Gastritis overview
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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
Gastritis is a histologic diagnosis of inflammation of the gastric mucosa, defined by a significant inflammatory infiltrate. It is distinct from gastropathy, in which epithelial injury occurs with little or no inflammation, as in chemical (reactive) injury from NSAIDs or bile. The term "gastritis" was first used in 1728 by the German physician Georg Ernst Stahl. The discovery of Helicobacter pylori by Robin Warren and Barry Marshall in 1982 led to the modern understanding and classification of the gastritides. The Sydney System was introduced in 1990 and updated at the 1994 Houston workshop. The OLGA (Operative Link on Gastritis Assessment) staging system followed in 2005.
Chronic gastritis is classified along three complementary axes. The updated Sydney System provides the histologic classification by topography, morphology, and etiology. OLGA/OLGIM staging converts the severity and topography of atrophy and intestinal metaplasia into stages 0–IV of gastric cancer risk. Endoscopic classifications (Kyoto score, Kimura–Takemoto, and EGGIM) predict H. pylori status and cancer risk in real time and guide, but do not replace, biopsy sampling. Among the atrophic forms, H. pylori–associated gastritis is antral-predominant or multifocal, whereas autoimmune gastritis (AIG) is corpus-restricted.
Most clinically important gastritis arises from three mechanisms: H. pylori infection, the leading cause worldwide and the main driver of the inflammation-to-cancer sequence; AIG, a T cell–mediated destruction of corpus parietal cells; and reactive (chemical) gastropathy from NSAIDs, aspirin, bile reflux, and alcohol. Clinical outcome depends mainly on where inflammation sits in the stomach and how it alters gastric acid secretion. Chronic inflammation involving the corpus drives the Correa cascade of atrophy, intestinal metaplasia, dysplasia, and intestinal-type gastric adenocarcinoma. Less common causes include lymphocytic, eosinophilic, granulomatous, and collagenous gastritis; non–H. pylori infections, mainly in immunocompromised hosts; and radiation, caustic, and ischemic injury. Gastritis must be differentiated from peptic ulcer disease, gastroesophageal reflux disease (GERD), gastroenteritis, Crohn's disease, gastrinoma, gastric adenocarcinoma, and primary gastric lymphoma.
The epidemiology of gastritis is best described by etiologic subtype. Global adult H. pylori prevalence fell from 52.6% before 1990 to 43.9% in 2015–2022, but prevalence in children and adolescents (~35%) has not declined. In the United States, H. pylori positivity is falling overall but remains disproportionately high in non-Hispanic Black and Hispanic individuals. Chronic atrophic gastritis affects ~5% of people in low–gastric-cancer-incidence populations and up to ~50% in high-incidence populations. AIG has a pooled global prevalence of ~3.9%, with a female predominance and overlap with other autoimmune diseases. Eosinophilic gastritis is rare, at ~6.3 per 100,000 in the US. The dominant risk factors are chronic H. pylori infection and autoimmunity. NSAIDs, aspirin, critical illness, bile reflux, and heavy alcohol use mainly cause reactive or erosive gastropathy. Cigarette smoking, a high-salt diet, increasing age, male sex, and a family history of gastric cancer act as cofactors for progression toward atrophy, intestinal metaplasia, and cancer. There is insufficient evidence to recommend routine screening for gastritis.
Gastritis usually persists throughout life, and spontaneous remission is rare. Complications include peptic ulcers, gastrointestinal bleeding, gastrointestinal perforation, gastric polyps, anemia, vitamin B12 deficiency, pernicious anemia, gastric outlet obstruction, and stomach cancer. Prognosis depends on the type and cause of gastritis. Reactive gastritis improves once offending agents are removed. AIG carries an increased risk of carcinoid tumors and gastric adenocarcinoma. Untreated H. pylori–associated gastritis may progress to peptic ulcer disease, adenocarcinoma, and MALT lymphoma.
Most patients with gastritis are asymptomatic, and dyspeptic symptoms correlate poorly with histologic findings. When present, symptoms include epigastric pain, dyspepsia, nausea, vomiting, bloating, early satiety, and, with bleeding, hematemesis or melena. Physical examination is often normal but may show pallor, epigastric tenderness, or tachycardia with bleeding. H. pylori can be detected by endoscopic biopsy-based tests (histology, rapid urease testing, culture, and PCR) or by nonendoscopic tests (urea breath test, fecal antigen test, and serology). CT may show gastric wall edema or a halo sign, and an upper gastrointestinal series may help exclude ulcers.
Treatment is directed by etiology. Offending agents such as NSAIDs and alcohol should be discontinued, and proton pump inhibitors should be prescribed only for a valid indication and deprescribed promptly. For H. pylori gastritis, the 2024 American College of Gastroenterology guideline and the 2022 Maastricht VI/Florence consensus recommend optimized bismuth quadruple therapy as the preferred empiric first-line regimen. Vonoprazan-based and rifabutin-based regimens are alternatives, and clarithromycin-based triple therapy is no longer recommended empirically. All regimens are given for 14 days, followed by a test of cure. AIG requires lifelong vitamin B12 and iron replacement with endoscopic surveillance. Other subtypes have specific therapies, such as dietary elimination and corticosteroids for eosinophilic gastritis and IV ganciclovir for CMV gastritis. Surgery is reserved for rare, life-threatening complications, including phlegmonous gastritis, emphysematous gastritis with necrosis, refractory postgastrectomy bile reflux gastritis, and uncontrolled stress-related hemorrhage. Prevention focuses on avoiding NSAIDs, alcohol, and smoking, on good hygiene to limit H. pylori transmission, and on confirming eradication after treatment.
Historical Perspective
In 1728, a German physician named Georg Ernst Stahl first used the term "gastritis" to describe inflammation of the inner lining of the stomach. In 1982, Robin Warren and Barry Marshall discovered Helicobacter pylori which further led to the identification and classification of different gastritides. in 1990, A New Classification of Gastritis called the Sydney System was presented to the World Congress of Gastroenterology in Sydney and was later published as six papers in the Journal of gastroenterology and hepatology. In 1994, at the international workshop on the histopathology of gastritis held at Houston, The updated Sydney System for the classification and grading of gastritis was introduced. In 2005, gastritis staging using the OLGA (Operative Link on Gastritis Assessment) staging system for reporting gastric histology was introduced.
Classification
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]
Pathophysiology
Most clinically important gastritis arises from three mechanisms: Helicobacter pylori–associated gastritis, autoimmune gastritis (AIG), and reactive (chemical) gastropathy. H. pylori is the most common cause worldwide and the main driver of the inflammation-to-cancer sequence. AIG is T cell–mediated destruction of corpus parietal cells, producing atrophy confined to the corpus. Reactive gastropathy is non-immune epithelial injury from NSAIDs, bile reflux, and alcohol, usually with little true inflammation. Clinical outcome depends mainly on where the inflammation sits in the stomach and how it changes gastric acid secretion, not simply on whether the organism is present.[9] Chronic inflammation involving the corpus drives the Correa cascade: atrophy, then intestinal metaplasia, then dysplasia, then intestinal-type gastric adenocarcinoma. Histologic staging of this cascade with OLGA/OLGIM identifies patients at high cancer risk.[10][11]
Causes
Gastritis is gastric mucosal injury accompanied by a significant inflammatory infiltrate. Gastropathy is epithelial or mucosal injury with little or no inflammation, as seen in chemical (reactive) injury from NSAIDs or bile.[8] Current classification is based on cause, as set out in the Kyoto Global Consensus and the Real-World Gastritis Initiative (RE.GA.IN.).[12][13]
- Helicobacter pylori infection is the leading cause of chronic gastritis worldwide.
- Autoimmune gastritis is the main non-infectious cause of corpus-restricted atrophic gastritis.
- Reactive (chemical) gastropathy from NSAIDs, aspirin, or bile reflux is the most frequent diagnosis where H. pylori is uncommon.
Less common causes include:
- Lymphocytic, eosinophilic, granulomatous, and collagenous gastritis
- Non–H. pylori infections, mainly in immunocompromised hosts
- Radiation, caustic, and ischemic injury
Differentiating Gastritis overview from Other Diseases
Gastritis must be differentiated from peptic ulcer disease, gastric cancer, gastroesophageal reflux disease (GERD), gastroenteritis, crohn's disease, gastrinoma, gastric adenocarcinoma and primary gastric lymphoma.
Epidemiology and Demographics
The epidemiology of gastritis is best described by etiologic subtype rather than by the older acute vs chronic division, which does not track with cause, demographics, or cancer risk. Helicobacter pylori–associated gastritis is the dominant entity worldwide. Nearly all chronically infected individuals have histologic chronic active gastritis.[14] Global adult H. pylori prevalence fell from 52.6% before 1990 to 43.9% in 2015–2022, but prevalence in children and adolescents (~35%) has not declined in any WHO region.[15] In the United States, H. pylori positivity is falling overall, but it remains disproportionately high in non-Hispanic Black and Hispanic individuals, and the racial gap has widened.[16]
Chronic atrophic gastritis (CAG) is the shared pre-neoplastic phenotype of long-standing H. pylori infection and autoimmune gastritis (AIG). Its prevalence ranges from ~5% in low–gastric-cancer-incidence populations to ~50% in high-incidence populations.[7] AIG has a pooled global prevalence of ~3.9%, with a female predominance and strong overlap with other autoimmune diseases.[17] Eosinophilic gastritis (EoG) is rare, at ~6.3 per 100,000 in the US. It is more common in females and young children and is frequently underdiagnosed.[18]
Risk Factors
Gastritis is best stratified by etiology rather than by symptom-based lists, because etiology determines cancer risk, surveillance, and treatment.[13] The two dominant, clinically decisive risk factors are chronic Helicobacter pylori infection and autoimmunity.[7] NSAIDs and aspirin, critical illness, bile reflux, and heavy alcohol use mainly produce reactive (chemical) or erosive gastropathy, an epithelial injury pattern with minimal inflammation.[19][8] Cigarette smoking, high-salt diet, increasing age, male sex, and family history of gastric cancer act mainly as cofactors that promote progression of chronic gastritis toward atrophy, intestinal metaplasia, and cancer.[20][21]
Screening
There is insufficient evidence to recommend routine screening for gastritis.
Natural History, Complications, and Prognosis
Natural History
Gastritis is a common inflammatory disease. Gastritis usually persists throughout life and the chance of spontaneous remission is rare. Gastritis is most commonly associated with Helicobacter pylori infection. The gastric mucosa undergoes inflammatory changes which may finally lead to atrophic gastritis. Chronic gastritis is commonly observed as a manifestation of progression of many gastric conditions. Gastric secretory functions are usually impaired due to inflammation and atrophy of the gastric mucosa. Increase in the prevalence of gastritis is attributed to the increasing age and the onset varies among different ethnicities. The increased risk of developing duodenal and peptic ulcers have been observed in individuals with persistent gastritis. Biopsies and routine evaluations may help predict the progression of gastritis to the conditions such as the peptic ulcer disease.
Complications
Complications of gastritis may include, peptic ulcers, gastrointestinal perforation, gastrointestinal bleeding, gastric polyp, anemia due to erosive gastritis, vitamin B12 deficiency, pernicious anemia, gastric outlet obstruction, increased risk of developing benign or malignant growths in the lining of the stomach which may lead to stomach cancer.
Prognosis
Prognosis for gastritis is majorly dependent upon the type of gastritis and etiological factors. In acute gastritis, the condition improves upon refraining from risk factors such as NSAIDs, alcohol, cigarette smoking, acidic food, and beverages. In autoimmune gastritis, prognosis for vitamin B12 deficiency when treated with cyanocobalamin therapy is good. Although in autoimmune gastritis, there is an increased risk for carcinoid tumors and gastric adenocarcinoma. In chronic gastritis associated with Helicobacter pylori infection, the prognosis is good. The triple therapy regimen may not be as effective when compared to quadruple bismuth-based regimen which has proven to be very effective comparatively. Helicobacter pylori infection associated chronic gastritis, if left untreated may progress to develop peptic ulcer disease, adenocarcinoma and MALT lymphoma.
Diagnosis
History and Symptoms
It is important to reviews a patient's history regarding medications, alcohol intake, smoking, and other risk factors that may be associated with gastritis.. Symptoms of gastritis may be silent or manifest as abdominal discomfort, nausea, vomiting, and/or gastrointestinal bleeding. Individuals with gastritis experience abdominal pain and gastric disturbances. Symptoms as a result of gastritis are upper abdominal pain or discomfort, dyspepsia (indigestion), nausea, vomiting of blood or dark brown/coffee-ground like vomitus, bloating sensation in the upper abdomen, belching, heartburn, loss of appetite, malena (dark stools), gastric hemorrhage, fever, lethargy, halitosis, epigastric pain or abdominal pain, early satiety, fatigue and diarrhea.
Physical Examination
Patients with gastritis may appear pale. Some patients may appear fatigued and in distress if associated with abdominal pain. Vital signs generally appear to be normal. If associated with gastrointestinal bleed, vital signs include tachycardia. Pallor may observed in patients presenting with melena and hematemesis. On examination of the eyes, conjunctival pallor may be observed. Halitosis may be observed in case of chronic gastritis. Chest tenderness may be present on palpation in case of Helicobacter pylori infection associated gastritis. Abdominal pain or discomfort may be observed. Epigastric tenderness may be present. Gastritis associated with gastric ulcers may result in blood loss and the stool test may be guaiac-positive.
Diagnostic Tests
Endoscopic diagnostic tests are biopsy-based diagnostic methods for gastritis associated with H. pylori infection. These include histology, rapid urease testing, culture and polymerase chain reaction (PCR).
The nonendoscopic diagnostic testing methods for gastritis associated with H. pylori include antibody tests, urea breath test, and fecal antigen test.
Imaging Findings
CT scan
CT scan may be helpful in the diagnosis of gastritis. Findings on CT scan suggestive of gastritis include gastric wall edema and halo sign.
X- ray
An x-ray may be helpful in the diagnosis of gastritis. Series of x-rays of the esophagus, stomach and duodenum known as the upper gastrointestinal series or barium swallow aid in determining the condition. In barium swallow procedure, the patient is made to ingest a white liquid which contains barium. The ingested barium liquid lines the gastrointestinal tract and helps in visualizing the ulcers better when the x-ray is taken.
Other Diagnostic Studies
In Helicobacter pylori infection which is the most common cause of gastritis, a non-invasive test such as the urea breath test is used to determine the presence of H. pylori in the stomach.
Treatment
Medical Therapy
Gastritis encompasses a heterogeneous group of conditions, and treatment is directed by the underlying etiology. Offending agents (particularly NSAIDs and alcohol) should be discontinued. Proton pump inhibitors (PPIs) form the backbone of acid suppression across most subtypes but should be prescribed only when a valid indication exists and deprescribed promptly thereafter.
For Helicobacter pylori gastritis — the most common form worldwide — the 2024 American College of Gastroenterology (ACG) guideline and the 2022 Maastricht VI/Florence Consensus Report establish optimized bismuth quadruple therapy (BQT) as the preferred empiric first-line regimen, replacing clarithromycin-based triple therapy which is no longer recommended empirically due to rising global resistance rates. Vonoprazan-based dual or triple therapy and rifabutin-based triple therapy are recognized alternative first-line regimens. All eradication regimens must be given for 14 days, followed by mandatory test of cure.[14][22]
For other subtypes: autoimmune gastritis requires lifelong parenteral vitamin B12 and iron replacement, with endoscopic surveillance for gastric cancer and neuroendocrine tumors; NSAID-associated gastropathy is managed with risk-stratified PPI co-therapy or COX-2 selective inhibitors; stress-related mucosal disease in the ICU is treated with PPI or H2RA while qualifying risk factors persist, then discontinued at ICU discharge per the 2024 SCCM/ASHP guideline; eosinophilic gastritis is treated with dietary elimination and corticosteroids, with dupilumab as an emerging option; CMV gastritis requires IV ganciclovir in immunocompromised hosts; and bile reflux gastropathy is managed with ursodeoxycholic acid and sucralfate. Rational PPI deprescribing and gastroprotection in patients on antiplatelet or anticoagulant therapy must also be kept in consideration.
Surgery
Surgery is reserved for rare, life-threatening complications of gastritis that have failed or are not amenable to medical management. The principal surgical indications are: (1) phlegmonous gastritis with refractory sepsis, gastric gangrene, or perforation; (2) emphysematous gastritis with gastric ischemia or necrosis confirmed on imaging or endoscopy; (3) symptomatic postgastrectomy bile reflux gastritis refractory to maximal medical therapy; and (4) upper gastrointestinal hemorrhage from stress-related mucosal disease that is not controlled by endoscopic or interventional radiologic means. Understanding the specific surgical indications, procedural options, and postoperative considerations is essential for optimal patient outcomes in these uncommon but critically ill presentations.
Primary Prevention
Effective measures for the primary prevention of gastritis include avoiding long term or extended use of medications such as NSAIDs, abstenance from alcohol, cessation of cigarette smoking, coffee or acidic beverages, spicy foods and avoiding stress. Inculcating healthy eating habits, exercising regularly and maintaining healthy body weight may help in avoiding gastritis. Effective measures for primary prevention of the H. pylori infection include hand washing (antibacterial soaps), avoid contaminated food and water, maintain proper hygiene (hand sanitizers, antiseptic washes) and avoid close contact with infected family members ( e.g., kissing, by sharing eating utensils and drinking glasses).
Secondary Prevention
The secondary prevention strategies for gastritis following H. pylori infection to prevent recurrence of peptic ulcer disease and gastric cancer include the use of antibiotics to prevent recurrence of infection and the post treatment confirmation of H. pylori eradication after treatment using diagnostic tests.
References
- ↑ 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.
- ↑ 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). - ↑ 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.
- ↑ 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.
- ↑ 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). - ↑ 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 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 Washington MK, Peek RM (2022). "Gastritis and gastropathy". Yamada's Textbook of Gastroenterology (7th ed.).
- ↑ Malfertheiner P, Camargo MC, El-Omar E; 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). - ↑ Sundar R, Nakayama I, Markar SR, Shitara K, van Laarhoven HWM; et al. (2025). "Gastric cancer". Lancet. doi:10.1016/S0140-6736(25)00052-2.
- ↑ Rugge M, Sugano K, Scarpignato C; et al. (2019). "Gastric cancer prevention targeted on risk assessment: Gastritis OLGA staging". Helicobacter. 24 (2): e12571. doi:10.1111/hel.12571. PMID 30773732.
- ↑ Sugano K, Tack J, Kuipers EJ; et al. (2015). "Kyoto global consensus report on Helicobacter pylori gastritis". Gut. 64 (9): 1353–67. doi:10.1136/gutjnl-2015-309252. PMID 26187502.
- ↑ 13.0 13.1 Rugge M, Genta RM, Malfertheiner P; 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). - ↑ 14.0 14.1 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). - ↑ Chen YC, Malfertheiner P, Yu HT, Kuo CL, Chang YY, Meng FT, Wu YX, Hsiao JL, Chen MJ, Lin KP, Wu CY, Lin JT, O'Morain C, Megraud F, Lee WC, El-Omar EM, Wu MS, Liou JM (2024). "Global prevalence of Helicobacter pylori infection and incidence of gastric cancer between 1980 and 2022". Gastroenterology. 166 (4): 605–619. doi:10.1053/j.gastro.2023.12.022. PMID 38176660 Check
|pmid=value (help). - ↑ Shah SC, Halvorson AE, Lee D, Bustamante R, McBay B, Gupta R, Denton J, Dorn C, Wilson O, Peek R Jr, Gupta S, Liu L, Hung A, Greevy R, Roumie CL (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. doi:10.1016/j.cgh.2023.05.016. PMID 37245717 Check
|pmid=value (help). - ↑ Li M, Huang Y, Liang X, Lu H. Prevalence of autoimmune gastritis worldwide: a systematic review and meta-analysis. Helicobacter. 2025.
- ↑ Jensen ET, Martin CF, Kappelman MD, Dellon ES (2016). "Prevalence of eosinophilic gastritis, gastroenteritis, and colitis: estimates from a national administrative database". J Pediatr Gastroenterol Nutr. 62 (1): 36–42. doi:10.1097/MPG.0000000000000865. PMC 4654708. PMID 25988554.
- ↑ Bjarnason I, Scarpignato C, Holmgren E, Olszewski M, Rainsford KD, Lanas A (2018). "Mechanisms of Damage to the Gastrointestinal Tract From Nonsteroidal Anti-Inflammatory Drugs". Gastroenterology. 154 (3): 500–514. doi:10.1053/j.gastro.2017.10.049. PMID 29221664.
- ↑ Thrift AP, Wenker TN, El-Serag HB (2023). "Global burden of gastric cancer: epidemiological trends, risk factors, screening and prevention". Nat Rev Clin Oncol. 20: 338–349.
- ↑ Huang RJ, Balasubramanian V, Shum MV, Ji HP, Hwang JH. Incidence of non-cardia gastric cancer among commercially-insured individuals aged 18-64 with chronic atrophic gastritis. PLoS One. 2024.
- ↑ Malfertheiner P, Megraud F, Rokkas T, Gisbert JP, Liou JM, Schulz C, Gasbarrini A, Hunt RH, Leja M, O'Morain C, Rugge M, Suerbaum S, Tilg H, Sugano K, El-Omar EM (2022). "Management of Helicobacter pylori infection: the Maastricht VI/Florence consensus report". Gut. 71 (9): 1724–1762. doi:10.1136/gutjnl-2022-327745. PMID 35944890 Check
|pmid=value (help).