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  • PMSA EDITORIAL TEAM 2020

Peptic Ulcer of Helicobacter Pylori Origin

Author: Nikil Naveel Chand (Umanand Prasad School of Medicine & Health Sciences Year 3 Student)


A peptic ulcer is an excoriated area of stomach or intestinal mucosa caused principally by the digestive action of gastric juice or upper small intestinal secretions. Most common ulceration sites are the cardia, pylorus, and the marginal area walls of the stomach. In addition, peptic ulcers frequently occur along the lesser curvature of the antral end of the stomach or, more rarely, in the lower end of the esophagus where stomach juices frequently reflux [1]. A type of peptic ulcer called a marginal ulcer also often occurs wherever a surgical opening such as a gastrojejunostomy has been made between the stomach and the jejunum of the small intestine.

Epidemiology

The incidence has fallen in developing countries with the reduction of H.pylori infection rates. However there is a rise of peptic ulcer disease incidence among patients who use NSAIDS [2].

Causes

Helicobacter pylori (most common cause)

● NSAIDs

● Endocrine cell hyperplasia

● Viral infection ( Herpes simplex virus, Cytomegalovirus)

Pathogenesis

H. pylori infection most often presents as a predominantly antral gastritis with normal or increased acid production. Local gastrin production may be increased, but hypergastrinemia (increased serum gastrin) is uncommon [3]. When inflammation remains limited to the antrum, increased acid production results in greater risk of duodenal peptic ulcer. In other patients, gastritis may progress to involve the gastric body and fundus [2, 3]. This multifocal atrophic gastritis is associated with patchy mucosal atrophy, reduced parietal cell mass and acid secretion, intestinal metaplasia, and increased risk of gastric adenocarcinoma [1, 2, 3].

Failure of 2 physiological feedback mechanisms

  1. When excess acid enters the duodenum, it inhibits gastric secretion and peristalsis in the stomach, both by nervous reflexes and by hormonal feedback from the duodenum, thereby decreasing the rate of gastric emptying [2].

  2. The presence of acid in the small intestine liberates secretin from the intestinal mucosa, which then passes by way of the blood to the pancreas to promote rapid secretion of pancreatic juice. This juice also contains a high concentration of sodium bicarbonate, thus making still more sodium bicarbonate available for neutralization of the acid [2].

Therefore, a peptic ulcer can be caused in either of two ways: (1) excess secretion of acid and pepsin by the gastric mucosa or (2) diminished ability of the gastroduodenal mucosal barrier to protect against the digestive properties of the stomach acid–pepsin secretion.

Specific Causes of Peptic Ulcer

At least 75 percent of people with peptic ulcers have been found to have chronic infection of the terminal portions of the gastric mucosa and initial portions of the duodenal mucosa, most often caused by the bacterium Helicobacter pylori [3]. Once this infection begins, it can last a lifetime unless it is eradicated by antibacterial therapy. Furthermore, the bacterium is capable of penetrating the mucosal barrier by virtue of its virulence factors to burrow through the barrier and by releasing ammonium that liquefies the barrier and stimulates the secretion of hydrochloric acid [3]. As a result, the strong acidic digestive juices of the stomach secretions can then penetrate into the underlying epithelium and literally digest the gastrointestinal wall, thus leading to peptic ulceration [2].

Virulence factors of Helicobacter pylori

  1. Flagella, which allow the bacteria to be motile in viscous mucus [3]

  2. Urease, which generates ammonia from endogenous urea and thereby elevates local gastric pH and enhances bacterial survival [3]

  3. Adhesins that enhance bacterial adherence to surface foveolar cells [3]

  4. Toxins, such as cytotoxin-associated gene A (CagA), that may be involved in disease progression [3]

Host factors also lead to H.pylori infection. Genetic polymorphism that lead to increased expression of the proinflammatory cytokines tumor necrosis factor (TNF) and interleukin-1β (IL-1β) or decreased expression of the anti-inflammatory cytokine interleukin-10 (IL-10) are associated with development of pangastritis, atrophy, and gastric cancer [2].

Iron deficiency may also be a risk factor for H. pylori–associated gastric cancer. The course of H. pylori gastritis is, therefore, the result of interplay between gastroduodenal mucosal defenses, inflammatory responses, and bacterial virulence factors [1, 2, 3].

Treatment

Antibiotic medications to kill H. pylori. If H. pylori is found in your digestive tract, your doctor may recommend a combination of antibiotics to kill the bacterium. These may include amoxicillin (Amoxil), clarithromycin (Biaxin), metronidazole (Flagyl), tinidazole (Tindamax), tetracycline and levofloxacin [4,5].

Medications that block acid production and promote healing. Proton pump inhibitors — also called PPIs — reduce stomach acid by blocking the action of the parts of cells that produce acid. Example: lansoprazole (Prevacid), rabeprazole (Aciphex), esomeprazole (Nexium) and pantoprazole (Protonix) [5] Long-term use of proton pump inhibitors, particularly at high doses, may increase your risk of hip, wrist and spine fracture. Ask your doctor whether a calcium supplement may reduce this risk [4, 5].

Medications to reduce acid production. Acid blockers — also called histamine (H-2) blockers — reduce the amount of stomach acid released into your digestive tract, which relieves ulcer pain and encourages healing [5] Available by prescription or over the counter, acid blockers include the medications famotidine (Pepcid AC), cimetidine (Tagamet HB) and nizatidine (Axid AR) [4, 5].

Antacids that neutralize stomach acid. Your doctor may include an antacid in your drug regimen. Antacids neutralize existing stomach acid and can provide rapid pain relief. Side effects can include constipation or diarrhea, depending on the main ingredients [4,5]. Antacids can provide symptom relief but generally aren't used to heal your ulcer [5].

Medications that protect the lining of your stomach and small intestine. In some cases, your doctor may prescribe medications called cytoprotective agents that help protect the tissues that line your stomach and small intestine. Options include the prescription medications sucralfate (Carafate) and misoprostol (Cytotec) [4,5].

Most common combination of drugs used to fight against Helicobacter pylori infection the triple therapy or the Quadruple therapy [5].


Triple Therapy

● An antibiotic amoxicillin

● Clarithromycin

● A proton pump inhibitor omeprazole, lansoprazol

Quadruple therapy

Proton pump inhibitor

Tetracycline

Metronidazole

Bismuth salt

In conclusion it could be said that PUD is a common clinical problem. Two of the most important causative factors are H.pylori and NSAID’s. Patients may present with dyspepsia and pain. Therefore, it is essential for medical professionals to be able to identify peptic ulcer caused by H.pylori. The use of triple therapy or quadruple therapy should be used to improve the patient’s condition. H.pylori eradication reduces the risk of recurrence.

References

1.Elsevier. (2018). Davidson's principles and practice of medicine. [Place of publication not identified].

2.Kumar, P., & Clark, M. (2017). Clinical medicine. London: Bailliere Tindall.

3.Kumar, V., De_Rosa, G., Eusebi, V., Aster, J., Abbas, A., Cotran, R., & Robbins, S. (2015). Robbins e Cotran Le basi patologiche delle malattie. Milano: Edra.

4.Peptic ulcer - Diagnosis and treatment - Mayo Clinic. (2020). Retrieved 11 August 2020, from https://www.mayoclinic.org/diseases-conditions/peptic-ulcer/diagnosis-treatment/drc-20354229

5.Stomach ulcer - Treatment. (2020). Retrieved 11 August 2020, from https://www.nhs.uk/conditions/stomach-ulcer/treatment/


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