hamedan Be’sat Hospital from 2011 to the end of 2018 while showing chronic gastrointestinal symptoms such as abdominal pain, nausea and vomiting as well as weak responses to medications regarding presence and severity of H. pylori, histological findings of gastritis severity, active and non-active gastritis types as well as atrophy and metaplasia.
Results: Out of 1006 biopsies, it was found that 766 samples (76.1%) had different degrees of H. pylori colonization. Moreover, it was revealed that the highest degree of H. pylori was moderate (49.9%) in the group with mean age of 8.94, and, moreover, the lowest degree of H. pylori belonged to the rare (1.9%) and severe (2.5%) categories in the mean age groups of 7 and 10.48, respectively. Also, it was found that the highest and lowest gastritis degrees were non-atrophic (46.7%) and atrophic (0.2%). Other gastritis types were respectively erosive gastritis (0.4%), lymphocytic (0.4%), ulcer (0.4%), hemorrhagic (0.4%) and reactive gastritis (1.7%). According to findings, as age increases, so does the prevalence of H. pylori colonization and active inflammation. A significant relationship was reported to be between severity of H. pylori and gastritis. It was, moreover, indicated that moderate and severe gastritis occurred more in moderate and severe colonization of H. pylori (p<0.001). The prevalence of atrophy and metaplasia were 0.2 and 0.1, respectively.
Conclusion: H. pylori colonization is followed by severity of gastritis, activity as well as chronic abdominal and intestinal complications. Given the high prevalence of this infection in the developing countries and high risks of its acquisition in childhood, it can impose a higher economic and medical burden on the society.
References
1. 1. Bahremand S, Nematollahi LR, Fourutan H, Tirgari F, Nouripour S, Mir E, et al. Evaluation of triple and quadruple Helicobacter pylori eradication therapies in Iranian children: a randomized clinical trial. Eur J Gastroenterol Hepatol. 2006;18(3):511-4.
2. Amieva M, Peek Jr RM. Pathobiology of Helicobacter pylori–induced gastric cancer. Gastroenterology. 2016;150(1):64-78.
3. Beceiro S, Radin JN, Chatuvedi R, Piazuelo MB, Horvarth DJ, Cortado H, Gu Y, Dixon B, Gu C, Lange I, Koomoa DL. TRPM2 ion channels regulate macrophage polarization and gastric inflammation during Helicobacter pylori infection. Mucosal immunology. 2017;10(2):493-9.
4. Kang H, Kim H. Astaxanthin and β-carotene in Helicobacter pylori-induced Gastric Inflammation: A Mini-review on Action Mechanisms. Journal of cancer prevention. 2017;22(2):57-64.
5. Malaty HM, El-Kasabany A, Graham DY, Miller CC, Reddy SG, Srinivasan SR, et al. Age at acquisition of Helicobacter pylori infection: a follow-up study from infancy to Adulthood. Lancet. 2002;359(2):931-5.
6. Fakher Yasseri H. determination of helicobacter-pylori prevalence in histologic gastritis and intestinal metaplasia and related to age and sex study on 576 patients with non-ulcer dyspepsia at endoscopy department of Firozgar Hospital. Razi Journal of Medical Sciences. 2002;9(30):379-87.
7. Costa Lopes AI, Palha A, Monteiro L, Olcastro M, Pelerito A, Fernandes A. Helicobacter pylori genotypes in children from a population at high gastric cancer risk: no association withgastroduodenal histopathology. Am J Gastroenterol. 2006;101(15):2113-22.
8. Stolte M, Eidt S. Helicobacter pylori and the evolution of gastritis. Scand J Gastroenterol Suppl. 1996;214(5):13-6.
9. Blaser MJ. Hypothesis: the changing relationships of Helicobacter pylori and humans: implications for health and disease. J Infect Dis. 1999;179(11):1523-30.
10. Yolanda J, Jesús NC, Verónica A, Martínez V, Manuel VR, Covarrubias L. Chronic Gastritis Associated with Helicobacter pylori in Mexican Children: Histopathological Patterns. Pediatric and Developmental Pathology. 2011;14(2):93-8.
11. Alborzi A, Soltani J, Pourabbas B. Prevalence of Helicobacter pylori infection in children (south of Iran). Diagn Microbiol Infect Dis. 2006;54(4):259-61.
12. Kato S, Nakajima S, Nishino Y. Association between gastric atrophy and Helicobacter pylori infection in Japanese children: a retrospective multicenter study. Dig Dis Sci. 2006;51(1):99-104.
13. Bardhan PK. Epidemiological features of Helicobacter pylori infection in developing countries. Clinical Infectious Diseases. 1997;25(5):973-8.
14. Koh H, Noh TW, Baek SY, Chung KS. Nodular gastritis and pathologic findings in children and young adults with Helicobacter pylori infection. Yonsei Med J. 2007;48(2):240-6.
15. Bedoya A, Garay J, Sanzon F. Histopathology of gastritis in Helicobacter pylori infected children from populations at high and low gastric cancer risk. Hum Pathol. 2003;34(3):206-13.
16. Harrold LR, Gurwitz JH, Field TS, Andrade SE, Fish LS, Jarry PD, et al. The diffusion of a novel therapy into clinical practice: the case of sildenafil. Archives of internal medicine. 2000;160(22):3401-5.
17. Zamani A, Bahremand Sh, Ojaghi Haghighi SM, Daneshjou K, Tirgari F, Ghasemi M. Endoscopic findings in children with Helicobacter pylori infection and abdominal tenderness. Tehran Univ Med Sci J. 2008;65(14):60-5.
18. Bahú M, da Silveira TR, Maguilnick I, Ulbrich-Kulczynski J. Endoscopic nodular gastritis: an endoscopic indicator of high-grade bacterial colonization and severe gastritis in children with Helicobacter pylori. Journal of pediatric gastroenterology and nutrition. 2003;36(2):217-22.
19. Yi Yu, Su L, Wang X, Wang X, Xu C. Association between Helicobacter pylori infection and pathological changes in the gastric mucosa in Chinese children. Internal Medicine. 2014;53(2):83-8.
20. Linz B, Balloux F, Moodley Y. An African origin for the intimate association between humans and Helicobacter pylori. Nature. 2007;445(7130):915-21.
21. Engin T, Deniz E. Endoscopic and Histopathologic Findings Associated with H. pylori Infection in Very Young Children. Digestiv Diseases and Sciences. 2009;54(1):111-7.
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