Helicobacter pylori infection classification
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahad Hasan, M.D.[2] Yamuna Kondapally, M.B.B.S[3]
Overview
Helicobacter pylori (H. pylori) infection is now recognized as an infectious disease in its own right, regardless of symptoms, by the Maastricht VI/Florence Consensus and the World Health Organization 11th revision of the International Classification of Diseases (ICD-11).[1] Current classification uses four clinically useful axes: formal disease and coding status, etiology-based classification of the gastritis it causes (Kyoto Global Consensus), topographic and histologic gastritis phenotype (updated Sydney System), and stage of the premalignant Correa cascade together with the resulting clinical outcome. All persistently infected individuals develop chronic gastritis, but only a minority (approximately 10–15%) progress to clinically significant disease such as peptic ulcer disease, gastric adenocarcinoma, or gastric MALT lymphoma.[2][3]
Classification
Etiologic Classification of Gastritis (Kyoto Global Consensus)
The Kyoto Global Consensus (2015) recommended classifying chronic gastritis and duodenitis by etiology rather than descriptive histology, and proposed this framework for ICD-11.[4] Principal etiologic categories relevant to H. pylori include:
- H. pylori-induced gastritis: the predominant cause of chronic gastritis worldwide
- Drug-induced gastritis (e.g., NSAIDs)
- Autoimmune gastritis (AIG)
The consensus also defined H. pylori-associated dyspepsia as a distinct entity, separate from idiopathic functional dyspepsia.[4][5]
| Feature | H. pylori-associated atrophic gastritis | Autoimmune gastritis |
|---|---|---|
| Topography of atrophy | Begins in the antrum, extends proximally to the corpus | Corpus-predominant with antral sparing |
| Mechanism | Chronic bacterial infection–driven inflammation | Autoantibody-mediated parietal cell destruction |
The two conditions can coexist; H. pylori testing and treatment are recommended in all patients diagnosed with autoimmune gastritis.[2]
Topographic and Histologic Phenotype
The anatomic distribution of gastritis is a core element of the updated Sydney System and predicts the dominant downstream complication.[6][7]
| Phenotype | Acid secretion | Dominant clinical association |
|---|---|---|
| Antral-predominant gastritis | Increased | Duodenal ulcer |
| Corpus-predominant gastritis or pangastritis | Reduced (hypochlorhydria), with progressive atrophy | Gastric ulcer and gastric adenocarcinoma |
On histology, the updated Sydney System separately grades activity (neutrophilic infiltration, reflecting active inflammation) and chronic inflammation (lymphocytes and plasma cells), alongside atrophy, intestinal metaplasia, and H. pylori density.[6] Chronic active gastritis is the near-universal consequence of persistent colonization.
Premalignant Staging: the Correa Cascade
Progression to noncardia gastric cancer follows a defined histopathologic sequence:[2][7]
Normal mucosa → chronic non-atrophic gastritis → atrophic gastritis (AG) → gastric intestinal metaplasia (GIM) → dysplasia → gastric adenocarcinoma
- AG, GIM, and dysplasia are collectively termed gastric premalignant conditions (GPMC); staging a patient along this cascade determines surveillance needs beyond eradication alone.[2]
- Chronic H. pylori gastritis is the dominant risk factor for noncardia gastric adenocarcinoma, with an attributable risk of approximately 75–89%.[2]
- Noninvasive serologic staging schemes (e.g., combining H. pylori serostatus with pepsinogen I/II ratio) are used in some Asian programs but are not reliably validated in North American populations.[2]
Classification by Clinical Outcome
| Category | Entity | Comment |
|---|---|---|
| Gastroduodenal (benign) | Chronic gastritis | Universal in untreated persistent infection; usually asymptomatic[3] |
| Duodenal ulcer | H. pylori implicated in >75% of cases[2] | |
| Gastric ulcer | Associated with corpus-predominant gastritis and NSAID co-exposure[8] | |
| H. pylori-associated dyspepsia | Distinct from idiopathic functional dyspepsia[4] | |
| Gastric malignancy | Noncardia gastric adenocarcinoma | Attributable risk approximately 75–89%[2] |
| Gastric MALT lymphoma (extranodal marginal-zone B-cell lymphoma) | Closely linked to chronic H. pylori gastritis[3][8] | |
| Extragastric (variable evidence quality) | Unexplained iron deficiency anemia | Established indication for testing[2] |
| Immune thrombocytopenic purpura | Established indication for testing[2] | |
| Vitamin B12 deficiency | Association reported; evidence less consistent[3] |
Areas of Uncertainty
- Universal versus indication-based treatment: Maastricht VI endorses an "infectious disease, therefore treat" stance for all infected individuals,[1] whereas the American College of Gastroenterology frames management around indication-based testing, with treatment of all who test positive.[2]
- The relationship between H. pylori and gastroesophageal reflux disease, irritable bowel syndrome, and asthma, including possible protective associations, remains contested.[3]
References
- ↑ 1.0 1.1 Malfertheiner P, Megraud F, Rokkas T, Gisbert JP, Liou JM, Schulz C; et al. (2022). "Management of Helicobacter pylori infection: the Maastricht VI/Florence consensus report". Gut. 71 (9): 1724–1762. doi:10.1136/gutjnl-2022-327745. PMID 35944925 Check
|pmid=value (help). - ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 Chey WD, Howden CW, Moss SF, Morgan DR, Greer KB, Grover S, Shah SC (2024). "ACG Clinical Guideline: Treatment of Helicobacter pylori Infection". Am J Gastroenterol. 119 (9): 1730–1753. doi:10.14309/ajg.0000000000002968. PMID 39626064 Check
|pmid=value (help). - ↑ 3.0 3.1 3.2 3.3 3.4 Robinson K, Atherton JC (2021). "The Spectrum of Helicobacter-Mediated Diseases". Annu Rev Pathol. 16: 123–144. doi:10.1146/annurev-pathol-032520-024949. PMID 33197219 Check
|pmid=value (help). - ↑ 4.0 4.1 4.2 Invalid
<ref>tag; no text was provided for refs namedpmid26187502 - ↑ Invalid
<ref>tag; no text was provided for refs namedpmid32170476 - ↑ 6.0 6.1 Dixon MF, Genta RM, Yardley JH, Correa P (1996). "Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994". Am J Surg Pathol. 20 (10): 1161–1181. doi:10.1097/00000478-199610000-00001. PMID 8827022.
- ↑ 7.0 7.1 Malfertheiner P, Camargo MC, El-Omar E, Liou JM, Peek R, Schulz C; et al. (2023). "Helicobacter pylori infection". Nat Rev Dis Primers. 9 (1): 19. doi:10.1038/s41572-023-00431-8. PMID 37081005 Check
|pmid=value (help). - ↑ 8.0 8.1 Crowe SE (2019). "Helicobacter pylori Infection". N Engl J Med. 380 (12): 1158–1165. doi:10.1056/NEJMcp1710945. PMID 30893536.