Peptic ulcer classification
|
Peptic ulcer Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Surgery |
|
Case Studies |
|
2017 ACG Guidelines for Peptic Ulcer Disease |
|
Guidelines for the Indications to Test for, and to Treat, H. pylori Infection |
|
Guidlines for factors that predict the successful eradication when treating H. pylori infection |
|
Guidelines to document H. pylori antimicrobial resistance in the North America |
|
Guidelines for evaluation and testing of H. pylori antibiotic resistance |
|
Guidelines for when to test for treatment success after H. pylori eradication therapy |
|
Guidelines for penicillin allergy in patients with H. pylori infection |
|
Peptic ulcer classification On the Web |
|
American Roentgen Ray Society Images of Peptic ulcer classification |
|
Risk calculators and risk factors for Peptic ulcer classification |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Fahad Hasan, M.D.[2] Manpreet Kaur, MD [3]
Overview
Peptic ulcer disease is classified along three clinically distinct axes: etiology, anatomic location, and endoscopic morphology. Etiologic classification is the clinically relevant framework because it drives management. The categories are H. pylori-associated, NSAID/aspirin-induced, and idiopathic.[1][2] The Forrest classification grades bleeding ulcers by their endoscopic stigmata of hemorrhage. It is the most clinically actionable system because it determines the need for endoscopic hemostasis and post-procedure proton pump inhibitor dosing.[3][4] The Sakita–Miwa classification stages gastric ulcer healing. It is used mainly in research and after endoscopic submucosal dissection (ESD).[5][6]
Classification
Etiologic classification
- H. pylori-positive ulcers: approximately 42% of cases.[1][2][7]
- NSAID/aspirin-induced ulcers: approximately 36% of cases.[1][2][7]
- Idiopathic ulcers (H. pylori-negative, NSAID-negative): approximately 22% of cases. This proportion is increasing, which older schemes built on the H. pylori/NSAID dichotomy did not emphasize.[1][8]
- Less common causes:[2][8]
- Acid hypersecretory states, including Zollinger-Ellison syndrome and systemic mastocytosis
- Malignancy: gastric cancer or gastric lymphoma
- Inflammatory: Crohn's disease and eosinophilic gastroduodenitis
- Infectious: cytomegalovirus or herpes simplex virus in immunocompromised hosts, and non-H. pylori Helicobacter (NHPH) infection
- Mechanical/iatrogenic: radiation, Cameron ulcers associated with hiatal hernia, and anastomotic (marginal) ulcers after gastric resection
- Stress ulcers in critically ill patients
Anatomic classification
Peptic ulcers occur in the stomach, most commonly along the lesser curvature, or in the duodenum, most commonly in the duodenal bulb.[1][2] The Johnson classification subtypes gastric ulcers by location and acid output. It is of historical and surgical interest but has limited bearing on modern medical management, which depends on H. pylori status and NSAID exposure rather than acid-secretory subtype.[9][10]
| Type | Location | Acid output |
|---|---|---|
| I | Lesser curvature, gastric body | Normal or low |
| II | Gastric body ulcer with active or healed duodenal ulcer | Hypersecretory |
| III | Prepyloric | Hypersecretory |
| IV | Juxtacardial/subcardial (added later)[10] | — |
Forrest classification: endoscopic stigmata of hemorrhage
The Forrest classification grades bleeding peptic ulcers by endoscopic appearance. Each grade predicts rebleeding risk and directs the decision to perform endoscopic hemostasis. US endoscopists often use the descriptive terms (spurting, oozing, visible vessel, adherent clot, flat spot, clean base) interchangeably with the Forrest grades.[11][12]
| Forrest class | Endoscopic finding | Approximate rebleeding risk without endoscopic therapy | Endoscopic management |
|---|---|---|---|
| IA | Active spurting | ~55–90% | Endoscopic hemostasis required[3][11][12][4] |
| IB | Active oozing | ~30% | Endoscopic hemostasis recommended[3][13] |
| IIA | Non-bleeding visible vessel | ~43–50% | Endoscopic hemostasis required[3][11][12] |
| IIB | Adherent clot | ~22–33% | Attempt clot removal to unmask the underlying stigma, then treat accordingly. ACG and ESGE differ on routine endotherapy (see below).[3][14][4] |
| IIC | Flat pigmented spot | ~10% | No endoscopic therapy needed[3][12] |
| III | Clean base | ~5% | No endoscopic therapy needed[3][12] |
- High-risk stigmata (IA, IB, IIA) carry mortality of up to 11% and rebleeding rates above 40% if untreated.[12] The adherent clot (IIB) is also grouped with the high-risk lesions, whereas the flat pigmented spot (IIC) and clean base (III) are low risk.[15]
- Recurrent bleeding after successful hemostasis in a post hoc analysis of randomized trial data: 22.5% (IA), 17.7% (IIB), 11.3% (IIA), and 4.9% (IB).[3]
- Documentation: the ACG/AGA 2025 quality indicators state that the Forrest class should be recorded in the procedure report, because it dictates both the need for endotherapy and post-procedure PPI dosing.[3]
- ESGE 2026 update: introduces Forrest-stratified recommendations. These include over-the-scope clips as monotherapy for high-risk stigmata (IA/IB) and endoscopic therapy for adherent clots (IIB) when technically feasible.[14]
- Reproducibility: interobserver agreement for Forrest stigmata is low to moderate.[15]
Sakita–Miwa classification: gastric ulcer healing stage
This six-stage system tracks the endoscopic appearance of gastric ulcer healing over time. It remains in use in ESD and ulcer-healing research, but it has no direct implications for acute management.[5][6]
| Stage | Phase | Endoscopic findings |
|---|---|---|
| A1 | Active | Mucus-coated ulcer, marginal edema, no regenerating epithelium |
| A2 | Active | Mucus-coated ulcer with a discrete margin and less edema; a red halo and converging folds may appear |
| H1 | Healing | Regenerating epithelium covers less than 50% of the ulcer floor, with or without converging folds |
| H2 | Healing | Regenerating epithelium covers most of the ulcer floor |
| S1 | Scarring | Red scar with complete re-epithelialization and visible capillaries |
| S2 | Scarring | White scar with mature re-epithelialization |
Areas of uncertainty and guideline disagreement
- Adherent clot (Forrest IIB): management remains unsettled. ACG did not reach a recommendation on routine endotherapy. ESGE 2026 suggests clot removal with hemostasis when the endoscopist has adequate technical competence.[3][14][4]
- Interobserver variability: agreement is limited when distinguishing oozing from spurting, or an adherent clot from a visible vessel. This reduces the reproducibility of risk stratification.[15]
Clinical pearls and pitfalls
- Forrest IA, IB, and IIA require endoscopic hemostatic therapy. Forrest IIC and III do not, and treating them endoscopically is not indicated.[3][12][4]
- An adherent clot should prompt attempted removal to unmask the underlying stigma.[14][12]
- Failing to document the Forrest class compromises post-procedure PPI dosing decisions and communication of rebleeding risk.[3]
- Gastric ulcers require biopsy of the ulcer edge to exclude malignancy, regardless of Forrest class or Sakita–Miwa stage.[1]
- Johnson subtype does not dictate modern medical therapy. H. pylori and NSAID status are the actionable etiologic classifiers.[1][2]
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Vakil N (2024). "Peptic ulcer disease: a review". JAMA. 332 (21): 1832–1842. doi:10.1001/jama.2024.19094.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Malfertheiner P, Chan FK, McColl KE (2009). "Peptic ulcer disease". Lancet. 374 (9699): 1449–61. doi:10.1016/S0140-6736(09)60938-7.
- ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 Yadlapati R, Early D, Iyer PG; et al. (2025). "Quality indicators for upper GI endoscopy". Am J Gastroenterol. 120 (2): 290–312. doi:10.14309/ajg.0000000000003252.
- ↑ 4.0 4.1 4.2 4.3 4.4 Laine L, Barkun AN, Saltzman JR, Martel M, Leontiadis GI (2021). "ACG clinical guideline: upper gastrointestinal and ulcer bleeding". Am J Gastroenterol. 116 (5): 899–917. doi:10.14309/ajg.0000000000001245.
- ↑ 5.0 5.1 Miyake T, Suzaki T, Oishi M (1980). "Correlation of gastric ulcer healing features by endoscopy, stereoscopic microscopy, and histology, and a reclassification of the epithelial regenerative process". Dig Dis Sci. 25 (1): 8–14. doi:10.1007/BF01312726.
- ↑ 6.0 6.1 6.2 Komori H, Ueyama H, Nagahara A; et al. (2019). "A prospective randomized trial of a potassium competitive acid blocker vs proton pump inhibitors on the effect of ulcer healing after endoscopic submucosal dissection of gastric neoplasia". J Int Med Res. 47 (4): 1441–1452. doi:10.1177/0300060519828514.
- ↑ 7.0 7.1 Almadi MA, Lu Y, Alali AA, Barkun AN (2024). "Peptic ulcer disease". Lancet. 404 (10447): 68–81. doi:10.1016/S0140-6736(24)00155-7.
- ↑ 8.0 8.1 Sugimoto M, Kamada T, Ito M; et al. (2026). "Evidence-based clinical practice guidelines for peptic ulcer disease 2026". J Gastroenterol. 61 (10): 1361–1381. doi:10.1007/s00535-026-02504-3.
- ↑ Albillos A, Alvarez-Mon M, Rossi I; et al. (1990). "Different HCl and pepsinogen I secretion patterns in anatomically defined gastric ulcer subsets". Am J Gastroenterol. 85 (5): 535–8.
- ↑ 10.0 10.1 Csendes A, Braghetto I, Smok G (1987). "Type IV gastric ulcer: a new hypothesis". Surgery. 101 (3): 361–6.
- ↑ 11.0 11.1 11.2 Ghassemi KA, Jensen DM (2022). "Approach to the patient with gastrointestinal bleeding". Yamada's Textbook of Gastroenterology (7th ed.).
- ↑ 12.0 12.1 12.2 12.3 12.4 12.5 12.6 12.7 Yen AW, Leung JW (2022). "Endoscopic diagnosis and treatment of nonvariceal upper gastrointestinal hemorrhage". Yamada's Textbook of Gastroenterology (7th ed.).
- ↑ Lu MH, Chiang HC (2024). "Turn over the new leaf of the treatment in peptic ulcer bleeding: a review of the literature". Ther Adv Gastroenterol. 17: 17562848241275318. doi:10.1177/17562848241275318.
- ↑ 14.0 14.1 14.2 14.3 Gralnek IM, Morris J, Laursen SB; et al. (2026). "Endoscopic diagnosis and management of peptic ulcer bleeding: European Society of Gastrointestinal Endoscopy (ESGE) Guideline – Update 2026". Endoscopy. 58 (8): 899–924. doi:10.1055/a-2863-8314.
- ↑ 15.0 15.1 15.2 Gralnek IM, Barkun AN, Bardou M (2008). "Management of acute bleeding from a peptic ulcer". N Engl J Med. 359 (9): 928–37. doi:10.1056/NEJMra0706113.