Health Risks of Chronic H. pylori Infection
Chronic H. pylori infection is a recognized human carcinogen that causes gastric cancer in 71-95% of cases, making it the most dreaded and clinically significant outcome, along with peptic ulcer disease, atrophic gastritis, and MALT lymphoma. 1, 2
Gastric Cancer Risk: The Most Critical Outcome
Gastric cancer represents the end-stage of a progressive inflammatory cascade that H. pylori initiates and maintains throughout a lifetime of infection 1:
- The carcinogenic pathway progresses: chronic active gastritis → atrophic gastritis → intestinal metaplasia → intraepithelial neoplasia → invasive gastric adenocarcinoma 1, 2
- All infected individuals develop gastritis and remain at risk for potentially life-threatening diseases 1
- Gastric cancer risk increases exponentially with age, with the infection typically acquired in childhood resulting in decades of carcinogenic exposure 1
- H. pylori increases gastric cancer risk approximately 2.5-fold, with gastric cancer being the third most common cause of cancer death worldwide 2, 3
Geographic Variation in Cancer Risk
The lifetime risk varies dramatically by population 1:
- United States: approximately 0.6% lifetime risk to age 75
- Japan and China: can reach 20% lifetime risk
- High-risk subpopulations in the U.S. (Native Americans, blacks, Hispanics, immigrants from high-risk countries) retain elevated risk similar to their countries of origin 1, 2
Peptic Ulcer Disease
- Lifetime risk of peptic ulcer disease is approximately 17% in H. pylori-infected individuals 2
- Eradication of H. pylori cures peptic ulcer disease and prevents ulcer recurrences, transforming it from a chronic disease into a "one-off" curable condition 1
- Dual therapy with amoxicillin and lansoprazole or triple therapy with clarithromycin has been shown to eradicate H. pylori and reduce duodenal ulcer recurrence 4
Atrophic Gastritis and Premalignant Conditions
Atrophic gastritis represents a critical point in the carcinogenic cascade 1:
- The risk of progression from atrophic gastritis to gastric adenocarcinoma is 0.1-0.3% per year 2
- Corpus-predominant H. pylori gastritis substantially increases gastric cancer risk compared to antral-predominant patterns 2
- Intestinal metaplasia represents a "point of no return" with gastric cancer developing 10.9 times more frequently in its presence, and it is generally considered irreversible even after H. pylori eradication 2
- Patients with pernicious anemia (type A autoimmune atrophic gastritis) are at particularly high risk and warrant specific surveillance 1, 3
MALT Lymphoma
- H. pylori infection is causally linked to gastric mucosa-associated lymphoid tissue (MALT) lymphoma 1, 5
- Eradication therapy is indicated for patients with this diagnosis 1
Critical Window for Prevention
Eradication of H. pylori infection halts the progression of gastritis, alters the natural history of disease, and reduces overall gastric cancer risk 1, 2:
- The intervention is most effective before development of preneoplastic conditions (atrophy and intestinal metaplasia) 2
- With eradication, the mucosa heals, which does not eliminate existing risk but halts the exponential increase of risk with age 1
- Gastric atrophy may be reversible only in the corpus, but intestinal metaplasia is uniformly considered irreversible 2
Population-Level Impact
Mass eradication programs in high-risk populations have demonstrated dramatic reductions 1:
- 67% reduction in peptic ulcer
- 77% reduction in premalignant gastric lesions
- 53% reduction in gastric cancer incidence
- 25% reduction in gastric cancer deaths
High-Risk Groups Requiring Eradication
H. pylori eradication to prevent gastric cancer should be undertaken in 1:
- First-degree relatives of gastric cancer patients (2-3 times increased risk; 10-fold if multiple relatives affected)
- Patients with previous gastric neoplasia (MALT lymphoma, adenoma, cancer) already treated
- Patients with high-risk gastritis patterns: severe pan-gastritis, corpus-predominant gastritis, severe atrophy
- Patients requiring chronic acid suppression for more than 1 year
- Patients with strong environmental risk factors (heavy smoking, occupational dust/coal/quartz/cement exposure)
Important Clinical Caveats
- False positive tests can occur with achlorhydria due to overgrowth of non-H. pylori urease-producing organisms (e.g., pernicious anemia, atrophic gastritis), leading to apparent treatment failures 1, 2
- Hereditary diffuse gastric cancer (less than 1% of cases with CDH-1 mutations) is not related to H. pylori infection and requires genetic consultation and prophylactic gastrectomy 1, 2
- Antibiotic resistance is the most important factor responsible for falling eradication success rates, with treatment failure occurring in more than 20% of patients even with recommended regimens 1, 6