The Role of the Helicobacter Pylori Infection in Ulcer Development and Treatment

Abstract

The treatment of peptic ulcer disease has changed dramatically since Helicobacter pylori-induced gastritis was identified as a significant contributing factor. One course of antimicrobial therapy that eradicates the H. pylori infection is more effective than ongoing suppression of acid secretion in preventing ulcer recurrence. It is widely recognized that Helicobacter pylori is the cause of chronic active type B gastritis and is likely the most prevalent bacterial infection in the world. While some people develop either a duodenal or gastric ulcer, many patients live with persistent superficial gastritis. A relatively little percentage of the lymphoid. In certain cases, the data indicates that chronic superficial gastritis advances to atrophy, the loss of gastric acid secretory capacity, and the formation of gastric cancer. In other cases, the reaction to H. pylori infection seems to progress to become a mucosal associated lymphoid tissue (MALT) lymphoma. Peptic ulcer disease (PUD) is most caused by Helicobacter pylori infection and nonsteroidal anti-inflammatory drug (NSAID) use. When there is a low risk of stomach cancer due to age under 55 and the lack of alarm symptoms, the test-and-treat approach for H. pylori detection is recommended.

Keywords

Introduction

TYPES OF PEPTIC ULCER

1. Acute peptic ulcer

• Cushing ulcer: Gastric, duodenal, or esophageal ulcer arising in patients with intracranial injury or operations.
• Curling ulcer: It occurs mostly in the proximal duodenum and is associated with severe burns and trauma.

2. Chronic peptic ulcer

• Gastric ulcer: It is a sore that is on the inside of the stomach.
• Duodenal ulcer: The peptic ulcer having a sore on the upper part of the small intestine.
• Esophageal ulcer: Open sores or lesions in the lining of the esophagus.
• Bleeding ulcer:
  • Internal bleeding is caused by a peptic ulcer which has been left untreated.
  • Most dangerous type of ulcers.
• Refractory ulcer: These are peptic ulcers that have not healed after at least 3 months of treatment.

The Role of H. pylori in Peptic Ulcer Disease

The idea that H. pylori-induced gastritis plays a significant role in the development of peptic ulcer disease, particularly duodenal ulcers, is supported by three lines of evidence. More than 95 percent of patients with duodenal ulcers and more than 80 percent of patients with gastric ulcers are infected with H. pylori, except for those who have gastrointestinal conditions or are taking non-steroidal anti-inflammatory medications [3,4,5]. Patch closure or definitive surgery are the two main treatments for perforated ulcers. As stated earlier, simple closure is linked to an intolerably elevated ulcer recurrence rate [35]. Either patch closure or definitive surgery are the two main treatments for perforated ulcers. As was already established, simple closure is linked to an unacceptable rate of ulcer recurrence [6].

Hypotheses to Explain H. pylori-Negative Peptic Ulcer Perforations

Even when case-control studies are considered, the frequency of H. pylori infection in perforated peptic ulcers varies significantly among studies, as was previously demonstrated. These contentious findings could be caused by several factors, including variations in the frequency of NSAID use, the type of perforated ulcer under consideration (gastric or duodenal), the sensitivity and specificity of H. pylori diagnostic techniques, or the potential that the infection would have been eliminated by ulcer perforation management procedures.

NSAID USE

The concurrent use of NSAIDs, a known independent cause of ulcer complications, may be one reason why the prevalence of H. pylori in some ulcer perforation studies is lower than anticipated. Many studies, however, have not used a systematic questionnaire to prospectively measure NSAID use or to report the prevalence of H. pylori differently for patients who take NSAIDs and those who do not.

As an exception, Ng et al.’s study [7] showed intraoperative and antral biopsies revealed a 70% H. pylori infection rate in patients with perforated peptic ulcers; however, if NSAID users were taken out of the equation, this number increased to 80% (although the infection was found in only 23% of cases in patients using these medications). According to other research, NSAID use is common among individuals with perforated peptic ulcers, particularly those who are not infected [8].

Ulcer Site (Duodenal or Gastric Ulcer)

The most significant etiologic factor for non-complicated duodenal ulcers is H. pylori infection, although NSAIDs appear to have a less significant effect [9,10,11]. However, H. pylori infection is far less common in stomach ulcer disease, indicating that factors from the body—primarily NSAIDs—are to blame for a comparatively high percentage of stomach ulcers [12].

DIAGNOSIS OF INFECTION

Endoscopic biopsies of gastric mucosa or non-invasive techniques can be used to diagnose H. pylori infection of the stomach [13]. The clinical scenario determines which test is best for a particular patient. There are non-invasive techniques for diagnosing: serologic testing and urea breath tests are used to detect H. pylori infection. Enzyme-linked immunosorbent assays and other quick serologic tests can identify the circulating antibody response caused by a chronic infection [14–20]. These tests are almost as sensitive and specific as methods involving biopsy and have been adapted for use in the physician’s office [21].

TREATMENT OF INFECTION

It is challenging to completely remove H. pylori, and effective treatment necessitates the simultaneous use of two or more antimicrobial medications [22–25]. Eradication has typically been defined in therapeutic studies as the absence of organisms that can be detected by breath testing or tissue samples at least one month after treatment is finished [26,27]. The absence of infectious organisms during or just after therapy may simply indicate that the infection has been suppressed and may not indicate a long-term recovery [26,28].

Currently available treatment regimens for H. pylori do not completely eliminate the infection in all patients, and many of them have a comparatively high frequency of adverse effects. Novel therapies that use either brand-new medications or novel combinations of already-approved medications will undoubtedly be developed in the future. Numerous medication combinations are presently undergoing extensive testing. The necessity to evaluate novel agent combinations in infected humans complicates the research process because sensitivity in vitro does not accurately predict antimicrobial effectiveness in vivo [29–31].

Amoxicillin

Both in vitro and in vivo, H. pylori is extremely sensitive to amoxicillin. It has topical or intraluminal activity, inhibits the formation of bacterial cell walls, and is most effective when used in an acidic environment, though active when the pH is neutral [32].

Tetracycline

Tetracycline, which inhibits bacterial protein synthesis and, like amoxicillin, seems to act luminally or topically, is likewise highly effective against H. pylori. At low pH, it is active [33].

Clarithromycin

A macrolide antibiotic called clarithromycin prevents bacteria from synthesizing proteins. Although it has a comparable antibacterial range as erythromycin, it is more efficient against H. pylori, more acid-soluble, and better absorbed. Resistance may arise, just like with metronidazole, when only clarithromycin is administered [34].

CONCLUSION

All patients with confirmed peptic ulcer disease who exhibit signs of H. pylori infection should receive antimicrobial therapy against the bacteria. The first regimen—triple therapy using bismuth, metronidazole, and tetracycline—is the option chosen based on research that is currently available. Clarithromycin may be used in place of metronidazole for people who have a history of taking it.

Antisecretory medication is also advised for patients with active, symptomatic peptic ulcers to aid in healing and alleviate symptoms. Second-choice regimens combine an antisecretory agent with two antibacterial medications, such as metronidazole, amoxicillin, or clarithromycin. An H/K-ATPase antagonist, like omeprazole, is preferred.

It is not advised to use omeprazole in conjunction with a single antimicrobial medication, particularly amoxicillin, as this combination is less effective.

REFERENCES

1. Pharmacotherapy- A pathophysiologic approach by Joseph T.DiPiro, Gary C.Yee, L.Michael Post T.Haines, Thomas D.Nolin, Vicki Ellingrod- 11th Edition.
2. Clinical pharmacy and Therapeutics edited by Roger Walker and Cate Whittlesea - 5th Edition.
3. Peterson WL. Helicobacter pylori and peptic ulcer disease. N Engl J Med 1991;324:10438.
4. Veldhuyzen van Zanten SJ, Sherman PM. Helicobacter pylori infection as a cause of gastritis, duodenal ulcer, gastric cancer and nonuleer dyspepsia: a systematic overview. Can Med Assoc J 1994;150:177-85.
5. Graham DY. Helicobacter pylori: its epidemiology and its role in duodenal ulcer disease. J Gastroenterol Hepatol 1991;6:105-13
6. Ananthakrishnan N, Angami K. Is ulcer recurrence after simple closure of perforated duodenal ulcer predictable? Indian J Gastroenterol 1993;12:80-2.
7. Ng EK, Chung SC, Sung JJ, et al. High prevalence of Helicobacter pylori infection in duodenal uleer perforations not caused by non-steroidal antiinflammatory drugs. Br J Surg 1996;83:1779-81.
8. Debongnie JC, Wibin E, Timmermans M, Mairesse J, Dekoninck X. Are perforated gastroduodenal ulcers related to Helicobacter pylori infection? Acta Gastroenterol Belg 1995;58:208-12.
9. Kuipers EJ, Thijs JC, Festen HP. The prevalence of Helicobacter pylori in peptic ulcer disease. Aliment Pharmacol Ther 1995:9:59-69.
10. Gisbert JP, Blanco M, Mateos JM, et al. H. pylorinegative duodenal ulcer prevalence and causes in 774 patients. Dig Dis Sci 1999;44:2295-302
11. Schubert TT, Bologna SD, Nensey Y, Schubert AB, Mascha EJ, Ma CK. Ulcer risk factors. interactions between Helicobacter pylori infection, nonsteroidal use, and age. Am J Med 1993;94:413-8.
12. Borody TJ, Brandl S, Andrews P, Jankiewicz E, Ostapowicz N. Helicobacter pylori-negative gastric ulcer. Am J Gastroenterol 1992;87:1403-6.
13. Brown KE, Peura DA. Diagnosis of Helicobacter pylori infection. Gastroenterol Clin North Am 1993;22:105-15.
14. Cutler A, Schubert A, Schubert T. Role of Helicobacter pylori serology in evaluating treatment suceess. Dig Dis Sei 1993;38:2262-6.
15. Schembri MA, Lin SK, Lambert JR. Comparison of commercial diagnostic tests for Helicobaeter pylori antibodies. J Clin Microbiol 1993;31:2621-4.
16. Von Wulffen H. An assessment of serological tests for detection of Helicobacter pylori. Eur J Clin Microbiol Infeet Dis 1992;11:577-82.
17. Taha AS, Reid J, Boothmann P, et al. Serological diagnosis of Helicobacter pylori evaluation of four tests in the presence or absence of non-steroidal anti-inflammatory drugs. Gut 1993;34:461-5.
18. Graham DY, Malaty HM, Evans DG, Evans DJ Jr, Klein PD, Adam E. Epidemiology of Helicobacter pylori in an asymptomatic population in the United States: effect of age, race, and sociocconomie status. Gastroenterology 1991;100:1495-501.
19. Perez-Perez GI, Dworkin BM, Chodos JE, Blaser MJ. Campylobacter pylori antibodies in humans. Ann Intern Med 1988;109:11-7.
20. Graham DY, Evans DG, Evans DJ. Better, accurate, more rapid and convenient physician-office serologic test for detection of H. pylori infection. Gastroenterology 1994;106:Suppl:A83. abstract.
21. Burette A, Glupczynski Y, Deprez C. Evaluation of various multidrug eradication regimens for Helicobacter pylori. Eur J Gastroenterol Hepatol 1992;4:817-23.
22. Chiba N, Rao BV, Rademaker JW, Hunt RH. Meta-analysis of the efficacy of antibiotic therapy in eradicating Helicobacter pylori. Am J Gastroenterol 1992:87:1716-27.
23. Tytgat GNJ. Treatments that impact favourably upon the cradication of Helicobacter pylori and ulcer recurrence. Aliment Pharmacol Ther 1994;8:359-68.
24. Penston JG. Helicobacter pylori eradication - understandable caution but no excuse for inertia. Aliment Pharmacol Ther 1994;8:369-89.
25. Bell GD. Anti-Helicobacter pylori therapy: clearance, elimination, or eradication? Lancet 1991;337:310-1.
26. Noach LA, Langenberg WL, Bertola MA, Dankert J, Tytgat GN. Impact of metronidazole resistance on the eradication of Helicobacter pylori. Scand J Infect Dis 1994:26:321-7.
27. Graham DY, Klein PD, Evans DG, et al. Simple noninvasive method to test efficacy of drugs in the eradication of Helicobacter pylori infection: the example of combined bismuth susalicylate and nitrofurantoin. Am J Gastroenterol 1991:86:1158-62.