Научная статья на тему 'PREVALENCE OF HELICOBACTER PYLORI (HP) IN PATIENTS WITH DIFFERENT GASTRIC PATHOLOGIES (GASTRIC CANCER & PEPTIC ULCER DISEASES)'

PREVALENCE OF HELICOBACTER PYLORI (HP) IN PATIENTS WITH DIFFERENT GASTRIC PATHOLOGIES (GASTRIC CANCER & PEPTIC ULCER DISEASES) Текст научной статьи по специальности «Фундаментальная медицина»

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Ключевые слова
helicobacter pylori / gastric cancer / peptic ulcer disease / duodenal ulcer / gastric ulcer.

Аннотация научной статьи по фундаментальной медицине, автор научной работы — Jahanarah Khatoon, Mohd. Saquib

Introduction-A total of 150 adult patients, comprising 90 males and 60 females, underwent upper gastrointestinal endoscopy at the Integral Institute of Medical Sciences and Research (IIMSR) Lucknow. The patients were categorized into three distinct groups: Group I Gastric cancer (GC) with 50 patients (17 intestinal types, 17 male; 33 diffuse type, 21 male), Group IIPeptic ulcer diseases (PUD) with 50 patients (16 duodenal ulcers, 12 male; 34 gastric ulcers, 18 male), and Group IIIFunctional dyspepsia (FD) with 50 patients (33 male). Material & MethodsDefinitive diagnosis of H. pylori infection in patients was made when either culture was positive or any two of remaining four tests including Histopathology, Urease C PCR, Real time PCR and Rapid urease Test (RUT) were found to be positive. According to above criteria, H. pylori infection was detected in 122 (51%) of 240 adult patients. Result-The overall prevalence of H. pylori infection in the study population was found to be 55% (82 out of 150). Specifically, H. pylori infection rates were 40% (20 out of 50) in the FD group (Group I), 68% (34 out of 50) in the PUD group (Group II), and 56% (28 out of 50) in the GC group (Group III). Within the subgroups of PUD and GC, the infection rates were 75% in duodenal ulcers (12 out of 16), 65% in gastric ulcers (22 out of 34), 76% in intestinal-type GC (13 out of 17), and 45% in diffuse-type GC (15 out of 33). Conclusion In our study, we find that H. pylori prevalence increases with advanced forms of gastric pathologies, suggesting that H. pylori infection may play an important role in the pathogenesis of gastric diseases (gastric cancer and peptic ulcer diseases).

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Текст научной работы на тему «PREVALENCE OF HELICOBACTER PYLORI (HP) IN PATIENTS WITH DIFFERENT GASTRIC PATHOLOGIES (GASTRIC CANCER & PEPTIC ULCER DISEASES)»

INTERNATIONAL SCIENTIFIC AND PRACTICAL CONFERENCE "STATUS AND DEVELOPMENT PROSPECTS OF FUNDAMENTAL AND APPLIED MICROBIOLOGY: THE VIEWPOINT OF YOUNG SCIENTISTS" _25-26 SEPTEMBER, 2024_

PREVALENCE OF HELICOBACTER PYLORI (HP) IN PATIENTS WITH DIFFERENT GASTRIC PATHOLOGIES (GASTRIC CANCER & PEPTIC ULCER DISEASES)

Jahanarah Khatoon, 2Mohd. Saquib

1Assistant Professor (Ph. D) Department of Biosciences, Integral University, Lucknow, Uttar

Pradesh, India

2Assistant Professor, (MBBS, MD) Department of Microbiology, Integral Institute of Medical Sciences and Research (IIMSR), Lucknow, Uttar Pradesh, India https://doi.org/10.5281/zenodo.13837668

Abstract. Introduction-A total of 150 adult patients, comprising 90 males and 60 females, underwent upper gastrointestinal endoscopy at the Integral Institute of Medical Sciences and Research (IIMSR) Lucknow. The patients were categorized into three distinct groups: Group I -Gastric cancer (GC) with 50 patients (17 intestinal types, 17 male; 33 diffuse type, 21 male), Group II- Peptic ulcer diseases (PUD) with 50 patients (16 duodenal ulcers, 12 male; 34 gastric ulcers, 18 male), and Group III- Functional dyspepsia (FD) with 50patients (33 male).

Material & Methods- Definitive diagnosis of H. pylori infection in patients was made when either culture was positive or any two of remaining four tests including Histopathology, Urease C PCR, Real time PCR and Rapid urease Test (RUT) were found to be positive. According to above criteria, H. pylori infection was detected in 122 (51%) of240 adult patients.

Result-The overall prevalence of H. pylori infection in the study population was found to be 55% (82 out of 150). Specifically, H. pylori infection rates were 40% (20 out of 50) in the FD group (Group I), 68% (34 out of 50) in the PUD group (Group II), and 56% (28 out of 50) in the GC group (Group III). Within the subgroups of PUD and GC, the infection rates were 75% in duodenal ulcers (12 out of 16), 65% in gastric ulcers (22 out of34), 76% in intestinal-type GC (13 out of 17), and 45% in diffuse-type GC (15 out of 33).

Conclusion - In our study, we find that H. pylori prevalence increases with advancedforms of gastric pathologies, suggesting that H. pylori infection may play an important role in the pathogenesis of gastric diseases (gastric cancer and peptic ulcer diseases).

Keywords: helicobacter pylori, gastric cancer, peptic ulcer disease, duodenal ulcer, gastric ulcer.

Introduction: Helicobacter pylori (H. pylori) is a bacterium that infects the human stomach which is colonizing well over ad more than half the world's population [1]. Indeed, the existence of spiral-shaped or curved bacilli within the stomach tissues of animals and man was foreshadowed about 10 decades ago [2]. Spiral organisms inhabiting the tissues of patients with gastric ulcers were reported by Fung and his co-worker, in 1979, on the luminal surfaces of epithelial tissues. However, before the identification of H. pylori in the early 1980s, diseases of the stomach such as gastritis and peptic ulcers were blamed on unhealthy eating, over-consumption of certain drinks like coffee, or a busy lifestyle. For these ailments were certain medications prescribed such as antacids and proton pump inhibitors to circumvent the fluid secretion in the stomach and subsequently eliminate the specific complaint. Bacteria were first located in the stomach tissues in 1874 but this was dismissed as it was thought that nothing could survive in such a hostile acidic environment. In patients suffering from gastritis and/or ulcer disease, the antrum was successfully

INTERNATIONAL SCIENTIFIC AND PRACTICAL CONFERENCE "STATUS AND DEVELOPMENT PROSPECTS OF FUNDAMENTAL AND APPLIED MICROBIOLOGY: THE VIEWPOINT OF YOUNG SCIENTISTS" _25-26 SEPTEMBER, 2024_

used for isolation of H. pylori and experiments that followed fulfilled Koch's postulates for gastritis, most importantly the antibiotic therapy documented the establishment of H. pylori as a gastric pathogen [3]. For this discovery, Marshall & Warren were awarded the Nobel Prize (2005) in the Medicine and Physiology. H. pylori is confirmed as a leading cause of gastric disorders such as gastritis and the more serious peptic ulcer diseases.

Methods & Materials

Study population

Group I - Patients suffering from functional dyspepsia (FD). Patients with functional dyspepsia were regarded as disease controls in all patients during the entire study.

Group II - Patients suffering from peptic ulcer disorder (PUD)

Group III - Patients suffering from gastric cancer (GC).

The diagnosis of any disease from gastroduodenal diseases was done clinically, endoscopically, and histopathologically. The study was approved by the ethics committee of the institute and informed consent were obtained from all patients. Patients of all three groups who had received antimicrobials, H2 antagonists, proton pump inhibitors and non-steroidal antiinflammatory drugs within the last four weeks prior to endoscopy were enrolled in the study. A pro forma- questionnaire for endoscopic examination was filled for all eyeball patients who underwent endoscopic examination (Appendix-I). The preparation of all the reagents and solutions has been mentioned in appendix-II.

Specimen: Antral biopsies

During each endoscopic examination (Olympus, Japan), the following surgical procedures were performed: 6 antral biopsies were obtained for the following tests:

• Two formalin-fixed biopsies were obtained, one for RUT for diagnosis of H. pylori, one more for culture for the diagnosis of H. pylori

• One fresh frozen biopsy for purifying DNA for PCR enriching for H. pylori

• One fresh frozen biopsy for the harvest of RNA for expression studies

• Two formalin-fixed biopsies for Histopathology

Results

Isolation and Identification of H. pylori: For the diagnosis of H. pylori infection, the following tests were utilized: RUT, culture, histopathology, H. pylori specific ureC PCR, and other Real-Time PCR (Q PCR). Diagnosis for H. pylori was established if culture results were positive or if culture results were negative but at least two of four other tests RUT, histopathology and PCR and Q-PCR were positive.

Prevalence of H. pylori infections: In total, a set of 150 adult patients (90 males and 60 females) were to perform upper GI endoscopy, at Integral Institute of Medical Sciences and Research (IIMSR), Lucknow. They were divided into 3 groups: GC 50 (17 intestinal type, 17 male; 33 diffuse type, 21 male), PUD 50 (16 DU, 12 male; 34 GU, 18 male) and FD 50 (33 male).

The overall prevalence of H. pylori infection in the study population was found to be 55% (82 out of 150). Specifically, H. pylori infection rates were 40% (20 out of 50) in the FD group (Group I), 68% (34 out of 50) in the PUD group (Group II), and 56% (28 out of 50) in the GC group (Group III). Within the subgroups of PUD and GC, the infection rates were 75% in duodenal ulcers (12 out of 16), 65% in gastric ulcers (22 out of 34), 76% in intestinal-type GC (13 out of 17), and 45% in diffuse-type GC (15 out of 33).

INTERNATIONAL SCIENTIFIC AND PRACTICAL CONFERENCE "STATUS AND DEVELOPMENT PROSPECTS OF FUNDAMENTAL AND APPLIED MICROBIOLOGY: THE VIEWPOINT OF YOUNG SCIENTISTS" _25-26 SEPTEMBER, 2024_

The incidence of H. pylori infection was significantly elevated in patients with PUD and GC when compared to those with FD, with rates of 68% versus 40% (P = 0.01) and 56% versus 40% (P = 0.024), respectively. However, no significant difference was noted between the GC and PUD groups (68% versus 56%, P = 0.345). Among the various study groups, a positive correlation was identified in H. pylori-infected patients with DU, GU, and intestinal-type GC when compared to the control group of FD. Additionally, subgroup analysis revealed that H. pylori infection was more closely associated with the intestinal type of GC than with the diffuse type, while no significant differences were found between DU and GU (refer to Table 1).

Table 1. Demographic details of different groups of patients with and without Helicobacter

pylori (HP) infection.

Disease Group Age (mean ± SD) Sex (M : F) H. pylori status (HP+ve : HP-ve)

Group I FD(n= 50) 42.1±12.9 33: 23 20 (40%): 30(60%)

Group II

PUD(n= 50) 48.1±12.3 38: 12 34(68%): 16 (32%)

Subgroups-DU(n= 16) GU(n= 32) 45.15± 12.3 47.34±23.12 12: 04 18: 08 12(75%): 04 (25%) 22(65%): 12 (35%)

Group III

GC (n= 50) 54.2 ±12.7 38: 12 28(56%): 12 (24%)

Subgroups-

Intestinal (n= 38) Diffuse (n= 32) 58.20 ±14.71 42.56± 12.10 17:13 21:14 13(76%): 4 (23%) 15(45%): 20 (63%)

Total (n= 240) 47.34±14.71 153:87 122(51%):118(49%)

Discussion

The prevalence of H. pylori infection has been extensively studied, highlighting its significant role in the development of gastroduodenal diseases. However, the rates of H. pylori infection differ considerably across various human populations. In our research, we found that the infection rate of H. pylori was 55%. Notably, the infection rate was markedly higher in patients with peptic ulcer disease (PUD) at 68%, compared to those with gastric cancer (GC) at 57% and functional dyspepsia (FD) at 40%. These findings align with previous studies [4,5]. Kuipers et al [6] reported that 80% to 95% of patients with PUD were infected with H. pylori. Additionally,

INTERNATIONAL SCIENTIFIC AND PRACTICAL CONFERENCE "STATUS AND DEVELOPMENT PROSPECTS OF FUNDAMENTAL AND APPLIED MICROBIOLOGY: THE VIEWPOINT OF YOUNG SCIENTISTS" 25-26 SEPTEMBER, 2024

Sipponen et al. (1992)[7] conducted a study involving 54 patients with GC, revealing that 38 (70%) were infected with H. pylori. In our current study of 50 GC patients, 28 (56%) tested positive for H. pylori, a prevalence rate consistent with Sipponen et al. (1992) and corroborated by other experimental studies [4, 14]. Conversely, several tissue-based studies from the Indian subcontinent have not established a clear link between H. pylori infection and GC [8]. The presence of chronic atrophic gastritis and intestinal metaplasia in the stomach may reduce the likelihood of detecting

H. pylori, as these conditions can lead to a decrease or absence of H. pylori due to a lack of nutrients for the bacteria [9]. Furthermore, the bacteria may conceal themselves within mucosal cells, avoiding urease production in the lumen [9, 10]. These factors may explain the lower prevalence of H. pylori infection observed in tissue-based diagnoses. Our findings indicate that H. pylori infection rates were significantly higher in patients with PUD and GC compared to those with FD, although no significant difference was noted between GC and PUD. Additionally, within subgroups, in our analysis of the subgroups of peptic ulcer disease (PUD) and gastric cancer (GC), we found that H. pylori infection was more closely linked to the intestinal type of gastric cancer than to the diffuse type. No notable differences were identified between duodenal ulcers (DU) and gastric ulcers (GU). Previous studies have indicated that H. pylori infection is associated with severe gastric conditions, including duodenal ulcers, gastric ulcers, chronic gastritis, and atrophic gastritis [11]. Both atrophic gastritis and gastric ulcers are recognized as early events in the carcinogenic process. Supporting our results, multiple human studies have established a significant correlation between H. pylori infection and gastric adenocarcinoma [12]. This association has been observed in both intestinal and diffuse subtypes of gastric carcinoma [13, 14, 15].

Conclusion

In our study, we find that H. pylori prevalence increases with advanced forms of gastric pathologies, suggesting that H. pylori infection might be a strong precursor in the pathogenesis of gastric cancer and peptic ulcer diseases. Hence, further studies are needed to validate these results and find out the exact molecular mechanism behind these gastric pathologies in H. pylori-infected individuals.

REFERENCES

I. Liang, S. C., A. J. Long, et al. (2007). "An IL-17F/A heterodimer protein is produced by mouse Th17 cells and induces airway neutrophil recruitment." J Immunol 179(11): 7791-9.

2. Salomon, R. and M. C. Salomon (1987). "[Campylobacter pylori]." G E N 41(3): 113-5.

3. Kuipers, E. J., A. M. Uyterlinde, et al. (1995). "Long-term sequelae of Helicobacter pylori gastritis." Lancet 345(8964): 1525-8.

4. Zhang, F., G. Meng, et al. (2008). "Interactions among the transcription factors Runx1, RORgammat and Foxp3 regulate the differentiation of interleukin 17-producing T cells." Nat Immunol 9(11): 1297-306.

5. Sipponen, P., K. Varis, et al. (1990). "Cumulative 10-year risk of symptomatic duodenal and gastric ulcer in patients with or without chronic gastritis. A clinical follow-up study of 454 outpatients." Scand J Gastroenterol 25(10): 966-73.

6. Kate, V., N. Ananthakrishnan, et al. (1998). "Helicobacter pylori infection and erosive gastritis." J Assoc Physicians India 46(5): 436-7.

7. Sipponen, P., Kosunen, T. U., Valle, J., Riihela, M., & Seppala, K. (1992). Helicobacter pylori infection and chronic gastritis in gastric cancer. Journal of clinical pathology, 45(4), 319-323.

INTERNATIONAL SCIENTIFIC AND PRACTICAL CONFERENCE "STATUS AND DEVELOPMENT PROSPECTS OF FUNDAMENTAL AND APPLIED MICROBIOLOGY: THE VIEWPOINT OF YOUNG SCIENTISTS"

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8. Balamourougane, P., KUNDARGI, V. S., KATE, V., & Ananthakrishnan, N. (2002). Drug therapy for H. pylori-Are nitroimidazoles useful in Indian patients?. Indian journal of pharmacology, 34(2), 111-114.

9. Konturek, S.J., Bielanski, W., Plonka, M., et al. (2003) Helicobacter pylori, non-steroidal antiinflammatory drugs and smoking in risk pattern of gastroduodenal ulcers. Scandinavian Journal of Gastroenterology, 38, 923-930. doi:10.1080/00365520310004696

10. Semino-Mora, C., Doi, S. Q., Marty, A., Simko, V., Carlstedt, I., & Dubois, A. (2003). Intracellular and interstitial expression of Helicobacter pylori virulence genes in gastric precancerous intestinal metaplasia and adenocarcinoma. The Journal of infectious diseases, 757(8), 1165-1177. https://doi.org/10.1086/368133

11. Kusters, J. G., van Vliet, A. H., & Kuipers, E. J. (2006). Pathogenesis of Helicobacter pylori infection. Clinical microbiology reviews, 19(3), 449-490. https://doi.org/10.1128/CMR.00054-05

12. Ilver, D., Arnqvist, A., Ogren, J., Frick, I. M., Kersulyte, D., Incecik, E. T., Berg, D. E., Covacci, A., Engstrand, L., & Borén, T. (1998). Helicobacter pylori adhesin binding fucosylated histo-blood group antigens revealed by retagging. Science (New York, N.Y.), 279(5349), 373-377. https://doi.org/10.1126/science.279.5349.373

13. Hu, Y., Wan, J. H., Li, X. Y., Zhu, Y., Graham, D. Y., & Lu, N. H. (2017). Systematic review with meta-analysis: the global recurrence rate of Helicobacter pylori. Alimentary pharmacology & therapeutics, 46(9), 773-779. https://doi.org/10.1111/apt.14319

14. Hung, I. F., & Wong, B. C. (2009). Assessing the risks and benefits of treating Helicobacter pylori infection. Therapeutic advances in gastroenterology, 2(3), 141-147.https://doi.org/10.1177/1756283X08100279

15. Tang, Y. L., Gan, R. L., Dong, B. H., Jiang, R. C., & Tang, R. J. (2005). Detection and location of Helicobacter pylori in human gastric carcinomas. World journal of gastroenterology: WJG, 11(9), 1387.

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