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.

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.

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]

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]

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

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.

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]

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]

There is insufficient evidence to recommend routine screening for gastritis.

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 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 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.

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.

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.

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.

CT scan may be helpful in the diagnosis of gastritis. Findings on CT scan suggestive of gastritis include gastric wall edema and halo sign.

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.

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.

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 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.

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).

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.

​​

In 1728, Georg Ernst Stahl, a German physician 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, the updated Sydney System for the classification and grading of gastritis was introduced at the International Workshop on the histopathology of gastritis held at Houston. In 2005, gastritis staging using the OLGA (Operative Link on Gastritis Assessment) staging system for reporting gastric histology was introduced.

• In 1728, George Stahl first noted inflammation of the inner lining of the stomach as “gastritis”.
• In 1771, Giovanni Morgagni described “erosive” and “ulcerating gastritis”.
• In 1855, Baron Carl von Rokitansky described “hypertrophic gastritis”.
• In 1870, Samuel Fenwick described gastric atrophy.
• In 1944, Warren & Meissner described intestinal metaplasia as feature of chronic gastritis.
• In 1947, Sir Ian Jeffreys Wood, performed first gastric biopsy with semi-flexible biopsy tube and defined “gastritis” by histopathology.
• In 1956, Louis Streifeneder and Eddy Palmer introduced flexible fiber optic endoscope.
• In 1982, Robin Warren and Barry Marshall discovered Helicobacter pylori which further led to the identification and classification of different gastritides.^[1]
• 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.^[2][3]
• In 1994, the updated Sydney system for the classification and grading of gastritis was introduced at the international workshop on the histopathology of gastritis held at Houston.^[3]
• In 2005, gastritis staging using the OLGA (Operative Link on Gastritis Assessment) staging system for reporting gastric histology was introduced. Gastritis staging combines the atrophy score which is determined by biopsy and the atrophy topography which is determined by directed biopsy mapping.^[4][5]

​​

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]

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]

Each variable is graded 0 (absent), 1 (mild), 2 (moderate), or 3 (marked).^[1]

Updated Sydney System: graded variables

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]

Chronic gastritis categories (updated Sydney System)

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

^[1][2]

• 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]

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]

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]

OLGA / OLGIM staging matrix

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

Comparison of histologic staging systems

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

^[13][14]

• 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]

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]

Endoscopic classification systems

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

^[5][17][6]

• 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]

H. pylori–associated atrophic gastritis (HpAG) and autoimmune gastritis (AIG) are distinguished mainly by topography and serology.^[9][7]

H. pylori–associated vs autoimmune atrophic gastritis

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]

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]

• 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]

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.^[1] 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.^[2][3]

• H. pylori crosses the mucus layer using flagellar motility and local alkalinization generated by urease.
• It then adheres to epithelial cells through adhesins (BabA, SabA, OipA) that bind Lewis blood-group antigens.^[1]
• Almost everyone with persistent colonization develops chronic gastritis. The topographic pattern determines the phenotype and its consequences:^[4][1]

Topographic phenotypes of chronic H. pylori gastritis

Phenotype	Approximate frequency	Acid secretion	Mechanism	Clinical consequence
Mild non-atrophic pangastritis	Most infected persons	Normal	Low-grade inflammation without atrophy	Usually asymptomatic; no major sequelae
Antral-predominant gastritis	~10–15%	Increased	Corpus is relatively spared, so parietal-cell mass is preserved. Antral inflammation impairs inhibitory control by somatostatin-secreting D cells, raising gastrin and acid output.	Duodenal ulcer phenotype
Corpus-predominant / multifocal atrophic gastritis	~1%	Decreased (hypochlorhydria or achlorhydria)	Inflammation of the oxyntic corpus leads to oxyntic atrophy. Low pepsinogen I and a low pepsinogen I/II ratio are physiologic markers.	Gastric ulcer and gastric cancer phenotype

• Acute infection causes transient hypochlorhydria, which helps the organism colonize.
• Chronic infection then diverges into one of two patterns:^[5][6]
  • the acid-hypersecretory antral pattern, or
  • the acid-hyposecretory corpus pattern, driven partly by IL-1β suppression of the parietal-cell proton pump.

• cag pathogenicity island and CagA
  • cag-positive strains assemble a type IV secretion system (T4SS) that injects CagA into epithelial cells.
  • Phosphorylated CagA activates SHP2–ERK signaling and also activates AKT and WNT signaling.
  • CagA inhibits PAR1b, which disrupts cell polarity and tight junctions. It also promotes genomic instability and epithelial–mesenchymal transition.
  • Downstream mutations can become self-sustaining. CagA can therefore act by a “hit-and-run” mechanism, in which malignant transformation no longer requires the organism.^[7]
  • cag-positive strains cause more severe gastritis, atrophy, ulceration, and distal cancer.^[7]
• VacA
  • VacA is present in nearly all strains. Its pathogenicity depends on genotype; s1/i1/m1 alleles are the most virulent.
  • It forms membrane pores, induces vacuolation and apoptosis, supplies nutrients to the bacteria, and promotes immune evasion.^[8][9]
• ADP-heptose and peptidoglycan
  • These CagA-independent molecules are translocated through the T4SS.
  • They activate ALPK1–TIFA–NF-κB signaling, a major pathway for initial mucosal inflammation and IL-8–driven neutrophil recruitment.^[7][1]

• Infection triggers an innate IL-8/neutrophil response. This is followed by a predominantly Th1/Th17 adaptive response (IFN-γ, TNF, IL-12, IL-17).^[1]
• The response is vigorous but fails to clear the organism. The result is persistent inflammation with lymphoid follicle formation.
• These follicles form mucosa-associated lymphoid tissue, the substrate for gastric MALT lymphoma.^[1]
• Chronic apoptosis, compensatory hyperproliferation, and altered differentiation set the stage for atrophy and metaplasia.^[1]

• AIG is a chronic, non–self-limiting, T cell–mediated disorder.
• It is restricted to the oxyntic (corpus/fundus) mucosa and spares the antrum, the mirror image of antral-predominant H. pylori gastritis.^[10]
• Autoantigen
  • The target is the parietal-cell H⁺/K⁺-ATPase (the gastric proton pump).
  • Autoreactive CD4⁺ Th1 cells recognize the proton pump through MHC class II.
  • Parietal cells die by apoptosis through Fas–FasL and perforin–granzyme mechanisms.^[11][10]
• Autoantibodies
  • Anti-parietal cell antibodies (PCA) and intrinsic factor antibodies (IFA) are serologic hallmarks, but their accuracy is suboptimal.
  • PCA has a high false-positive rate, and IFA has low sensitivity.
  • Diagnosis therefore rests on histologic corpus-restricted atrophy together with endoscopy and serology, not on antibodies alone.^[12][13]
• Functional consequences
  • Loss of parietal cells causes hypo-/achlorhydria, leading to malabsorption of iron, folate, and calcium.
  • Loss of intrinsic factor causes vitamin B12 malabsorption.
  • Low acid produces secondary hypergastrinemia. This drives enterochromaffin-like cell (ECL) hyperplasia and predisposes to type 1 gastric neuroendocrine tumors.^[10][14]
• Natural history
  • Asymptomatic AIG can precede corpus atrophy by 10–20 years.
  • Iron deficiency anemia typically comes before B12-deficient pernicious anemia. Pernicious anemia is one of several possible presentations, not the defining feature.^[11][15]
  • H. pylori may trigger AIG through molecular mimicry in some patients, but this remains uncertain.^[10]

• Reactive gastropathy is a non-immune injury pattern. It is now among the most common histologic gastric diagnoses, especially where H. pylori prevalence is low.^[16]
• Causes include:^[17]
  • NSAIDs and aspirin
  • bile (duodenogastric) reflux, notably after gastrectomy
  • alcohol
  • other drugs: bisphosphonates, oral iron, tetracycline/doxycycline, and SSRIs
• NSAIDs and aspirin
  • Cyclooxygenase inhibition depletes mucosal prostaglandins. This reduces mucus and bicarbonate secretion and mucosal blood flow.
  • COX-independent proinflammatory effects also contribute.
  • Luminal acid worsens the injury, which is the mechanistic rationale for acid suppression.^[17]
• Bile reflux
  • Bile salts solubilize the mucus layer and disrupt epithelial membranes, allowing acid to back-diffuse into the mucosa.^[18]
• Alcohol
  • Alcohol dissolves the mucus layer, increases mucosal permeability, and induces oxidative stress.

Feature	H. pylori gastritis	Autoimmune gastritis	Reactive gastropathy
Distribution	Antrum-predominant, pangastritis, or multifocal	Corpus/fundus only; antrum spared	Typically antrum
Inflammation	Chronic lymphoplasmacytic infiltrate with neutrophilic activity; lymphoid follicles	Lymphoplasmacytic infiltrate targeting oxyntic glands; progressive oxyntic atrophy	Scant acute and chronic inflammatory cells
Epithelial changes	Atrophy and metaplasia with chronicity	Pyloric and intestinal metaplasia; ECL-cell hyperplasia	Foveolar hyperplasia with corkscrew pits, mucin depletion, lamina propria smooth-muscle fibers, capillary congestion
Supporting references	[1]	[10]	[16][18]

• A dense surface eosinophilic band is typical of NSAID injury.^[18]

• Chronic inflammation involving the corpus drives a stepwise histologic sequence:^[2][19]
  1. non-atrophic gastritis
  2. atrophic gastritis
  3. intestinal metaplasia
  4. dysplasia
  5. intestinal-type adenocarcinoma
• H. pylori is the dominant initiator, with about 75% attributable risk; it is a WHO class 1 carcinogen. AIG drives an analogous pathway restricted to the corpus.^[2][19]
• Atrophy and its subtypes
  • Atrophy is loss of native glands.
  • The glands are replaced by fibrosis (non-metaplastic atrophy), pseudopyloric/pyloric metaplasia, or intestinal metaplasia.
  • Intestinal metaplasia is therefore a subtype of atrophy, not a separate lesion.^[20]
• Pyloric metaplasia and SPEM
  • Spasmolytic polypeptide-expressing metaplasia (SPEM; TFF2⁺/GIF⁺) arises when corpus chief cells are reprogrammed after oxyntic injury.
  • It can precede intestinal metaplasia or develop alongside it.
  • Single-cell data now describe region-specific, partly non-linear trajectories layered on the classic tissue-level cascade.^[21][7][22]
• Intestinal metaplasia subtype
  • Incomplete intestinal metaplasia carries a higher cancer risk than the complete type.^[23]
• Molecular changes
  • Chromosomal instability, copy-number alterations, telomere shortening, and DNA methylation accumulate across the cascade.
  • Intestinal metaplasia is often described as a relative “point of no return” that signals elevated risk.^[24]
• Gastric microbiota
  • In the achlorhydric corpus, the gastric microbiota becomes dysbiotic and genotoxic. It can perpetuate carcinogenesis even after H. pylori is lost.^[1][7]
• Progression rates
  • Non-dysplastic intestinal metaplasia progresses to cancer at a pooled rate of about 12.4 per 10,000 person-years.^[19]
  • Only about 1–3% of infected people ultimately develop gastric cancer.^[2]

• Updated Sydney System
  • It grades chronic inflammation, activity (neutrophils), atrophy, intestinal metaplasia, and H. pylori density as mild, moderate, or severe.^[25]
  • It uses a defined 5-biopsy protocol: antrum ×2, corpus ×2, and incisura ×1.
  • Antral and corpus specimens go in separate jars so that atrophy can be localized.^[26]
• OLGA and OLGIM
  • OLGA (atrophy) and OLGIM (intestinal metaplasia) combine severity and topography into stages 0–IV.
  • Stages III–IV mark high cancer risk. International guidelines endorse these stages for risk stratification.^[3][20]

System	What it scores	Strengths	Limitations
Updated Sydney System	Inflammation, activity, atrophy, intestinal metaplasia, H. pylori density; each graded mild/moderate/severe	Standardized, topographic biopsy protocol; provides the grading that OLGA/OLGIM are built on	Descriptive; does not by itself produce a cancer-risk stage
OLGA	Atrophy of all subtypes (non-metaplastic, pyloric, intestinal) in antrum and corpus, combined into stages 0–IV	Captures all atrophy, so OLGA stage is always at least the OLGIM stage; stages III–IV are high risk	Higher interobserver variability
OLGIM	Intestinal metaplasia only, in antrum and corpus, combined into stages 0–IV	Lower interobserver variability; strongly elevated cancer risk at stages III–IV; measurable risk even at stage II	May be less sensitive than OLGA

• Support for the table above:^[27][3]
• Routine OLGA/OLGIM reporting remains limited in US practice.^[26][28]

• Topography predicts phenotype.
  • Antral-predominant gastritis means high acid and a tendency to duodenal ulcer.
  • Corpus-predominant atrophic gastritis means low acid and a tendency to gastric ulcer and cancer.^[4]
• Pepsinogen as a marker. Low pepsinogen I and a low pepsinogen I/II ratio signal corpus atrophy.^[4]
• Corpus-restricted atrophy with antral sparing should prompt evaluation for AIG.
  • Antral atrophy in a presumed AIG case suggests concurrent H. pylori infection.^[10]
  • Corpus atrophy plus hypergastrinemia plus B12/iron deficiency suggests AIG and the risk of type 1 gastric NET.^[10]
• Reactive gastropathy is an injury pattern, not an infection. Foveolar hyperplasia with scant inflammation should prompt review of NSAIDs/aspirin, other culprit drugs, bile reflux, and alcohol.^[16]
• Timing of eradication. H. pylori eradication interrupts the cascade most effectively before atrophy or metaplasia develop. Once extensive metaplasia or dysbiosis is established, residual risk persists.^[1][19]

• Labeling endoscopic erythema “gastritis” without histology; much of it is reactive gastropathy.^[16]
• Ruling out AIG on negative PCA/IFA alone. Histology showing corpus atrophy is the anchor.^[12]
• Pooling antrum and corpus biopsies in one jar, which prevents topographic atrophy assessment and OLGA/OLGIM staging.^[26]

• It is debated whether intestinal metaplasia confers substantially more risk than pyloric metaplasia or atrophy alone. It is also unclear whether metaplasia without H. pylori is truly precancerous.^[21]
• Single-cell and lineage data are reframing the linear Correa cascade as a regionally stratified, partly parallel process. Diffuse-type cancer may bypass intestinal metaplasia altogether.^[29][22]
• A role for H. pylori in initiating AIG through molecular mimicry remains unproven.^[10]
• It is unsettled whether OLGA or OLGIM is the better predictor, and whether OLGIM stage II warrants surveillance.^[28][27]

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.^[1] Current classification is based on cause, as set out in the Kyoto Global Consensus and the Real-World Gastritis Initiative (RE.GA.IN.).^[2][3]

• 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

Life-threatening causes are conditions that can lead to death or permanent disability within 24 hours if left untreated.

• Phlegmonous gastritis and its gas-forming variant, emphysematous gastritis: bacterial infection of the gastric wall with mortality of approximately 40%.^[4]
• Caustic or corrosive ingestion (acids, alkalis)^[1]
• Stress-related mucosal disease in critical illness, major surgery, burns, or trauma. This is an erosive, ischemia- and acid-mediated gastropathy, not true inflammatory gastritis.
• Cytomegalovirus (CMV) and other opportunistic infections in immunocompromised patients, which can present as ulceration with bleeding^[4]

• H. pylori infection^[5]
• Autoimmune gastritis^[6]
• NSAIDs and aspirin, which cause reactive gastropathy^[1]
• Bile (duodenogastric) reflux^[7]

• H. pylori is the most common cause of chronic gastritis worldwide and is a WHO/IARC group 1 carcinogen.^[5]
  • It colonizes approximately 43% of the world population.
  • Infection is usually acquired in childhood and persists for life if untreated.
• It produces chronic active gastritis, which stays asymptomatic for decades in most carriers.^[5]
• Phenotype depends on topography:^[5][8]
  • Antral-predominant gastritis: acid output preserved or high; predisposes to duodenal ulcer.
  • Corpus-predominant gastritis or pangastritis: acid output reduced; predisposes to gastric ulcer, atrophy, and gastric adenocarcinoma.
• Bacterial virulence factors are the main determinants of inflammatory intensity and cancer risk. These are a functional cag pathogenicity island (CagA) and the vacuolating cytotoxin VacA.^[5]
• Long-standing infection drives the Correa cascade:^[9]
  • Non-atrophic gastritis → multifocal atrophic gastritis → intestinal metaplasia → dysplasia → adenocarcinoma.
  • The rate ratio for atrophic gastritis in infected versus uninfected persons is approximately 5.0.
  • Atrophy incidence in uninfected persons is below 1% per year.
• Helicobacter heilmannii is a less common cause of Helicobacter gastritis.^[4]

• Autoimmune gastritis (AIG) is immune-mediated destruction of parietal (oxyntic) cells.^[6][10]
  • It is restricted to the corpus and fundus and spares the antrum, which is the reverse of most H. pylori gastritis.
  • It is not self-limiting.
• Mechanism:^[6]
  • The gastric H⁺/K⁺ ATPase (proton pump) is the major autoantigen.
  • Autoreactive T cells drive parietal cell loss.
  • Anti-parietal cell antibodies (PCA) and anti-intrinsic factor antibodies (IFA) are produced.
• Consequences are hypo- or achlorhydria, loss of intrinsic factor, and hypergastrinemia. These lead to malabsorption of:^[11][12]
  • Iron, causing iron-deficiency anemia (often the earlier presentation, in younger patients)
  • Vitamin B12, causing pernicious anemia (a later presentation, in older patients)
  • Folate and calcium
• AIG accounts for approximately 20–27% of obscure or refractory iron-deficiency anemia.^[12]
• Pernicious anemia is a late complication of AIG, not a synonym for it.^[10]
• Other complications are type 1 gastric neuroendocrine tumors and increased gastric adenocarcinoma risk.^[6][13]
• Epidemiology:^[9]
  • Estimated prevalence is approximately 0.5–2% and rises with age.
  • Women are more often affected.
  • AIG is strongly associated with autoimmune thyroid disease (up to about one-third of these patients have AIG) and type 1 diabetes mellitus.
  • Racial and ethnic variation is less prominent than in H. pylori-associated atrophic gastritis.
• Potential and seronegative AIG are now recognized variants.^[10]
• H. pylori may trigger AIG through molecular mimicry, but this has not been proven.^[6][14]

Histologic features are:^[15][1]

• Foveolar hyperplasia (“corkscrew” glands)
• Lamina propria edema
• Smooth muscle fibers extending into the lamina propria
• Vascular ectasia
• Minimal inflammation

It is the most common histopathologic gastric change in large US biopsy cohorts, and its prevalence rises with age.^[16]

Causes:

• NSAIDs and aspirin are the most common medication cause.^[1][17]
  • Reactive gastropathy is found in up to approximately 45% of regular NSAID users.
  • Injury comes from direct topical damage (independent of prostaglandins) plus cyclooxygenase inhibition, and acid makes it worse.
• Bile (duodenogastric) reflux:^[7][18]
  • In the intact stomach, it injures the antrum.
  • After partial gastrectomy or gastrojejunostomy (Billroth II), it injures the corpus and anastomosis and contributes to gastric stump cancer.
• Other drugs and agents:^[15]
  • Bisphosphonates
  • Oral iron
  • Tetracyclines, especially doxycycline
  • 5-aminosalicylic acid
  • Antiplatelet agents such as clopidogrel
  • Selective serotonin reuptake inhibitors
  • Alcohol^[19]
• Gastrostomy tubes can cause localized reactive injury.^[15]

• Lymphocytic gastritis is associated with celiac disease and H. pylori. Some cases are drug-induced or idiopathic.^[1][20]
• Eosinophilic gastritis is linked to food or allergic sensitization and other allergic mechanisms.^[1]
• Granulomatous gastritis:^[1]
  • Leading identifiable causes are Crohn’s disease and sarcoidosis.
  • Other causes are foreign material and granulomatosis with polyangiitis.
  • Some cases are idiopathic (isolated granulomatous gastritis).
• Collagenous gastritis is rare. Its cause is unknown and may be autoimmune.^[1]

These infections occur mostly in immunocompromised hosts: HIV, transplant, chemotherapy, high-dose corticosteroids, diabetes mellitus, and malnutrition.^[7][4]

• Viral:^[4]
  • CMV is the most common, with characteristic “owl-eye” inclusions.
  • Herpes simplex virus involves the stomach rarely and causes punched-out ulcers.
• Bacterial (non–H. pylori):^[4]
  • Phlegmonous gastritis is caused by Streptococcus, Escherichia coli, Enterobacter, or Proteus.
    • Risk factors are immunosuppression, diabetes, alcoholism, hypochlorhydria, and recent instrumentation.
    • Emphysematous gastritis is the gas-forming variant.
  • Other bacterial causes are mycobacteria, syphilis, and Salmonella.
• Fungal and parasitic:^[1][4]
  • Fungi: Candida, mucormycosis, histoplasmosis, aspergillosis
  • Parasites: anisakiasis, strongyloidiasis
  • These occur mainly with immunocompromise or exposure in endemic areas.

• Radiation therapy to the upper abdomen causes radiation gastropathy.^[1]
• Ingestion of caustic or corrosive agents (acids, alkalis) or other chemical irritants causes direct injury.^[1]
• Gastric hypoperfusion and stress-related mucosal disease are erosive gastropathies, not inflammatory gastritis.

These factors modify disease rather than cause it on their own.

• Tobacco and high-salt diet are cofactors for non-autoimmune atrophic gastritis and accelerate H. pylori-associated atrophy.^[9][21]
• Alcohol contributes to reactive gastropathy.^[19]
• Coffee, acidic beverages, and spicy or fatty foods may provoke dyspeptic symptoms. They are not established causes of histologic gastritis in current classifications.^[3]

Category	Principal causes	Typical pattern	Key association
H. pylori	H. pylori; rarely H. heilmannii	Chronic active gastritis; antral-predominant or multifocal atrophy	Peptic ulcer; gastric adenocarcinoma; MALT lymphoma
Autoimmune	Anti-parietal cell immunity (H+/K+ ATPase)	Corpus-restricted atrophy with antral sparing	Iron or B12 deficiency; type 1 gastric NET; thyroid disease and type 1 diabetes
Reactive gastropathy	NSAIDs/aspirin, bile reflux, bisphosphonates, iron, doxycycline, alcohol	Foveolar hyperplasia with minimal inflammation	Remove the offending agent; not an infection
Other non-infectious	Celiac disease, allergy, Crohn’s disease, sarcoidosis	Lymphocytic, eosinophilic, granulomatous, or collagenous patterns	Systemic disease outside the stomach
Non–H. pylori infectious	CMV, HSV, phlegmonous bacteria, fungi, parasites	Ulcers or erosions; mural infection	Immunocompromise; phlegmonous form carries ~40% mortality
Physical/caustic/ischemic	Radiation, caustic ingestion, hypoperfusion, critical illness	Erosive gastropathy	Emergency presentations

^[2][14]

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.

Differentiating gastritis from other Diseases:

• Acute Gastritis
  • Crohn’s Disease
  • Gallstones (Cholelithiasis)
  • Cholecystitis
  • Gastric cancer
  • Peptic Ulcer Disease
  • Viral Gastroenteritis
  • Acute Complications of Sarcoidosis
  • B-Cell Lymphoma
• Chronic Gastritis
  • Atrophic Gastritis
  • Gastroesophageal Reflux Disease (GERD)
  • Crohn’s Disease
• Atrophic Gastritis
  • Chronic Gastritis
  • Functional (Nonulcer) Dyspepsia
  • Gastroesophageal Reflux Disease (GERD)
  • Pernicious Anemia
• Stress related/induced Gastritis
  • Alcoholic gastropathy
  • Nonsteroidal anti-inflammatory drug, (NSAID) induced gastritis
  • Peptic Ulcer Disease
  • Uremic gastropathy
• Helicobacter Pylori-associated Gastritis
  • Autoimmune gastritis
  • Nonspecific chronic inactive gastritis
  • Gastritis in patients with Crohn’s disease involving the stomach
  • Gastropathy in the setting of chronic conditions (eg, portal hypertensive gastropathy)
  • Lymphocytic gastritis
• Other differentials
  • Ménétrier disease (Rare disorder)
  • Aortic aneurysm (ruptured)
  • Candida
  • Crohn’s Disease
  • Cytomegalovirus (CMV) in HIV
  • Diseases of the biliary system
  • Drugs
  • Esophageal varices
  • Functional dyspepsia
  • Gastric carcinoma
  • Gastroduodenal ulcer
  • Intoxication
  • Liver failure
  • Lymphocytic gastritis
  • Mallory-Weiss Tear
  • Menetrier’s Disease
  • Pancreas carcinoma
  • Pancreatitis
  • Peptic ulcer
  • Perforated ulcer
  • Radiation
  • Reflux esophagitis
  • Renal Failure
  • Respiratory failure
  • Sarcoidosis
  • Sepsis
  • Shock
  • Surgery
  • Syphilis
  • Trauma
  • Tuberculosis
  • Volvulus
  • Zollinger-Ellison Syndrome

• The table below differentiates gastritis from other conditions:^{[1][2][3][4][5][6][7][8][9]}

Differential Diagnosis

Disease

Cause

Symptoms

Diagnosis

Other findings

Pain

Nausea & Vomiting

Heartburn

Belching or Bloating

Weight loss

Loss of Appetite

Stools

Endoscopy findings

Location

Aggravating Factors

Alleviating Factors

Acute gastritis

H. pylori NSAIDS Corticosteroids Alcohol Spicy food Viral infections Crohn’s disease Autoimmune diseases Bile reflux Cocaine use Breathing machine or ventilator Ingestion of corrosives

Epigastric pain

Food

Antacids

✔

✔

✔

–

✔

Black stools

Pangastritis or antral gastritis Erosive (Superficial, deep, hemorrhagic) Nonerosive (H. pylori)

–

Chronic gastritis

H. pylori Alcohol Medications Autoimmune diseases Chronic stress

Epigastric pain

Food

Antacids

✔

✔

✔

✔

✔

–

H. pylori gastritis Atrophy Intestinal metaplasia Lymphocytic gastritis Enlarged folds Aphthoid erosions

–

Atrophic gastritis

H. pylori Autoimmune disease

Epigastric pain

–

–

✔

–

✔

✔

–

H. pylori Mucosal atrophy Autoimmune Mucosal atrophy

Iron deficiency anemia Autoimmune gastritis diagnosis includes: Antiparietal and anti-IF antibodies Achlorhydria and hypergastrinemia Low serum cobalamine

Crohn’s disease

Autoimmune disease

Abdominal pain

–

–

–

–

–

✔

✔

Chronic diarrhea often bloody with pus or mucus Rectal bleeding

Mucosal nodularity with cobblestoning Multiple aphthous ulcers Linier or serpiginous ulcerations Thickened antral folds Antral narrowing Hypoperistalsis Duodenal strictures

Fever Fatigue Anemia (pernicious anemia)

GERD

Lower esophageal sphincter abnormalities Hiatal hernia Abnormal esophageal contractions Prolonged emptying of stomach Gastrinomas

Epigastric pain

Spicy food Tight fitting clothing

Antacids Head elevation during sleep

✔ (Suspect delayed gastric emptying)

✔

–

–

–

–

Esophagitis Barrette’s esophagus Strictures

Other symptoms: Dysphagia Regurgitation Nocturnal cough Hoarseness Complications Esophagitis Strictures Barrette esophagus

Peptic ulcer disease

H. pylori Smoking Alcohol Radiation therapy Medications Zollinger-Ellison syndrome

Epigastric pain sometimes extending to back Right upper quadrant pain

Duodenal ulcer Pain aggravates with empty stomach Gastric ulcer Pain aggravates with food

Antacids Duodenal ulcer Pain alleviates with food

✔

✔

–

–

–

Black stools

Gastric ulcers Discrete mucosal lesions with a punched-out smooth ulcer base with whitish fibrinoid base Most ulcers are at the junction of fundus and antrum 0.5-2.5cm Duodenal ulcers Well-demarcated break in the mucosa that may extend into the muscularis propria of the duodenum Found in the first part of duodenum <1cm

Other diagnostic tests Serum gastrin levels Secretin stimulation test Biopsy

Gastrinoma

Associated with MEN type 1

Abdominal pain

–

–

✔ (suspect gastric outlet obstruction)

✔

–

–

–

Black stools

Useful in collecting the tissue for biopsy

May present with symptoms of GERD or peptic ulcer disease Associated with MEN type 1 Diagnostic tests Serum gastrin levels Somatostatin receptor scintigraphy CT and MRI

Gastric Adenocarcinoma

H. pylori infection Smoked and salted food

Abdominal pain

–

–

✔

✔

✔

✔

✔

Black stools, or blood in stools

Esophagogastroduodenoscopy Multiple biopsies are taken to establish the diagnosis

Other symptoms Dysphagia Early satiety Frequent burping

Primary gastric lymphoma

H. pylori infection

Abdominal pain Chest pain

–

–

–

–

–

✔

–

–

Useful in collecting the tissue for biopsy

Other symptoms Painless swollen lymph nodes in neck and armpit Night sweats Fatigue Fever Cough or trouble breathing

​​

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.^[1] 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.^[2] 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.^[3]

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.^[4] AIG has a pooled global prevalence of ~3.9%, with a female predominance and strong overlap with other autoimmune diseases.^[5] 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.^[6]

H. pylori is the most common cause of gastritis worldwide and the most common chronic bacterial infection in humans.^[1]

• The crude global prevalence of H. pylori in adults fell from 52.6% (before 1990) to 43.9% (2015–2022). A systematic review of 1,748 studies from 111 countries estimated a ~15.9% decline in adults over three decades.^[2]
• An independent meta-analysis of 224 studies from 71 countries found a parallel decline, from 58.2% (1980–1990) to 43.1% (2011–2022). Prevalence was relatively static from 1991 to 2010, then fell sharply from 2011 to 2022, with the largest drop in the WHO African region.^[7]
• The decline is confined to adults. Prevalence in children and adolescents remained ~35.1% in 2015–2022, with no significant reduction in any WHO region. This reflects ongoing early-life transmission.^[2]
• Prevalence is inversely associated with income level, Human Development Index, and universal health coverage. Some low-resource settings still exceed 60–70%.^[1][7]
• Studies using serologic testing consistently report higher prevalence than studies using non-serologic (active-infection) testing.^[7]

Adult H. pylori prevalence by WHO region, 2010–2022^[2]

WHO region	Adult prevalence
African	52.7%
Eastern Mediterranean	52.6%
Southeast Asian	46.7%
Western Pacific	43.2%
Americas	42.5%
European	39.6%

• Historical North American prevalence estimates are 30–40%. Contemporary non-serologic testing gives lower figures.^[1]
• In a nationwide Veterans Health Administration cohort of 913,328 adults tested for H. pylori between 1999 and 2018, 25.8% tested positive. Positivity fell from 35.9% (1999–2006) to 18.4% (2013–2018).^[3]
• Positivity by race and ethnicity in this cohort:^[3]
  • Non-Hispanic Black: 40.2%
  • Hispanic: 36.7%
  • Non-Hispanic other: 27.7%
  • Non-Hispanic White: 20.1%
• The highest state-level rates were among non-Hispanic Black individuals in Mississippi (54%) and Alabama (50.9%).^[3]
• The disparity is widening. The gap between non-Hispanic Black and non-Hispanic White individuals was largest in the most recent period, 2013–2018 (32.1% vs 13.3%; ~2.4-fold).^[3]
• A reference-laboratory study of 624,444 samples (2005–2014) found 24.8% seroprevalence. Rates exceeded 30% in the southern US (e.g., Texas, New Mexico) and the Southeast.^[1]

• Higher prevalence in older adults reflects a birth cohort effect, not increased acquisition in later life.^[8]
• About 90% of infections are acquired in childhood, typically before age 10, and persist lifelong unless treated.^[8]
• In a longitudinal cohort, overall incidence was ~1.4%/year. Incidence peaked at ages 4–5 (2.1%/year) and fell to 0.3%/year by ages 21–23.^[8]
• Spontaneous clearance is uncommon but occurs, notably in advanced atrophic gastritis.^[8]

• Globally, H. pylori prevalence is modestly higher in men (OR ~1.12; 95% CI 1.09–1.15).^[1]

• First-generation immigrants from high-prevalence regions (e.g., Mexico, Central America) have higher prevalence than the destination population. This difference attenuates with longer residence and in subsequent generations.^[1]
• In a Houston cohort, first-generation immigrant status and Black or Hispanic race/ethnicity were the individual risk factors with the best predictive performance for H. pylori infection.^[9]

CAG is the convergent pre-neoplastic phenotype of long-standing H. pylori infection and of AIG, and an early step in the Correa cascade.^[4]

• Prevalence:
  • ~10–15% in the US^[4]
  • ~5% in populations with low gastric-cancer incidence^[4]
  • Up to ~50% in populations with high gastric-cancer incidence^[4]
  • ~25% (95% CI 18–32%) pooled worldwide (2010–2020 studies)^[10]
• H. pylori as the main driver: the incidence rate ratio for atrophic gastritis in infected vs uninfected individuals is 5.0 (95% CI 3.1–8.3). Annual incidence in uninfected persons is <1%.^[4]
• Other risk factors for non-autoimmune CAG: older age, tobacco use, high-salt diet, and possibly chronic bile reflux.^[4]
• Gastric cancer risk:
  • Progression from CAG to gastric adenocarcinoma is estimated at ~0.1–0.3%/year. Risk rises with atrophy severity and extent and with concomitant intestinal metaplasia.^[4]
  • A meta-analysis of 23 studies found a 4.12-fold increased risk of incident gastric cancer with CAG (OR 4.12; 95% CI 3.20–5.30). Risk estimates were higher when CAG was diagnosed histologically rather than serologically.^[11]
  • A meta-analysis reported a pooled standardized incidence ratio for gastric cancer of 20.7 (95% CI 14.0–30.2), substantially higher with extensive than with antral-predominant atrophy.^[12]
  • In a US commercially insured cohort aged 18–64 with CAG (107,835 individuals), the crude incidence of non-cardia gastric cancer was 98 per 100,000 person-years.^[13] Risk was higher in men, in those aged 50–64, and in patients with anemia, smoking, or a family history of digestive neoplasms.^[13]

AIG is a corpus-restricted, antral-sparing chronic atrophic gastritis mediated by anti-parietal cell and anti-intrinsic factor autoimmunity. It is substantially less common than H. pylori–associated CAG.^[4]

• Prevalence depends heavily on the diagnostic method:
  • Histology/endoscopy-based estimates: ~0.5–2%^[4]
  • Pooled global prevalence (47 studies; 15,817 individuals): 3.85% (95% CI 2.94–5.04%)^[5]
  • Pooled estimates by method: 5.4% by serology alone, 2.71% by histology, and 1.81% by combined serology and histology^[5]
  • Individual serology-only population studies report figures as high as ~19.5%, which overestimates true disease^[14]
• Geography: AIG was historically considered a Western disease but is now recognized globally.^[15] Pooled prevalence by region:^[5]
  • Africa: 8.46%
  • Australia: 8.08%
  • Europe: 4.94%
  • Americas: 2.82%
  • Asia: 2.23%
• Age and sex: prevalence increases with age and is rare before age 30. There is a consistent female predominance.^[14]
• Race/ethnicity: marked racial or ethnic variation is not considered characteristic of AIG.^[4] However, a Houston safety-net cohort identified non-White race, female sex, older age, non-tobacco use, and absence of H. pylori as factors associated with AIG.^[16]
• High-risk populations:^[4][15]
  • Unexplained iron deficiency anemia: up to ~50% have AIG
  • Autoimmune thyroid disease: up to one-third have AIG
  • Also associated with type 1 diabetes mellitus, vitiligo, Addison disease, celiac disease, and autoimmune liver disease
• Pernicious anemia (late-stage AIG) has an estimated prevalence of ~0.15–1% in the general population and ~2% in people older than 60.^[4][14]
• Neoplastic risk:
  • Type 1 gastric neuroendocrine tumors are consistently increased, with an estimated incidence of ~0.4–0.7%/year in chronic atrophic gastritis.^[4]
  • In a US cohort, gastric malignancy risk (mainly neuroendocrine tumors) was 2.7-fold higher in AIG than in non-autoimmune atrophic gastritis.^[16]
  • Whether AIG independently increases gastric adenocarcinoma risk, after accounting for H. pylori, remains debated (see below).^[16]

EoG is a rare type-2 (Th2) immune–mediated eosinophilic gastrointestinal disorder. It is defined histologically by gastric eosinophilia (≥30 eosinophils/HPF in ≥5 HPFs) in the appropriate clinical context, after secondary causes are excluded.^[17]

• Prevalence: ~6.3 per 100,000 in US administrative-database estimates.^[6]
• Trend: prevalence appears to be rising. Evolving case definitions and likely underdiagnosis limit precise estimates.^[17][18]
• Demographics: there is a female predominance (~7.9 vs 5.4 per 100,000). EoG is diagnosed more often in children than adults, with the highest prevalence in children younger than 5. It is associated with atopic comorbidities.^[6][17]
• Underdiagnosis:
  • In a US claims cohort of 4,108 patients with eosinophilic gastritis and/or duodenitis, the mean time from symptom onset to diagnosis was 3.6 years.^[19]
  • The diagnosis was missed at the index esophagogastroduodenoscopy in 38.2% of these patients.^[19]
  • Prior misdiagnosis as irritable bowel syndrome, functional dyspepsia, or peptic ulcer independently predicted delay.^[19]
  • Because gastric involvement is patchy, sampling with multiple (≥8) gastric biopsies is recommended.^[17]

• True AIG prevalence is unknown. Estimates diverge several-fold between serology-based and histology-based studies. No Western population-based, histologically confirmed prevalence study exists.^[14][5]
• Independent adenocarcinoma risk in AIG is contested. Many studies suggesting elevated risk did not exclude concomitant or prior H. pylori infection. Neuroendocrine tumor risk, by contrast, is consistently elevated.^[16]
• US H. pylori testing targets differ by guidance.
  • The Houston Consensus Conference and ACG identify partially different high-risk groups.^[9]
  • In external validation, only Black or Hispanic race/ethnicity (AUROC 0.57) and first-generation immigrant status (AUROC 0.59) showed meaningful predictive value as individual risk factors.^[9]
  • A combined model improved performance only modestly (AUROC 0.64).^[9]
• Western CAG cancer-risk data are methodologically limited. Studies separate atrophy from intestinal metaplasia, and autoimmune from H. pylori etiology, inconsistently.^[12]

Gastritis is best stratified by etiology rather than by symptom-based lists, because etiology determines cancer risk, surveillance, and treatment.^[1] The two dominant, clinically decisive risk factors are chronic Helicobacter pylori infection and autoimmunity.^[2] 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.^[3][4] 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.^[5][6]

• Risk factors differ by histologic entity:
  • Inflammatory gastritis (immune-cell infiltrate): H. pylori infection and autoimmunity.^[2]
  • Reactive/chemical gastropathy (epithelial injury, minimal inflammation): NSAIDs/aspirin, bile reflux, alcohol, and stress-related mucosal disease of critical illness.^[3][4]
• Distinguishing these entities matters because only inflammatory gastritis (particularly corpus-predominant or atrophic forms) carries meaningful long-term neoplastic risk.^[1]

• Single most important and most prevalent cause of chronic gastritis worldwide; classified as a WHO class I carcinogen.^[7]
• Estimated to infect ~43% of adults globally and ~18% of US adults.^[8]
• Usually acquired in childhood and persists for life if untreated; most infected hosts have chronic–active gastritis that remains asymptomatic for decades.^[7]
• Acquisition risk is higher with lower socioeconomic status, household crowding, and birth in or immigration from high-prevalence regions.^[4]
• Gastritis phenotype determines downstream disease:^[7][9]
  • Antral-predominant gastritis → acid hypersecretion → duodenal ulcer risk
  • Corpus-predominant gastritis or pangastritis → atrophy, hypochlorhydria, and gastric cancer risk
• Infection strongly drives atrophic gastritis: incidence rate ratio 5.0 (95% CI 3.1–8.3) in infected versus uninfected individuals, with <1% annual incidence in uninfected persons.^[2]
• Strain virulence factors (functional cag pathogenicity island, CagA, VacA) modulate the severity of inflammation and oncogenic potential.^[7]

• Corpus-restricted atrophic gastritis driven by autoreactive CD4+ T cells targeting the parietal-cell H+/K+ ATPase, causing oxyntic gland loss, hypo-/achlorhydria, and intrinsic factor deficiency; pernicious anemia is a late-stage manifestation.^[10][11]
• Risk factors and associations:
  • Older age (prevalence rises with age).^[11]
  • Female sex.^[11][12]
  • Coexisting autoimmune disease, especially autoimmune thyroid disease (up to one-third of these patients have autoimmune gastritis) and type 1 diabetes mellitus.^[2][11]
  • Genetic predisposition: familial clustering, twin concordance, and HLA haplotypes shared with other autoimmune conditions.^[11]
• Estimated prevalence ~0.5–2% (higher in serology-based studies); unlike H. pylori-associated atrophy, it lacks marked racial/ethnic variation.^[2][12]
• Now recognized as a global disorder with a broad clinical spectrum and its own risk of gastric adenocarcinoma and type 1 gastric neuroendocrine tumors.^[13]

• With H. pylori, one of the two leading causes of gastroduodenal mucosal injury.^[9]
• Mechanism: COX-1 inhibition with loss of mucosal prostaglandin protection, plus COX-independent topical injury; antral histology in H. pylori-negative users is typically reactive/chemical gastropathy.^[3]
• 15–30% of long-term NSAID users develop endoscopic ulcers, and serious GI complications occur in 1–4% of users annually.^[14]
• Risk is dose- and duration-dependent; aspirin carries risk comparable to other NSAIDs, and dual antiplatelet therapy raises it further.^[15]
• Risk amplifiers:^[14][15]
  • Prior ulcer or GI complication (strongest; OR up to ~13.5)
  • Advancing age
  • Concomitant corticosteroids, anticoagulants, SSRIs, or combined NSAID/aspirin use
  • Concurrent H. pylori infection (synergistic)
• GI toxicity varies by agent: lower with ibuprofen, etodolac, nabumetone, and COX-2–selective inhibitors; higher with piroxicam, indomethacin, and ketorolac.^[14]

• Acute, multifactorial mucosal injury driven by splanchnic hypoperfusion, reduced mucosal defenses, and acid back-diffusion; it is distinct from the poorly defined “stress” of outpatient dyspepsia.^[16]
• Upper GI mucosal lesions are found in 75–100% of ICU patients, but clinically important bleeding is uncommon (1.5% in a 2,252-patient prospective cohort).^[16][17]
• Major independent risk factors:^[17]
  • Respiratory failure requiring mechanical ventilation >48 hours (OR 15.6)
  • Coagulopathy (OR 4.3)
• Bleeding occurred in 3.7% of patients with one or both major factors versus 0.1% of those without.^[17]
• Additional risk factors: severe head or spinal cord injury, multiple trauma, extensive burns, hepatic failure, shock, sepsis, acute kidney injury, prolonged ICU stay, and high-dose corticosteroids.^[16]
• Early enteral nutrition appears protective.^[16]

• Bile (duodenogastric) reflux produces reactive gastropathy and is associated with antral metaplastic change; it may contribute to nonautoimmune atrophic gastritis, particularly after gastric surgery.^[2][18]
• Heavy alcohol use causes acute hemorrhagic/erosive gastropathy;^[19] heavy drinking independently predicts upper GI symptoms (OR ~2.4),^[20] and high intake (≥4 drinks/day) is associated with gastric cancer (pooled OR 1.37).^[8]
• Cigarette smoking promotes atrophic gastritis in H. pylori-positive individuals and progression along the Correa cascade; current smokers have ~25–50% higher gastric cancer risk, with dose- and duration-dependence and normalization ~10 years after cessation.^[21][5]
• High-salt diet damages the mucosa, promotes H. pylori colonization, and interacts more than multiplicatively with H. pylori for gastric cancer risk (interaction OR 2.62).^[8][22]
• Increasing age is associated with greater prevalence and severity of atrophic gastritis and independently predicts progression to cancer.^[2][6]
• Male sex (HR 1.86) and family history of digestive neoplasm (HR 1.45) independently predict progression of chronic atrophic gastritis to non-cardia gastric cancer.^[6]

• Whether H. pylori triggers autoimmune gastritis (e.g., via molecular mimicry with H+/K+ ATPase) remains unresolved; H. pylori-dependent and -independent pathways are both proposed.^[10][13]
• Whether H. pylori adds to short-term NSAID injury is contested; the interaction is likely additive rather than causal.^[3]
• Sepsis as an independent risk factor for stress-related mucosal disease is inconsistently supported.^[16]
• Everyday psychological stress is a weak, poorly validated contributor.^[23]
• Evidence that moderate alcohol, caffeine, or acidic beverages cause histologic chronic gastritis is weak and confounded.^[19]

Risk factor	Predominant lesion
H. pylori infection	Chronic–active gastritis → atrophy, metaplasia
Autoimmunity	Corpus-restricted atrophic gastritis
NSAIDs/aspirin	Reactive gastropathy, erosions, ulcers
Critical illness (ventilation >48 h, coagulopathy)	Stress-related mucosal disease
Bile reflux	Reactive gastropathy
Heavy alcohol use	Acute erosive/hemorrhagic gastropathy
Cigarette smoking	Progression of atrophic gastritis
High-salt diet	Progression of H. pylori gastritis
Age, male sex, family history of gastric cancer	Progression of atrophic gastritis
Psychological stress, caffeine, moderate alcohol	—

There is insufficient evidence to recommend routine screening for gastritis

There is insufficient evidence to recommend routine screening for gastritis.

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Gastritis may be seen as a commonly occurring inflammatory disease in many individuals. Gastritis usually persists throughout life and the chance of spontaneous healing is rare. Gastritis is mostl associated with the presence of Helicobacter pylori infection. The gastric mucosa undergoes inflammation and may lead to atrophic gastritis. Chronic gastritis is a condition which is commonly observed as a manifestation of pathogenesis of many gastric disease conditions. Gastric secretory functions are usually impaired due to the gastric mucosa undergoing inflammation and atrophy. 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 further conditions such as the peptic ulcer disease. 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 for gastritis is majorly dependent upon the type of gastritis and etiological factors. In Acute gastirtis, the condition improves upon refraining from risk factors such as NSAIDs, alcohol, cigarette smoking, acidic food, and beverages. In Autoimmune gastirtis, prognosis is usually good for vitamin B12 deficiency when treated with cyanocobalamin therapy. Although in Autoimmune gastritis, there is an increased risk for carcinoid tumors and gastric adenocarcinoma. In Chronic gastirtis associated with Helicobacter pylori infection, the prognosis is good. The triple therapy regimen may not be effective when compared to quadruple bismuth-based regimen is has proven to be very effective comparatively. In individuals with Helicobacter pylori infection associated chronic gastritis, if left untreated may progress to develop peptic ulcer disease, adenocarcinoma and MALT lymphoma.

Gastritis is a common inflammatory disease. Gastritis usually persists throughout life and the chance of spontaneous healing 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. ^[1][2][3]

• Acute gastritis Complications:
  • Ulcer bleed
  • Bleeding as a result of gastric erosion
  • Anemia as a result of the bleeding from the ulcer or due to the gastric erosion
  • Gastric outlet obstruction

• Chronic gastritis Complications:
  • Atrophic gastritis
  • Peptic ulcers
  • Gastrointestinal Perforation
  • Gastrointestinal Bleeding
  • Anemia due to erosive gastritis
  • Stomach cancer
  • Vitamin B12 deficiency
  • Pernicious anemia
  • Increased risk of developing benign or malignant growths in the lining of the stomach.

• Atrophic gastritis Complications:
  • Atrophic gastirtis as a result of Helicobacter pylori infection:
    • Gastric ulceration
    • Gastric cancer (adenocarcinoma)
  • Atrophic gastritis as a result of atrophic gastritis due to Autoimmune gastritis:
    • Gastric polyp
    • Gastric cancer (adenocarcinoma)
    • Pernicious anemia

• Stress Induced gastritis Complications:
  • Rarely, stress-induced gastritis may lead to severe bleeding that can prove fatal and leads to a life-threatening situation.

• Helicobacter pylori-associated gastirtis Complications:
  • Chronic Helicobacter pylori-associated gastritis increases the risk for mucosa-associated lymphoid tissue (MALT) lymphoma.
  • Gastric and duodenal ulcers
  • Gastric adenocarcinoma
  • Pseudomembranous colitis following H. pylori treatment
  • B12 and iron deficiency anemia
  • Post Treatment complication of of Helicobacter pylori infection is Clostridium difficile infection

• 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. ^[4]
  • In Autoimmune gastritis, prognosis is usually good for vitamin B12 deficiency when treated with cyanocobalamin therapy. Although in autoimmune gastritis, there is an increased risk for carcinoid tumors and gastric adenocarcinoma. ^{[5] [6]}
  • In Chronic gastirtis associated with Helicobacter pylori infection, the prognosis is good.
    • The triple therapy regimen may not be effective when compared to quadruple bismuth-based regimen is has proven to be very effective comparatively. ^[7]
    • In individuals with Helicobacter pylori infection associated chronic gastritis, if left untreated may progress to develop peptic ulcer disease, adenocarcinoma and MALT lymphoma.

​