What are complications of H pylori- associated chronic gastritis?

Updated: Jun 07, 2019
  • Author: Akiva J Marcus, MD, PhD; Chief Editor: BS Anand, MD  more...
  • Print

As previously mentioned, 50% of the world's population is infected with H pylori. The overwhelming majority of those infected do not develop significant clinical complications and remain carriers with asymptomatic chronic gastritis. Some individuals who carry additional risk factors may develop peptic ulcers, gastric mucosa–associated lymphoid tissue (MALT) lymphomas, or gastric adenocarcinomas.

An increased duodenal acid load may precipitate and wash out the bile salts, which normally inhibit the growth of H pylori. Progressive damage to the duodenum promotes gastric foveolar metaplasia, resulting in sites for H pylori growth and more inflammation. This cycle renders the duodenal bulb increasingly unable to neutralize acid entering from the stomach until changes in the bulb structure and function are sufficient for an ulcer to develop. H pylori can survive in areas of gastric metaplasia in the duodenum, contributing to the development of peptic ulcers. [11]

MALT lymphomas may develop in association with chronic gastritis secondary to H pylori infection. The stomach usually lacks organized lymphoid tissue, but after infection with H pylori, lymphoid tissue is universally present. Acquisition of gastric lymphoid tissue is thought to be due to persistent antigen stimulation from byproducts of chronic infection with H pylori. [25]

The continuous presence of H pylori results in the persistence of MALT in the gastric mucosa, which eventually may progress to form low- and high-grade MALT lymphomas. MALT lymphomas are monoclonal proliferations of neoplastic B cells that have the ability to infiltrate gastric glands. Gastric MALT lymphomas typically are low-grade T-cell–dependent B-cell lymphomas, and the antigenic stimulus of gastric MALT lymphomas is thought to be H pylori.

Another complication of H pylori gastritis is the development of gastric carcinomas, especially in individuals who develop extensive atrophy and intestinal metaplasia of the gastric mucosa. It is well accepted that a multistep process initiated by H pylori related chronic inflammation of the gastric mucosa progresses to chronic atrophic gastritis, intestinal metaplasia, dysplasia, and finally leading to the development adenocarcinoma. Although the relationship between H pylori and gastritis is constant, only a small proportion of individuals infected with H pylori develop gastric cancer; the exact mechanism for this relationship with gastric carcinogenesis remains unclear, but host genetic background may play a role. [8] The incidence of gastric cancer usually parallels the incidence of H pylori infection in countries with a high incidence of gastric cancer and is consistent with H pylori being the cause of the precursor lesion, chronic atrophic gastritis. [25, 26]

H pylori-related chronic gastritis may also increase the risk of endothelial dysfunction, and thus vascular disease, due to abnormalities in flow-mediated dilation and carotid intima media thickness, as well as elevated levels of soluble vascular cell adhesion molecule-1 (sVCAM-1) and intercellular adhesion molecule-1 (ICAM-1). [27]

Persistence of the organisms and associated inflammation during long-standing infection is likely to permit the accumulation of mutations in the genome of the gastric epithelial cells, leading to an increased risk of malignant transformation and progression to adenocarcinoma. Studies have provided evidence of the accumulation of the mutations in the gastric epithelium secondary to oxidative DNA damage associated with chronic inflammatory byproducts and secondary to deficiency of DNA repair induced by chronic bacterial infection.

Although the role of H pylori in peptic ulcer disease is well established, the role of the infection in non-ulcer or functional dyspepsia remains highly controversial. A recent meta-analysis demonstrates that H pylori eradication therapy is associated with an improvement of dyspeptic symptoms in patients with functional dyspepsia in Asian, European, and American populations. [28] Although this study illustrates that H pylori eradication may be beneficial for symptom relief in some populations, routine H pylori testing and treatment in nonulcer dyspepsia are not currently widely accepted. Therefore, H pylori eradication strategies in patients with nonulcer dyspepsia must be considered on a patient-by-patient basis.

Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!