Gastritis Due to Helicobacter pylori Infection

How to Cite This Chapter: Agarwal A, Leontiadis GI, Dąbrowski A, Marlicz K. Gastritis Due to Helicobacter pylori Infection. McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. Accessed May 30, 2024.
Last Updated: July 21, 2019
Last Reviewed: August 9, 2019
Chapter Information

Definition, Etiology, PathogenesisTop

The prevalence of Helicobacter pylori is highest in developing countries, with Africa having the highest pooled prevalence globally (70.1%) and Oceania having the lowest (24.4%). Approximately 4.4 billion individuals were estimated to be infected globally as of 2015. The prevalence of H pylori infection is also determined by geography, age, strain virulence, environmental factors, and socioeconomic status.

H pylori infection is associated with gastric mucin degradation, epithelial cytotoxicity, and increased mucosal permeability. It causes inflammatory reactions and increased gastric acid secretion by stimulating gastrin-secreting G cells.

Acute gastritis may progress to a chronic phase, leading to mucosal atrophy and hypochlorhydria or achlorhydria. Early H pylori infection and uncomplicated chronic gastritis are usually asymptomatic. Complications and long-term sequelae include peptic ulcer disease (PUD), gastric cancer, gastric mucosa-associated lymphoid tissue (MALT) lymphoma, immune thrombocytopenia, iron deficiency anemia, and in very rare cases bacterial overgrowth secondary to achlorhydria. Chronic H pylori infection predisposes affected individuals to atrophic and autoimmune gastritis.

Clinical Features and Natural HistoryTop

Clinical features associated with H pylori–related gastritis are similar to that of gastritis due to other causes (see Acute Hemorrhagic/Erosive and Stress-Related Gastropathy).


Endoscopy is used for gastric mucosal assessment and biopsy for histopathologic and H pylori testing (biopsies should include the prepyloric region). It is recommended for patients with dyspepsia aged >60 years, and for those <60 years with alarming symptoms (anemia, weight loss, dysphagia, emesis). Mucosal biopsies can be tested using the rapid urease test and with direct culture and molecular studies.

The endoscopic features of acute gastritis usually include enlarged and stiffened folds as well as erosions and erythema of the mucosa. In chronic gastritis the antral mucosa is nodular and has a “cobblestone” appearance (due to “follicular” inflammation of the gastric mucosa), and areas of intestinal metaplasia, either multifocal or limited to the prepyloric region, are observed. Histologic examination of gastric mucosa specimens is necessary to assess the severity of chronic gastritis and to diagnose potential epithelial dysplasia. Details of the diagnosis of H pylori infection: see Peptic Ulcer Disease.

The urea breath test and fecal antigen test are 2 noninvasive tests for active infection that may be also used to monitor treatment response. Because proton pump inhibitor (PPI) therapy may interfere with test results, if possible it should be withheld for 1 to 2 weeks after treatment when confirming H pylori eradication.


1. Eradication therapy: see Peptic Ulcer Disease. Eradication testing is now recommended following completion of treatment using urea breath test, fecal antigen test, or biopsy-based confirmatory testing. Eradication failure has been associated with medication nonadherence, smoking, and alcohol use, among other variables. Eradication of H pylori leads to regression of inflammatory infiltrates, but regression of intestinal metaplasia and reduction of the risk of gastric cancer have not been proven.

2. Nonsteroidal anti-inflammatory drug (NSAID) discontinuation is generally recommended.

Prognosis is usually very good with appropriate therapy.

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