H. pylori infection is usually acquired in childhood and, if it is not treated, persists for life. Almost every colonized person develops chronic active gastritis, although most remain asymptomatic.^[1][2] The pattern of gastritis largely determines the long-term outcome:

• Antral-predominant gastritis predisposes to duodenal ulcer.
• Corpus-predominant or atrophic gastritis predisposes to gastric ulcer, intestinal metaplasia, and non-cardia gastric adenocarcinoma.^[3]

The major complications are peptic ulcer disease (lifetime risk about 10–20%), distal gastric adenocarcinoma (about 1–2%), and gastric MALT lymphoma (<1%).^[4] Overall prognosis is favorable. Confirmed eradication cures most ulcer disease, lowers gastric cancer incidence and mortality, and induces remission in most patients with early-stage gastric MALT lymphoma. Residual cancer risk persists when atrophy or intestinal metaplasia is already established.^[5][6]

• Most infections are acquired in childhood (usually before age 10) and persist throughout life without spontaneous clearance in adults.^[1]
• Acute infection is almost never recognized clinically. It is followed by chronic active gastritis in virtually all persistently colonized persons.^[3]
• Chronic gastritis stays asymptomatic for decades in most people. Only a minority develop clinically significant disease, depending on:
  • bacterial virulence factors (notably cagA and vacA)
  • host genetics
  • environmental cofactors^[1][2]

^[3]

• Intestinal-type gastric adenocarcinoma develops through a multistep sequence:
  • non-atrophic chronic gastritis
  • atrophic gastritis
  • intestinal metaplasia
  • dysplasia
  • invasive adenocarcinoma^[1]
• In a prospective Japanese cohort of 1,526 patients followed with serial endoscopy:^[7]
  • Gastric cancer developed in 2.9% of infected patients and in none of the uninfected patients.
  • Severe atrophy, corpus-predominant gastritis, and intestinal metaplasia identified the highest-risk patients.
  • Patients with duodenal ulcer did not develop gastric cancer.
• In a U.S. Veterans Affairs cohort of 371,813 infected patients, cumulative incidence of non-proximal gastric adenocarcinoma after detection of H. pylori was:^[8]
  • 0.37% at 5 years
  • 0.50% at 10 years
  • 0.65% at 20 years

• H. pylori remains a leading cause of gastric and duodenal ulcers, and eradication heals ulcers and prevents recurrence.^[2]
• NSAIDs are an independent and often coexisting cause, so both should be evaluated in every ulcer patient.^[2]
• Ulcer complications (bleeding, perforation, gastric outlet obstruction) are the main source of acute morbidity from untreated infection.^[1]

• H. pylori is classified by the WHO International Agency for Research on Cancer as a group 1 (definite) carcinogen.^[2]
• It is the strongest known risk factor for non-cardia gastric adenocarcinoma and accounts for the large majority of these cancers.^[1][2]
• Among infected U.S. veterans, risk of future gastric cancer was higher with:^[8]
  • older age
  • racial and ethnic minority groups
  • smoking
• H. pylori is associated with both intestinal-type and diffuse-type adenocarcinoma.^[1]

• Gastric mucosa-associated lymphoid tissue lymphoma is a low-grade extranodal marginal zone B-cell lymphoma driven by chronic H. pylori–induced lymphoid proliferation.^[1]
• Eradication is the recognized initial therapy for early-stage, H. pylori–positive disease and achieves remission in about 75% of patients.^[9]

• Chronic infection drives atrophic gastritis and intestinal metaplasia, the precursor lesions of intestinal-type adenocarcinoma.^[1]
• Severe or extensive (corpus-involving) metaplasia and dysplasia carry the highest risk.^[7]
• Endoscopic surveillance (often about every 3 years) is suggested for individuals with high-risk intestinal metaplasia or dysplasia, and for those with resected dysplasia or early cancer.^[10]

• Iron-deficiency anemia: H. pylori is an established cause of unexplained or refractory iron deficiency anemia.^[1][11]
• Vitamin B12 deficiency: Atrophic corpus gastritis with achlorhydria can impair B12 absorption.^[1]
• Immune thrombocytopenic purpura: ITP is an established extragastric association.^[1][11]

• Most infected individuals remain asymptomatic lifelong.
• Lifetime risks are about:^[4]
  • 10–20% for ulcer disease
  • 1–2% for distal gastric cancer
  • <1% for MALT lymphoma
• Gastric cancer risk is concentrated in patients with:^[7]
  • corpus-predominant atrophic gastritis
  • intestinal metaplasia
  • dysplasia

• Confirmed cure is required. Cancer-risk reduction depends on documented eradication. Post-treatment test-of-cure (urea breath test, stool antigen, or biopsy-based testing) at least 4 weeks after therapy is recommended for all treated patients.^[8][11]
• Timing of eradication. Benefit is greatest when eradication precedes atrophy and intestinal metaplasia. Once these changes are established, residual cancer risk persists, so continued endoscopic surveillance is needed in high-risk mucosa.^[6][10]
• Latency of benefit. The cancer-prevention effect is delayed by years and is not evident in short-term follow-up.^[12]
• Generalizability. Most randomized evidence comes from high-incidence East Asian populations; Western prospective trial data are limited.^[5][6]