Peptic ulcer overview
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Peptic ulcer Microchapters |
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Diagnosis |
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Treatment |
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Surgery |
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Case Studies |
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2017 ACG Guidelines for Peptic Ulcer Disease |
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Guidelines for the Indications to Test for, and to Treat, H. pylori Infection |
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Guidlines for factors that predict the successful eradication when treating H. pylori infection |
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Guidelines to document H. pylori antimicrobial resistance in the North America |
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Guidelines for evaluation and testing of H. pylori antibiotic resistance |
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Guidelines for when to test for treatment success after H. pylori eradication therapy |
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Guidelines for penicillin allergy in patients with H. pylori infection |
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Peptic ulcer overview On the Web |
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American Roentgen Ray Society Images of Peptic ulcer overview |
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 a defect in muscularis mucosa of gastrointestinal tract. Peptic ulcer is classified into 2 depending upon the location of ulcer, gastric ulcer and duodenal ulcer. The most common cause of peptic ulcer disease is H.pylori infection which is acquired in childhood but presents in adulthood. Other causes of peptic ulcer disease are chronic use of NSAID, family history of peptic ulcer disease. Persistant use of NSAIDS or chronic infection with H.Pylori results in inflammation of antral mucosa and ultimately causes the ulcer. The most common symptoms of peptic ulcer disease include episodic epigastric pain, heartburn, loss of appettite, gastroesophageal reflux, waterbrash, hematemesis and melena. Common physical examination findings of peptic ulcer disease include epigastric tenderness, tachycardia. Endoscopy is the gold standard test for the diagnosis of the peptic ulcer disease. Treatment of helicobacter pylori with antimicrobial agents is indicated for patients with gastric or duodenal ulceration. Pharmacologic therapies for peptic ulcer disease due to H. pylori is either triple or quadruple pharmacologic agents that include a Proton pump inhibitors plus a combination of antimicrobial agents.
Historical Perspective
Hundred years ago, Polish clinical researcher, professor W.Jaworski was the first to describe the spiral-shaped microorganism at Cracow Jagiellonian University but it was later confirmed in the animal by G.Bizzazero. Asklepios was the first to describe an association between GI bleeding and peptic ulcer disease. In 1982 Warren and B.J marshall cultured the organism and found a strong association between Helicobacter pylori and inflammation of gastric mucosa, not due to spicy food and stress and were awarded the noble prize.
Classification
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]
Pathophysiology
Peptic ulcer disease develops when aggressive luminal factors (acid, pepsin, bile) overwhelm the gastroduodenal mucosal barrier. That barrier depends on tight epithelial junctions, an adherent mucus layer, bicarbonate secretion, and prostaglandin-maintained mucosal blood flow.[7][8] Helicobacter pylori causes chronic active gastritis, and the anatomic pattern of that gastritis determines the ulcer type. Antral-predominant gastritis produces hypergastrinemia and acid hypersecretion, which leads to duodenal ulcer. Pangastritis produces hypochlorhydria and gastric ulcer, along with a risk of atrophy and gastric cancer.[9] NSAIDs and aspirin injure the mucosa through COX-1-mediated prostaglandin depletion and through direct topical toxicity. NSAID-associated ulcers are often painless until bleeding or perforation occurs.[10][11] In critical illness, stress-related mucosal injury results from mucosal hypoperfusion, independent of H. pylori or NSAID exposure.[1] H. pylori and NSAIDs act synergistically, so the combination carries greater risk of ulceration and bleeding than either factor alone.[7]
Causes
Peptic ulcer disease (PUD) results from an imbalance between mucosal defense and aggressive factors such as gastric acid, pepsin, and exogenous injury.[7]
The principal causes are:
- Helicobacter pylori infection, about 42% of cases.
- Aspirin or NSAID use, about 36% of cases.
- Idiopathic ulcers, unrelated to either, about 22% of cases.[1]
H. pylori and NSAIDs independently increase ulcer risk and act synergistically. PUD is rare when neither is present.[12]
Less common causes include:
- Stress-related mucosal disease in critical illness.[13]
- Zollinger-Ellison syndrome.
- Malignancy.[14]
- Rare inflammatory, infectious, and anatomic causes.[15]
Differentiating Peptic ulcer overview from Other Diseases
Peptic ulcer disease must be differentiated from other causes of acute upper gastrointestinal bleeding such as esophageal varices, Mallory-Weiss syndrome, gastrointestinal cancer, arteriovenous malformations, esophagitis, and esophageal ulcer. Peptic ulcer disease must also be differentiated from gastroesophageal reflux disease (GERD,pancreatitis, Zollinger-Ellison Syndrome, Cholelithiasis, gastric outlet syndrome, myocardial infarction ,pleural empyema and appendicitis.
Epidemiology and Demographics
Global age-standardized incidence, prevalence, and mortality of peptic ulcer disease (PUD) fell by 40.3%, 41.1%, and 61.5%, respectively, between 1990 and 2021.[16] Absolute case numbers continued to rise because of population growth and aging.[17] Men carry a higher burden than women across most age groups.[16] In the United States, PUD-related mortality fell sharply from 2001 to 2012, plateaued, and then rose from 2018 to 2020.[18] US racial and ethnic disparities largely track Helicobacter pylori exposure, which is highest in non-Hispanic Black and Hispanic individuals and in immigrants from endemic regions.[19][20]
Risk Factors
The two dominant, largely modifiable risk factors for peptic ulcer disease (PUD) are Helicobacter pylori infection and use of aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs). Together they account for roughly 70% to 78% of cases.[1][8] These two exposures interact synergistically, so combined exposure raises ulcer bleeding risk more than either alone.[21][2] In NSAID users, the strongest predictor of a future ulcer complication is a prior ulcer complication. Concomitant corticosteroids, anticoagulants, antiplatelet agents, or SSRIs and older age further amplify risk.[2][8] Additional independent associations include cigarette smoking, alcohol use, male sex, diabetes mellitus, and cardiovascular disease.[22] The proportion of idiopathic ulcers (negative for both H. pylori and NSAIDs) is rising as H. pylori prevalence declines.[1][8]
Screening
There is no role for universal, population-based screening for peptic ulcer disease (PUD), including routine endoscopic screening, in asymptomatic average-risk adults.[7] Instead, PUD prevention relies on targeted, risk-based testing for Helicobacter pylori (with treatment of all positive results) and on ulcer-risk assessment before starting chronic NSAID or low-dose aspirin therapy.[19][21] The 2024 American College of Gastroenterology (ACG) guideline and the 2018 Houston Consensus Conference define the populations in whom H. pylori testing is indicated, using non-invasive urea breath testing or stool antigen testing.[19][23] Population-wide H. pylori screen-and-treat programs are endorsed only in regions with high gastric cancer incidence.[24]
Natural History, Complications, and Prognosis
Natural History
The infection of Helicobacter pylori, a common cause of peptic ulcer disease is acquired usually during the childhood but presents in second to the fifth decade of life.Patient presents with episodic epigastric pain, indigestion, bloating, hematemesis and melena. Peptic ulcers tend to come back if untreated.
Complications
Peptic ulcer disease if not treated, the patient can develop complications like bleeding, perforation, obstruction, stricture.Chronic infection of Helicobacter pylori leads to gastric cancer, MALT lymphoma, Iron deficiency anemia, Idiopathic thrombocytopenic purpura.
Prognosis
Prognosis is good if the eradication therapy of Helicobacter pylori is taken. The recurrence rate of patients with peptic ulcer disease is less than 20%.
Diagnosis
Diagnostic Study of choice
Endoscopy is the gold standard test for the diagnosis of the peptic ulcer disease.
History and Symptoms
The hallmark of peptic ulcer disease is an episodic epigastric pain which cause awakening at night.A positive history of epigastric pain, use of drugs like NSAIDs including aspirin which inhibit cyclooxygenase, use of antiplatelets, steroids and family history of peptic ulcer disease is suggestive of peptic ulcer disease. The most common symptoms of peptic ulcer disease include episodic epigastric pain, heartburn, loss of appettite, gastroesophageal reflux, waterbrash, hematemesis and melena. Less common symptoms of peptic ulcer disease include intolerance to fatty food.
Physical Examination
Peptic ulcer disease patient appears in severe stress due to abdominal pain. Common physical examination findings of peptic ulcer disease include epigastric tenderness, tachycardia.Perforated peptic ulcer disease patient presents with classic triad of severe epigastric tenderness, tachycardia and abdominal rigidity. Clinical signs of perforated peptic ulcer comes in 3 stages: In the initial stage within first 2 hours, the patient presents with tachycardia, epigastric pain and cool extremities. In next 2 to 12 hours, the patient presents with lower right quadrant tenderness and abdominal rigidity. In more than 12 hours, the patient presents with abdominal distension, hypotension, and pyrexia with acute circulatory collapse.
Laboratory Findings
There is no specific diagnostic laboratory test for peptic ulcer disease but in the patient with the history of peptic ulcer disease, the laboratory test is used to rule out bleeding and to document the status of eradication therapy and to test refractory ulcers.
Imaging Findings
If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal tract (which always contains some air) to the peritoneal cavity (which normally never contains air). This leads to "free gas" within the peritoneal cavity. If the patient stands erect, as when having a chest X-ray, the gas will float to a position underneath the diaphragm. Therefore, gas in the peritoneal cavity, shown on an erect chest X-ray or supine lateral abdominal X-ray, is an omen of perforated peptic ulcer disease. An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as a gastroscopy, is carried out on patients in whom a peptic ulcer is suspected. By direct visual identification, the location and severity of an ulcer can be described. Moreover, if no ulcer is present, EGD can often provide an alternative diagnosis.
Other diagnostic studies
Testing of H.pylori infection is very important for treating ulcers. H.pylori tested by 2 methods : invasive and non-invasive. Rapid urease testing is invasive test which is used as diagnostic study of choice. Stool monoclonal antigen test is one of the non-invasive test which is used to diagnose active infection.
Treatment
Medical Therapy
The mainstay of treatment for peptic ulcer disease is pharmacotherapy. All patients with a gastric or duodenal peptic ulcer should be evaluated for Helicobacter pylori infection and for nonsteroidal anti-inflammatory drug (NSAID) or aspirin use, as these represent the two dominant etiologies. Treatment of H. pylori with antimicrobial agents is indicated for all patients with active gastric or duodenal ulceration who test positive for the infection.
The pharmacologic approach to H. pylori-associated PUD involves a combination of a proton pump inhibitor (PPI) or potassium-competitive acid blocker (PCAB) plus two or three antimicrobial agents. The 2024 American College of Gastroenterology (ACG) Clinical Guideline substantially revised first-line eradication strategy: standard PPI–clarithromycin triple therapy is no longer recommended empirically, given rising resistance rates to clarithromycin and levofloxacin in North America. Optimized bismuth quadruple therapy (BQT) is now the recommended first-line regimen; rifabutin-based triple therapy and vonoprazan-based regimens are endorsed as alternatives.[19] After treatment, confirmation of eradication is mandatory using a urea breath test or monoclonal fecal antigen test at least 4 weeks after completing antibiotics and at least 2 weeks after stopping all acid-suppressive therapy. If the patient remains infected, the regimen is planned according to prior antibiotic exposure, documented resistance, and remaining treatment options.
For non-H. pylori, non-NSAID (idiopathic) ulcers, long-term acid suppression is the foundation of therapy. The use of antimicrobial therapy is discouraged among asymptomatic H. pylori carriers without an established indication.
Endoscopic Management
The cornerstone of endoscopic risk stratification in peptic ulcer bleeding is the Forrest classification, first described in 1974, which categorizes ulcer stigmata and guides decisions regarding the need for endoscopic hemostasis. Pre-endoscopic risk stratification using validated scoring systems — most importantly the Glasgow-Blatchford Score (GBS) — allows identification of very-low-risk patients who may be safely managed as outpatients, as well as high-risk patients who require urgent inpatient endoscopy and intervention.[4][25]
Surgical Management
Surgery for peptic ulcer is principally indicated for the management of life-threatening complications, including upper gastrointestinal bleeding, perforation, and gastric outlet obstruction, as well as for ulcers that are refractory to maximal medical therapy or carry concern for underlying malignancy. Peptic ulcer disease has a lifetime prevalence in the general population of 5–10% and an annual incidence of 0.1–0.3%; despite a marked decline over the past three decades attributable to the discovery of Helicobacter pylori and the widespread use of proton pump inhibitors (PPIs), complications still arise in 10–20% of affected patients.[26]
Bleeding ulcers are treated first with endoscopic therapy; surgery is reserved for cases of failure or recurrence after endoscopic and angiographic management. Perforated peptic ulcer is a surgical emergency; immediate repair—preferentially by laparoscopic approach in haemodynamically stable patients—is the standard of care. Elective acid-reducing surgery (e.g., vagotomy and drainage) has been largely supplanted by modern pharmacotherapy, including optimized bismuth quadruple therapy and potassium-competitive acid blocker (vonoprazan)-based regimens for Helicobacter pylori eradication.[27]
Prevention
Primary prevention of PUD focuses on: (1) identification and eradication of H. pylori infection before ulcer development; (2) gastroprotective co-therapy or substitution of safer drug classes in patients requiring NSAIDs or low-dose aspirin; (3) modification of lifestyle risk factors, including smoking cessation and reduction of excessive alcohol intake; and (4) stress ulcer prophylaxis in high-risk critically ill patients.
References
- ↑ 1.0 1.1 1.2 1.3 1.4 Vakil N (2024). "Peptic ulcer disease: a review". JAMA. 332 (21): 1832–1842. doi:10.1001/jama.2024.19094. PMID 39466269 Check
|pmid=value (help). - ↑ 2.0 2.1 2.2 Malfertheiner P, Chan FK, McColl KE (2009). "Peptic ulcer disease". Lancet. 374 (9699): 1449–61. doi:10.1016/S0140-6736(09)60938-7. PMID 19683340.
- ↑ 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 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. PMID 33929377 Check
|pmid=value (help). - ↑ 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.
- ↑ 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 7.2 7.3 Lanas A, Chan FKL (2017). "Peptic ulcer disease". Lancet. 390 (10094): 613–624. doi:10.1016/S0140-6736(16)32404-7. PMID 28242110.
- ↑ 8.0 8.1 8.2 8.3 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.
- ↑ Crowe SE (2019). "Helicobacter pylori infection". N Engl J Med.
- ↑ Bjarnason I, Scarpignato C, Holmgren E; et al. (2018). "Mechanisms of damage to the gastrointestinal tract from nonsteroidal anti-inflammatory drugs". Gastroenterology.
- ↑ Wolfe MM, Lichtenstein DR, Singh G (1999). "Gastrointestinal toxicity of nonsteroidal antiinflammatory drugs". N Engl J Med.
- ↑ Huang JQ, Sridhar S, Hunt RH (2002). "Role of Helicobacter pylori infection and non-steroidal anti-inflammatory drugs in peptic-ulcer disease: a meta-analysis". Lancet. 359 (9300): 14–22.
- ↑ Bardou M, Quenot JP, Barkun A (2015). "Stress-related mucosal disease in the critically ill patient". Nat Rev Gastroenterol Hepatol. 12 (2): 98–107. doi:10.1038/nrgastro.2014.235. PMID 25560847.
- ↑ Kim HU (2015). "Diagnostic and treatment approaches for refractory peptic ulcers". Clin Endosc. 48 (4): 285–290. PMID 26240800.
- ↑ McColl KE (2009). "How I manage H. pylori-negative, NSAID/aspirin-negative peptic ulcers". Am J Gastroenterol. 104 (1): 190–193.
- ↑ 16.0 16.1 Hao W, Zheng C, Wang Z, Ma H (2025). "Global burden and risk factors of peptic ulcer disease between 1990 and 2021: an analysis from the global burden of disease study 2021". PLoS One. 20 (7): e0325821. doi:10.1371/journal.pone.0325821. PMC 12250541 Check
|pmc=value (help). - ↑ Xie X, Ren K, Zhou Z, Dang C, Zhang H (2022). "The global, regional and national burden of peptic ulcer disease from 1990 to 2019: a population-based study". BMC Gastroenterol. 22 (1): 58. doi:10.1186/s12876-022-02130-2. PMC 8832644 Check
|pmc=value (help). - ↑ Babar M, Raza M, Nadir MA; et al. (2025). "Trends and disparities in peptic ulcer disease-related mortality in the United States from 1999 to 2020: a cross-sectional study". Medicine (Baltimore). 104 (40): e42129. doi:10.1097/MD.0000000000042129. PMC 12499665 Check
|pmc=value (help). - ↑ 19.0 19.1 19.2 19.3 Chey WD, Howden CW, Moss SF; et al. (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). - ↑ Shah SC, Halvorson AE, Lee D; et al. (2024). "Helicobacter pylori burden in the United States according to individual demographics and geography: a nationwide analysis of the Veterans Healthcare System". Clin Gastroenterol Hepatol. 22 (1): 42–50.e26. doi:10.1016/j.cgh.2023.05.016. PMC 11552088 Check
|pmc=value (help). PMID 37245717 Check|pmid=value (help). - ↑ 21.0 21.1 Lanza FL, Chan FK, Quigley EM; Practice Parameters Committee of the American College of Gastroenterology (2009). "Guidelines for prevention of NSAID-related ulcer complications". Am J Gastroenterol. 104 (3): 728–38. doi:10.1038/ajg.2009.115. PMID 19240698.
- ↑ Tahery, et al. Case-control study of risk factors for peptic ulcer disease. BMC Gastroenterology. 2026.
- ↑ El-Serag HB, Kao JY, Kanwal F; et al. (2018). "Houston Consensus Conference on Testing for Helicobacter pylori Infection in the United States". Clin Gastroenterol Hepatol. 16 (7): 992–1002.e6. doi:10.1016/j.cgh.2018.03.013. PMID 29559361.
- ↑ Liou JM, Malfertheiner P, Lee YC; et al. (2020). "Screening and eradication of Helicobacter pylori for gastric cancer prevention: the Taipei global consensus". Gut. 69 (12): 2093–2112. doi:10.1136/gutjnl-2020-322368. PMID 33004546 Check
|pmid=value (help). - ↑ Gralnek IM, Stanley AJ, Morris AJ, Camus M, Lau J, Lanas A, Laursen SB, Radaelli F, Papanikolaou IS, Cúrdia Gonçalves T, Dinis-Ribeiro M, Awadie H, Braun G, de Groot N, Udd M, Sanchez-Yague A, Neeman Z, van Hooft JE (2021). "Endoscopic diagnosis and management of nonvariceal upper gastrointestinal hemorrhage (NVUGIH): European Society of Gastrointestinal Endoscopy (ESGE) Guideline – Update 2021". Endoscopy. 53 (3): 300–332. doi:10.1055/a-1369-5274. PMID 33567467 Check
|pmid=value (help). - ↑ Tarasconi A, Coccolini F, Biffl WL, Tomasoni M, Ansaloni L, Picetti E, Molfino S, Shelat V, Cimbanassi S, Weber DG, Abu-Zidan FM, Campanile FC, Di Saverio S, Baiocchi GL, Casella C, Kelly MD, Kirkpatrick AW, Leppaniemi A, Moore EE, Peitzman A, Pereira Fraga G, Ceresoli M, Maier RV, Wani I, Pattonieri V, Perrone G, Velmahos G, Sugrue M, Sartelli M, Kluger Y, Catena F (2020). "Perforated and bleeding peptic ulcer: WSES guidelines". World J Emerg Surg. 15 (1): 3. doi:10.1186/s13017-019-0283-9. PMID 31903027.
- ↑ Masoudpour H, Wassef J, Saladziute S, Sherman J (2025 Feb). "Surgical Therapy of Gastric Ulcer Disease". Surg Clin North Am. 105 (1): 173–186. doi:10.1016/j.suc.2024.06.013. PMID 39523072 Check
|pmid=value (help). Check date values in:|date=(help)