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Chronic gastritis caused by Helicobacter pylori
Last reviewed: 05.07.2025
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Helicobacter pylori is the main pathogenic microorganism of the stomach, causing gastritis, peptic ulcer disease, gastric adenocarcinoma and poorly differentiated gastric lymphoma.
Chronic gastritis caused by Helicobacter pylori may be asymptomatic or cause dyspepsia of varying severity. Diagnosis is made by a breath test with urea labeled with C14 or C13 and morphological examination of biopsy specimens during endoscopy. Treatment of chronic gastritis caused by Helicobacter pylori consists of proton pump inhibitors and two antibiotics.
[ What causes chronic gastritis caused by Helicobacter pylori?
Helicobacter pylori is a spiral-shaped, Gram-negative microorganism that has adapted to thrive in acidic conditions. In developing countries, it causes chronic infections and is usually acquired in childhood. In the United States, infection is less common in children, but incidence increases with age: approximately 50% of people aged 60 years are infected. Infection is particularly common in African Americans and Hispanics.
The organism has been isolated from stool, saliva, and dental plaque, suggesting oro-oral or feco-oral transmission. The infection tends to spread within families and among residents of shelters. Nurses and gastroenterologists are at high risk: the bacteria can be transmitted through insufficiently disinfected endoscopes.
Pathophysiology of chronic gastritis caused by Helicobacter pylori
The impact of Helicobacter pylori infection varies depending on the location within the stomach. Antral-predominant infection results in increased gastrin secretion, likely due to localized reduction in somatostatin synthesis. The resulting hypersecretion of hydrochloric acid predisposes to the development of prepyloric and duodenal ulcers. Corpus-predominant infection results in gastric mucosal atrophy and decreased acid production, possibly due to increased local secretion of interleukin 1b. Patients with corpus-predominant infection are predisposed to gastric ulcer and adenocarcinoma. Some patients have combined antral and corpus infection with associated clinical manifestations. Many patients with Helicobacter pylori infection do not develop any significant clinical manifestations.
Ammonia produced by Helicobacter pylori allows the organism to survive in the acidic environment of the stomach and to destroy the mucus barrier. Cytotoxins and mucolytic enzymes (e.g. bacterial protease, lipase) produced by Helicobacter pylori may play a role in mucosal damage and subsequent ulcerogenesis.
Infected individuals are 3-6 times more likely to develop gastric cancer. Helicobacter pylori infection is associated with intestinal-type adenocarcinoma of the body and antrum of the stomach, but not with cardiac cancer. Other associated malignancies include gastric lymphoma and mucosa-associated lymphoid tissue (MALT) lymphoma, a monoclonal limited B-cell tumor.
Diagnosis of chronic gastritis caused by Helicobacter pylori
Screening examination of asymptomatic patients does not guarantee diagnosis. Studies are performed to assess the course of peptic ulcer and gastritis. Post-treatment examination is also usually performed to confirm the death of the microorganism. Differential studies are performed to verify the diagnosis and the effectiveness of treatment.
Non-invasive tests for Helicobacter
Laboratory tests for Helicobacter and programmed serologic tests for Helicobacter pylori antibodies have a sensitivity and specificity of more than 85% and are considered the noninvasive tests of choice for the primary verification of Helicobacter pylori infection. However, since qualitative determination remains positive for up to 3 years after successful therapy and quantitative antibody levels do not decrease significantly for 6-12 months after treatment, serologic tests are not routinely used to assess treatment efficacy.
When determining urea in exhaled air, 13C or 14C-labeled urea is used. In an infected patient, the body metabolizes urea and releases labeled CO 2, which is exhaled and can be quantified in exhaled air 20-30 minutes after oral administration of labeled urea. The sensitivity and specificity of the method is more than 90%. The breath test for Helicobacter (for urea) is well suited for confirming the death of the microorganism after treatment. False-negative results are possible with previous use of antibiotics or proton pump inhibitors; therefore, subsequent studies should be carried out more than 4 weeks after antibacterial therapy and 1 week after therapy with proton pump inhibitors. H2 blockers do not affect the test results.
Invasive tests for Helicobacter
Gastroscopy is used for biopsy sampling of mucosal fragments for the purpose of performing a rapid urea test (URT or urease test) and histological staining of the biopsy. Bacterial culture has limited use due to the low resistance of the microorganism.
The rapid urea test, in which the presence of bacterial urea in biopsy specimens causes a staining change in special media, is the diagnostic method of choice for tissue specimens. Histologic staining of biopsy specimens should be performed in patients with negative BMT results but with clinical suspicion of infection, as well as with previous antibiotic therapy or treatment with proton pump inhibitors. The rapid urea test and histologic staining have a sensitivity and specificity of more than 90%.
Treatment of chronic gastritis caused by Helicobacter pylori
Patients with complications (e.g., gastritis, ulcer, malignancy) require treatment to eradicate the organism. Eradication of Helicobacter pylori may even cure mucosa-associated lymphoid tissue lymphoma (but not other infection-related malignancies) in some cases. Treatment of asymptomatic infection is controversial, but recognition of the role of Helicobacter pylori in cancer has led to recommendations for preventive treatment.
Treatment of chronic gastritis caused by Helicobacter pylori requires the use of mixed therapy, usually including antibiotics and acid suppressants. Proton pump inhibitors suppress H. pylori and increase the pH of the stomach, increasing the concentration of the drug in the tissues and the effectiveness of antibacterial drugs, creating an unfavorable environment for H. pylori.
A three-drug regimen is recommended. Oral omeprazole 20 mg twice daily or lansoprazole 30 mg twice daily, clarithromycin 500 mg twice daily, and metronidazole 500 mg twice daily or amoxicillin 1 g twice daily for 14 days cures the infection in more than 95% of cases. This regimen has excellent tolerability. Ranitidine bismuth citrate 400 mg orally twice daily can be used as an H2 - receptor antagonist to increase pH.
Four-drug therapy with a proton pump inhibitor twice daily, tetracycline 500 mg and basic salicylate or bismuth citrate 525 mg four times daily, and metronidazole 500 mg three times daily is also effective but more cumbersome.
Infected patients with duodenal or gastric ulcer require prolonged acid suppression for at least more than 4 weeks.
Treatment of chronic gastritis caused by Helicobacter pylori should be repeated if H. pylori persists. If repeated courses of treatment are ineffective, some authors recommend endoscopic culture to test its sensitivity to drugs.