Gastritis 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] Aravind Reddy Kothagadi M.B.B.S[3]
Overview
Chronic gastritis is classified along three complementary axes, each answering a different clinical question. The updated Sydney System gives the histologic classification: topography (antrum/incisura vs corpus), morphology (atrophic vs non-atrophic, metaplastic vs non-metaplastic, active vs inactive), and etiology.[1][2] Histologic staging with OLGA/OLGIM, and the newer OLGIMA, converts the severity and topography of atrophy and intestinal metaplasia (IM) into stages 0–IV of gastric cancer (GC) risk.[3][4] Endoscopic classification (Kyoto score, Kimura–Takemoto, and EGGIM) predicts Helicobacter pylori status and GC risk in real time and is now endorsed to guide, but not replace, biopsy sampling.[5][6]
Among the atrophic forms, the key distinction is between H. pylori–associated gastritis, which is antral-predominant or multifocal, and autoimmune gastritis, which is corpus-restricted.[7] Gastritis is a histologic diagnosis. Most patients are asymptomatic, and dyspeptic symptoms correlate poorly with histologic findings.[8]
Classification
Updated Sydney System
The updated Sydney System (Houston workshop, 1994; published 1996) is the international standard for classifying and reporting non-neoplastic gastric biopsies. It classifies chronic gastritis by topography, morphology, and etiology, and provides a visual analogue scale for semiquantitative grading.[1]
Graded morphologic variables
Each variable is graded 0 (absent), 1 (mild), 2 (moderate), or 3 (marked).[1]
| Feature | Definition | Grading anchor |
|---|---|---|
| Chronic inflammation | Lymphocytes and plasma cells in the lamina propria | Mild, moderate, or marked increase in density |
| Activity | Neutrophilic infiltration of pits and surface epithelium | Mild: <⅓ of pits/surface Moderate: ⅓–⅔ Marked: >⅔ |
| Atrophy | Loss of glands appropriate to the compartment (antral or oxyntic), including metaplastic atrophy | Mild, moderate, or marked loss |
| Intestinal metaplasia | Intestinal-type epithelium replacing gastric epithelium | Mild: <⅓ of mucosa Moderate: ⅓–⅔ Marked: >⅔ |
| H. pylori density | Organism load on the surface epithelium | Mild: scattered organisms over <⅓ of surface Moderate: intermediate Marked: large clusters or a continuous layer over >⅔ of surface |
Non-graded features are recorded as present or absent. They include surface epithelial damage, lymphoid follicles, foveolar hyperplasia, and granulomas.[8]
Etiologic and topographic categories
| Category | Principal etiology | Synonyms / notes |
|---|---|---|
| Non-atrophic | H. pylori (± other factors) | Superficial gastritis, diffuse antral gastritis; historically "type B" |
| Atrophic: autoimmune | Autoimmunity | Historically "type A"; corpus-restricted; pernicious anemia–associated |
| Atrophic: multifocal | H. pylori; dietary and environmental factors | Historically "type B/AB"; environmental metaplastic atrophic gastritis |
| Chemical (reactive gastropathy) | NSAIDs, bile reflux, other irritants | Historically "type C"; reflux/chemical gastropathy (minimal inflammation) |
| Lymphocytic | Celiac disease, H. pylori, drugs (e.g., ticlopidine), idiopathic | Varioliform appearance at endoscopy |
| Granulomatous (non-infectious) | Crohn's disease, sarcoidosis, vasculitis, foreign material, idiopathic | Isolated granulomatous gastritis when no cause is found |
| Eosinophilic | Food sensitivity and other allergy | — |
| Collagenous | Unknown (possible autoimmune mechanism) | Thickened subepithelial collagen band |
| Radiation | Radiation injury | — |
| Other infectious | Non–H. pylori bacteria, cytomegalovirus, fungi, parasites (e.g., anisakiasis) | Includes phlegmonous and emphysematous gastritis |
- The legacy "type A/B/C" labels predate the modern etiologic classification. They should be used only as historical synonyms, not as standalone diagnoses.[9]
- "Gastritis" is reserved for inflammatory processes. NSAID- or bile-induced injury is histologically a gastropathy with minimal inflammation and is often misreported as gastritis.[8]
Biopsy sampling required for classification and staging
Topographic classification and staging require correctly sited biopsies submitted in separate, labeled containers.[7][10]
- Antrum (2): lesser and greater curvature, within 2–3 cm of the pylorus
- Incisura angularis (1): an early site of atrophy, IM, and dysplasia
- Corpus (2): lesser curvature about 4 cm proximal to the incisura, and greater curvature about 8 cm distal to the cardia
- Containers: at least one jar for antrum/incisura and one for corpus; targeted biopsies of visible lesions go in a separate jar
- Corpus biopsies are especially important in patients taking proton pump inhibitors or potassium-competitive acid blockers, because H. pylori migrates proximally under acid suppression.[10]
- MAPS III accepts a pragmatic minimum of 2 antrum/incisura and 2 corpus biopsies in 2 vials. The incisura biopsy is optional when virtual chromoendoscopy is used.[6]
Histologic staging: OLGA, OLGIM, and OLGIMA
Staging combines the severity of atrophy or IM with its topography to assign stage 0–IV. Stages III–IV denote high GC risk.[3][4][11] Clinical priority has shifted from naming the type of gastritis to staging its cancer risk.[12]
The matrix below is shared by OLGA (scoring atrophy) and OLGIM (scoring IM only). The antrum score includes the incisura angularis.[3]
| Antrum (incl. incisura) ↓ | Corpus → | |||
|---|---|---|---|---|
| None (0) | Mild (1) | Moderate (2) | Severe (3) | |
| None (0) | Stage 0 | Stage I | Stage II | Stage II |
| Mild (1) | Stage I | Stage I | Stage II | Stage III |
| Moderate (2) | Stage II | Stage II | Stage III | Stage IV |
| Severe (3) | Stage III | Stage III | Stage IV | Stage IV |
| System | What is scored | Strengths | Limitations |
|---|---|---|---|
| OLGA (Operative Link on Gastritis Assessment) | Atrophy in the antrum/incisura and corpus. Atrophy includes non-metaplastic gland loss, pseudopyloric metaplasia, and IM. | Biologically most complete | Only moderate interobserver agreement for glandular atrophy |
| OLGIM (Operative Link on Gastric Intestinal Metaplasia Assessment) | IM only, using the same matrix | Higher interobserver agreement | Ignores non-metaplastic atrophy and can under-stage. OLGIM stage is never higher than OLGA stage. |
| OLGIMA (Operative Link on Gastric IM and Glandular Atrophy Assessment; 2026) | The most severe single finding (glandular atrophy or IM) in each compartment, rather than an average | In multicenter validation it captured all OLGIM III–IV patients and up-staged OLGIM 0–II patients with advanced glandular atrophy | New; not yet in routine use |
- A meta-analysis of prospective cohorts confirmed substantially higher GC risk for OLGA/OLGIM III–IV than for 0–II. It also found measurable excess risk for stage II compared with 0–I, which challenges a strict cutoff at stage III.[15]
- The Correa histopathology score incorporates IM extent and complete versus incomplete subtype. It correlates with OLGA/OLGIM and is used mainly in cohort studies of progression.[4]
- Guidelines differ on how to use stage clinically. MAPS III recommends endoscopic surveillance (every 3 years) for advanced stages (III–IV) or extensive atrophy/IM.[6] The AGA recommends against routine surveillance for IM in general (conditional recommendation, very-low-quality evidence) and favors shared decision-making in higher-risk subgroups.[16][13]
Endoscopic classification
High-definition endoscopy with virtual chromoendoscopy allows real-time classification and risk stratification. It is endorsed to guide biopsy sampling, not to replace histology.[6]
| System | Components | Interpretation |
|---|---|---|
| Kyoto classification (Japan Gastroenterological Endoscopy Society) | Composite score of 0–8: atrophy (0–2), IM (0–2), enlarged folds (0–1), nodularity (0–1), diffuse redness (0–2) | 0: normal (uninfected) stomach ≥2: H. pylori–infected gastritis ≥4: gastritis at elevated GC risk |
| Kimura–Takemoto | Extent and pattern of endoscopic atrophy: closed type (C1–C3) or open type (O1–O3) | C3 or open type indicates extensive atrophy and higher risk |
| EGGIM (Endoscopic Grading of Gastric Intestinal Metaplasia) | IM scored 0–2 in each of five areas (total 0–10) | EGGIM ≥5 indicates extensive IM |
- Individual Kyoto findings indicate infection status. Regular arrangement of collecting venules (RAC) predicts an uninfected stomach. Enlarged folds, nodularity, and diffuse redness predict current infection. Map-like redness predicts past, eradicated infection.[5][17]
- Endoscopic and histologic findings correlate but are not interchangeable. Kyoto atrophy and IM scores track Sydney atrophy and IM grades. Enlarged folds, nodularity, and diffuse redness correlate with corpus inflammation rather than atrophy.[18]
- A Kyoto score of ≥4 should prompt Sydney-protocol biopsies to stage GC risk.[5]
Etiologic phenotypes of chronic atrophic gastritis
H. pylori–associated atrophic gastritis (HpAG) and autoimmune gastritis (AIG) are distinguished mainly by topography and serology.[9][7]
| Feature | H. pylori–associated (HpAG) | Autoimmune (AIG) |
|---|---|---|
| Legacy label | Type B | Type A |
| Topography | Antral-predominant or multifocal; extends proximally | Corpus-restricted; antrum spared |
| Mechanism | Chronic H. pylori infection | Immune-mediated destruction of parietal cells |
| Serology / biomarkers | H. pylori testing positive | Anti-parietal cell antibodies ± anti-intrinsic factor antibodies; elevated gastrin; low pepsinogen I/II ratio |
| Acid secretion | Variable | Hypochlorhydria or achlorhydria |
| Key sequelae | Peptic ulcer, gastric adenocarcinoma, MALT lymphoma | Pernicious anemia (vitamin B12 deficiency), iron deficiency, type 1 gastric neuroendocrine tumors |
| Demographics / associations | Follows H. pylori prevalence | More common in women; associated with autoimmune thyroid disease and type 1 diabetes mellitus |
- Antral atrophy alongside corpus-restricted atrophy should raise suspicion of concurrent HpAG and AIG. The two frequently coexist.[7][19]
- Current AIG phenotyping goes beyond the classic dichotomy. It now includes potential AIG (anti-parietal cell antibody–positive, normal gastrin) and seronegative AIG (antibody-negative, elevated gastrin), both of which require histologic confirmation.[19]
Structured pathology reporting
Several report elements are the strongest determinants of risk category, so the pathology report should specify:[20][21]
- H. pylori status
- Severity (mild, moderate, or marked) of atrophy and IM in each compartment
- IM subtype: incomplete IM carries higher GC risk than complete IM
- Anatomic extent: limited (antrum/incisura only) vs extensive (corpus involvement), with extensive IM carrying higher risk
- OLGA/OLGIM stage where feasible. Such staging remains uncommon in US practice.[7]
Classification pitfalls
- Pooling biopsies from the antrum and corpus in one container prevents topographic classification and OLGA/OLGIM staging.[7]
- Omitting the incisura misses a common early site of atrophy, IM, and dysplasia.[7]
- Labeling reactive gastropathy as gastritis misdirects workup toward infection or autoimmunity.[8]
- Assuming eradication resets the stage. Established atrophy and IM persist after H. pylori eradication, and the staged risk remains.[7]
- Relying on serology alone for AIG misses potential and seronegative phenotypes.[19]
- Expecting symptoms to reflect histology. Gastritis is usually asymptomatic.[8]
References
- ↑ 1.0 1.1 1.2 1.3 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): 1161–81. PMID 8827022.
- ↑ 2.0 2.1 Rugge M, Savarino E, Sbaraglia M, Bricca L, Malfertheiner P (2021). "Gastritis: the clinico-pathological spectrum". Dig Liver Dis. 53 (10): 1237–1246. doi:10.1016/j.dld.2021.03.007. PMID 33785282 Check
|pmid=value (help). - ↑ 3.0 3.1 3.2 Rugge M, Meggio A, Pennelli G, Piscioli F, Giacomelli L, De Pretis G; et al. (2007). "Gastritis staging in clinical practice: the OLGA staging system". Gut. 56 (5): 631–6. doi:10.1136/gut.2006.106666. PMC 1942143. PMID 17142647.
- ↑ 4.0 4.1 4.2 Gawron AJ, Shah SC, Altayar O, Davitkov P, Morgan D, Turner K, Mustafa RA (2020). "AGA technical review on gastric intestinal metaplasia—natural history and clinical outcomes". Gastroenterology. 158 (3): 705–731.e5. doi:10.1053/j.gastro.2019.12.001. PMID 31816300.
- ↑ 5.0 5.1 5.2 5.3 Toyoshima O, Nishizawa T (2022). "Kyoto classification of gastritis: advances and future perspectives in endoscopic diagnosis of gastritis". World J Gastroenterol. 28 (43): 6078–6089. doi:10.3748/wjg.v28.i43.6078. PMID 36483157 Check
|pmid=value (help). - ↑ 6.0 6.1 6.2 6.3 6.4 Dinis-Ribeiro M, Libânio D, Uchima H; et al. (2025). "Management of epithelial precancerous conditions and early neoplasia of the stomach (MAPS III): European Society of Gastrointestinal Endoscopy (ESGE), European Helicobacter and Microbiota Study Group (EHMSG) and European Society of Pathology (ESP) guideline update 2025". Endoscopy. 57 (5): 504–554. doi:10.1055/a-2529-5025. PMID 40112834 Check
|pmid=value (help). - ↑ 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 Shah SC, Piazuelo MB, Kuipers EJ, Li D (2021). "AGA clinical practice update on the diagnosis and management of atrophic gastritis: expert review". Gastroenterology. 161 (4): 1325–1332.e7. doi:10.1053/j.gastro.2021.06.078. PMID 34454714 Check
|pmid=value (help). - ↑ 8.0 8.1 8.2 8.3 8.4 Washington MK, Peek RM (2022). "Gastritis and gastropathy". Yamada's Textbook of Gastroenterology (7th ed.).
- ↑ 9.0 9.1 Lenti MV, Rugge M, Lahner E, Miceli E, Toh BH, Genta RM, De Block C, Hershko C, Di Sabatino A (2020). "Autoimmune gastritis". Nat Rev Dis Primers. 6 (1): 56. doi:10.1038/s41572-020-0187-8. PMID 32647173 Check
|pmid=value (help). - ↑ 10.0 10.1 Nagula S, Parasa S, Laine L, Shah SC (2024). "AGA clinical practice update on high-quality upper endoscopy: expert review". Clin Gastroenterol Hepatol. 22 (5): 933–943. doi:10.1016/j.cgh.2023.10.034. PMID 38385942 Check
|pmid=value (help). - ↑ Rugge M, Correa P, Di Mario F, El-Omar E, Fiocca R, Geboes K; et al. (2008). "OLGA staging for gastritis: a tutorial". Dig Liver Dis. 40 (8): 650–8. doi:10.1016/j.dld.2008.02.030. PMID 18424244.
- ↑ Rugge M, Genta RM, Malfertheiner P, Dinis-Ribeiro M, El-Serag H, Graham DY; et al. (2024). "RE.GA.IN.: the Real-world Gastritis Initiative—updating the updates". Gut. 73 (3): 407–441. doi:10.1136/gutjnl-2023-331164. PMID 38383142 Check
|pmid=value (help). - ↑ 13.0 13.1 Matysiak-Budnik T, Camargo MC, Piazuelo MB, Leja M (2020). "Recent guidelines on the management of patients with gastric atrophy: common points and controversies". Dig Dis Sci. 65 (7): 1899–1903.
- ↑ Delgado Guillena PG, Cuatrecasas M, Montori S; et al. (2026). "The OLGIMA system for gastric cancer risk assessment. A useful method based on the histological Sydney consensus". Histopathology. 88 (4): 911–921. PMID 41293900 Check
|pmid=value (help). - ↑ Benites-Goñi H, Cabrera-Hinojosa D, Latorre G, Hernandez AV, Uchima H, Riquelme A (2025). "OLGA and OLGIM staging systems on the risk assessment of gastric cancer: a systematic review and meta-analysis of prospective cohorts". Ther Adv Gastroenterol. 18. doi:10.1177/17562848251325461.
- ↑ Gupta S, Li D, El Serag HB, Davitkov P, Altayar O, Sultan S, Falck-Ytter Y, Mustafa RA (2020). "AGA clinical practice guidelines on management of gastric intestinal metaplasia". Gastroenterology. 158 (3): 693–702. doi:10.1053/j.gastro.2019.12.003.
- ↑ 17.0 17.1 Toyoshima O, Nishizawa T, Koike K (2020). "Endoscopic Kyoto classification of Helicobacter pylori infection and gastric cancer risk diagnosis". World J Gastroenterol. 26 (5). doi:10.3748/wjg.v26.i5.466. PMID 32089624 Check
|pmid=value (help). - ↑ Toyoshima O, Nishizawa T, Yoshida S; et al. (2022). "Consistency between the endoscopic Kyoto classification and pathological updated Sydney System for gastritis". J Gastroenterol Hepatol. 37 (2). PMID 34569096 Check
|pmid=value (help). - ↑ 19.0 19.1 19.2 Lenti MV, Miceli E, Vanoli A, Di Sabatino A (2026). "Autoimmune gastritis: emerging insights and clinical management". Nat Rev Gastroenterol Hepatol. doi:10.1038/s41575-026-01200-0. PMID 41975068 Check
|pmid=value (help). - ↑ Shah SC, Wang AY, Wallace MB, Hwang JH (2025). "AGA clinical practice update on screening and surveillance in individuals at increased risk for gastric cancer in the United States: expert review". Gastroenterology. 168 (2): 405–416.e1. doi:10.1053/j.gastro.2024.11.001.
- ↑ Sugano K, Moss SF, Kuipers EJ (2023). "Gastric intestinal metaplasia: real culprit or innocent bystander as a precancerous condition for gastric cancer?". Gastroenterology. 165 (6): 1352–1366.e1. doi:10.1053/j.gastro.2023.08.028.