Gastritis

Table of Contents

1. How Gastritis Develops
2. Types: Erosive vs. Non-Erosive
3. Causes and Risk Factors
4. H. pylori and Gastritis
5. Symptoms
6. Diagnosis
7. Treatment
8. Dietary and Lifestyle Approaches
9. Autoimmune Gastritis
10. Complications
11. Key Research Papers
12. Connections
13. Featured Videos

How Gastritis Develops

Gastritis is inflammation of the gastric mucosa — the protective lining of the stomach. It is one of the most common digestive conditions worldwide, affecting people of all ages. The mucosa normally secretes a layer of mucus that shields the underlying tissue from stomach acid. When that barrier breaks down — through infection, medication use, or autoimmune attack — the acid begins to erode and inflame the lining.

Gastritis can be acute (sudden onset, usually short-lived) or chronic (slowly developing, often persisting for years without obvious symptoms). Both forms can cause permanent damage if left untreated. Chronic gastritis is particularly important because it can silently progress to intestinal metaplasia — a precancerous change — and ultimately to gastric cancer in a subset of patients.

Types: Erosive vs. Non-Erosive

Gastritis is broadly divided into two structural patterns based on what endoscopy and biopsy reveal:

• Erosive (reactive) gastritis — the mucosa develops visible sores or erosions. Common causes include nonsteroidal anti-inflammatory drugs (NSAIDs), alcohol, stress (physiologic), and bile reflux. Erosions can bleed, sometimes severely. The Sydney System classifies erosive gastritis by location (antrum, body, fundus) and severity.
• Non-erosive gastritis — the stomach lining looks grossly normal on endoscopy but biopsy reveals inflammatory cell infiltration. Helicobacter pylori infection is the dominant cause worldwide. Autoimmune gastritis also falls here: it targets the acid-secreting parietal cells in the body and fundus but spares the antrum.

A second axis of classification uses histology:

• Type A gastritis — autoimmune; involves the body/fundus; leads to achlorhydria and intrinsic-factor deficiency.
• Type B gastritis — H. pylori-driven; predominantly affects the antrum but can spread to the corpus over decades.
• Type C (chemical/reactive) gastritis — caused by nonsteroidal anti-inflammatory drugs, alcohol, or bile; typically antral with foveolar hyperplasia.

Causes and Risk Factors

• Helicobacter pylori infection — the leading global cause; colonizes up to 44% of the world population and is responsible for roughly 90% of duodenal ulcers and 60–80% of gastric ulcers.
• Nonsteroidal anti-inflammatory drugs (NSAIDs) — aspirin, ibuprofen, naproxen, and ketorolac inhibit cyclooxygenase-1 (COX-1), reducing prostaglandin synthesis. Prostaglandins (especially PGE2) stimulate mucus and bicarbonate secretion and promote mucosal blood flow. Without them, the stomach becomes vulnerable to acid injury. Risk is dose-dependent and increased with concurrent corticosteroids, anticoagulants, or advanced age.
• Alcohol — directly disrupts the mucosal barrier and stimulates acid secretion.
• Physiologic stress — critically ill patients (mechanical ventilation, coagulopathy, burns) develop stress-related mucosal disease through reduced splanchnic blood flow.
• Autoimmune disease — the immune system attacks parietal cells (producing anti-parietal cell and anti-intrinsic factor antibodies).
• Bile reflux — duodenogastric reflux exposes the stomach to bile salts, causing chemical injury.
• Radiation — abdominal radiation damages mucosal cells.
• Other infections — cytomegalovirus (CMV), tuberculosis, and fungal infections can cause granulomatous gastritis in immunocompromised patients.

H. pylori and Gastritis

Helicobacter pylori is a gram-negative, spiral-shaped bacterium that colonizes the gastric antrum (and sometimes the corpus) by burrowing under the mucus layer and adhering to epithelial cells. It survives stomach acid by producing urease, which splits urea into ammonia — creating a local alkaline microenvironment. The ammonia itself, along with bacterial toxins (CagA, VacA), directly damages mucosal cells and triggers a chronic inflammatory response dominated by neutrophils and mononuclear cells.

Long-standing H. pylori infection follows the Correa cascade: chronic active gastritis → chronic atrophic gastritis → intestinal metaplasia → dysplasia → gastric adenocarcinoma. This cascade takes decades and only a minority of infected individuals progress to cancer, but the absolute numbers are large given how many people carry the bacterium.

Detecting H. pylori

• Urea breath test (UBT) — the gold standard non-invasive test. The patient drinks labeled urea (¹³C or ¹⁴C); if H. pylori is present, its urease splits the urea and labeled CO₂ appears in expired air within 20–30 minutes. Sensitivity 95–100%, specificity 91–98%. Proton pump inhibitors are stopped 2 weeks before testing because they cause false negatives.
• Stool antigen test (HpSA) — detects H. pylori antigens in feces. Sensitivity ~94%, specificity ~97%. Convenient for test-of-cure 4 weeks after treatment.
• Serology (immunoglobulin G (IgG) antibody) — detects prior exposure, not active infection; cannot confirm eradication. Useful only in low-prevalence populations with clinical suspicion.
• Endoscopic biopsy with rapid urease test (CLO test, for “Campylobacter-like organism”) — biopsy specimens from the antrum and corpus are placed in a urea-containing gel; a color change indicates urease activity. Results in 1–24 hours. Simultaneous histology adds sensitivity.
• Culture — rarely used clinically but allows antibiotic susceptibility testing; important in areas with high clarithromycin resistance.

H. pylori Eradication Regimens

Older guidelines (including the 2017 American College of Gastroenterology guideline) made clarithromycin-based triple therapy for 14 days the standard first-line regimen:

• Proton pump inhibitor (e.g., omeprazole 20 mg twice daily or esomeprazole 40 mg twice daily)
• Clarithromycin 500 mg twice daily
• Amoxicillin 1 g twice daily (or metronidazole 500 mg twice daily if penicillin allergy)

Eradication rates with 14-day triple therapy are 80–85% in low-resistance areas but drop significantly where clarithromycin resistance exceeds 15–20%. In those settings, bismuth quadruple therapy (proton pump inhibitor + bismuth + tetracycline + metronidazole) or concomitant therapy (adding metronidazole to standard triple) are preferred. Eradication is confirmed with a UBT or stool antigen test at least 4 weeks after completing antibiotics and 2 weeks after stopping proton pump inhibitors.

The 2024 American College of Gastroenterology (ACG) guideline changed first-line treatment in North America. For people never treated before, bismuth quadruple therapy for 14 days is the preferred regimen when it is not known which antibiotics the germ resists. Rifabutin triple therapy, or 14 days of dual therapy built on a newer type of acid blocker (a potassium-competitive acid blocker), are suitable alternatives for people without a penicillin allergy. The guideline states that salvage (retreatment) regimens containing clarithromycin or levofloxacin should only be used if antibiotic susceptibility is confirmed. The guideline also addresses testing everyone after treatment to confirm the germ is gone. In Europe, the 2022 Maastricht VI/Florence consensus report likewise describes continuously rising antibiotic resistance and calls for susceptibility testing and careful choice of first-line and rescue treatments.

Symptoms

Many patients with gastritis — including those with H. pylori or chronic atrophic gastritis — have no symptoms at all. When symptoms do occur they typically include:

• Epigastric pain or burning — the most common complaint; may worsen or improve with eating depending on the type
• Nausea and vomiting
• Bloating and early satiety
• Loss of appetite
• Hiccups
• Dark or tarry stools (melena) — signals upper gastrointestinal (GI) bleeding from erosions
• Vomiting blood (hematemesis) — urgent medical situation

Autoimmune gastritis specifically may present with symptoms of vitamin B12 deficiency (fatigue, numbness, cognitive changes) or iron-deficiency anemia before gastrointestinal symptoms appear, because parietal cell destruction reduces both intrinsic factor and acid needed for iron absorption.

Diagnosis

• Upper endoscopy (esophagogastroduodenoscopy, EGD) — the definitive diagnostic tool; allows direct visualization of mucosal erythema, erosions, ulcers, atrophy, and intestinal metaplasia. Biopsies from at least the antrum and corpus are taken to assess for H. pylori, atrophy grade, and metaplasia using the updated Sydney System.
• Histopathology — hematoxylin-and-eosin staining graded using OLGA (operative link for gastritis assessment) or OLGIM (operative link for gastric intestinal metaplasia) staging systems to stratify cancer risk.
• H. pylori testing — UBT, stool antigen, or biopsy-based as described above.
• Blood tests — complete blood count (anemia from bleeding or B12 deficiency), serum B12, iron studies, gastrin level (elevated in autoimmune gastritis due to achlorhydria), anti-parietal cell antibodies, anti-intrinsic factor antibodies.
• Pepsinogen I/II ratio — a non-invasive serum marker; a low PGI (<30 μg/L) and low PGI/PGII ratio (<3) suggest corpus atrophy. Used in population screening programs in Japan and parts of Europe.

Treatment

• H. pylori eradication — for all confirmed H. pylori-positive patients. See the eradication regimens above. Successful eradication heals gastritis in most patients, reduces ulcer recurrence by 80–90%, and reduces gastric cancer risk in early-stage atrophy.
• Proton pump inhibitors — suppress acid production; first-line for symptom relief, nonsteroidal anti-inflammatory drug (NSAID)-associated gastritis, and as a component of H. pylori eradication. Examples: omeprazole, esomeprazole, pantoprazole, lansoprazole. Proton pump inhibitors are most effective when taken 30 minutes before a meal.
• H2-receptor antagonists — famotidine, ranitidine (now withdrawn due to N-nitrosodimethylamine (NDMA) contamination); less potent than proton pump inhibitors but useful for mild or nocturnal symptoms.
• Antacids — aluminum hydroxide, magnesium hydroxide; provide immediate but short-lived neutralization of existing acid. Not disease-modifying.
• Cytoprotective agents — sucralfate (coats and protects ulcer bases), misoprostol (prostaglandin analog; co-prescribed with nonsteroidal anti-inflammatory drugs in high-risk patients to restore mucosal protection).
• Discontinuing causative agents — stopping nonsteroidal anti-inflammatory drugs, alcohol, and other irritants removes the cause. When nonsteroidal anti-inflammatory drugs cannot be stopped, a cyclooxygenase-2 (COX-2) selective inhibitor (e.g., celecoxib) combined with a proton pump inhibitor is a common substitute.
• B12 supplementation — for autoimmune gastritis with pernicious anemia: intramuscular cyanocobalamin 1 mg monthly or high-dose oral B12 (1000–2000 μg daily, which is absorbed by passive diffusion without intrinsic factor).
• Iron supplementation — intravenous (IV) iron may be needed if oral absorption is impaired by achlorhydria.

Dietary and Lifestyle Approaches

• Nonsteroidal anti-inflammatory drugs — a leading cause of gastritis (see Causes); acetaminophen is considered a safer pain reliever for most people with gastritis.
• Alcohol — even moderate intake can keep the stomach lining inflamed.
• Coffee and carbonated beverages — stimulate acid production; some people cut back to see whether symptoms improve.
• Smaller, more frequent meals — reduce the load on the stomach at any one time.
• Low-acid foods — people with gastritis often report tolerating oatmeal, bananas, cooked vegetables and plain proteins well; spicy foods, citrus, and tomato-based products worsen symptoms in many people.
• Lying down after eating — waiting 2–3 hours before lying down is commonly suggested to reduce reflux and bile regurgitation.
• Stress — psychological stress does not directly cause gastritis but can worsen symptoms and delay healing. Mindfulness, yoga, and cognitive behavioral therapy have supporting evidence for functional gastrointestinal disorders.
• Probiotics — Lactobacillus and Bifidobacterium strains have shown modest benefit as adjuncts to H. pylori eradication therapy, reducing side effects and possibly improving eradication rates. Evidence for use outside of eradication therapy is limited.
• Fermented foods — yogurt, kefir, natto, miso and tempeh are made by fermenting food with live microbes, and yogurt and kefir commonly carry Lactobacillus and Bifidobacterium strains. They are listed here as food sources of such microbes; the evidence above comes from probiotic supplements, not from these foods.

Autoimmune Gastritis

Autoimmune gastritis (formerly called Type A gastritis or fundic atrophic gastritis) results from T-cell-mediated destruction of parietal cells in the gastric body and fundus. Parietal cells produce both hydrochloric acid and intrinsic factor — the glycoprotein required for vitamin B12 absorption in the terminal ileum. Their destruction leads to two parallel deficiencies:

• Achlorhydria — absence of stomach acid; impairs absorption of non-heme iron, calcium, and certain drugs; may cause bacterial overgrowth in the stomach.
• Pernicious anemia — B12 deficiency causing megaloblastic anemia and potentially irreversible subacute combined degeneration of the spinal cord if untreated.

Anti-parietal cell antibodies (present in ~90% of patients) and anti-intrinsic factor antibodies (more specific, ~50–70%) confirm the diagnosis. Autoimmune gastritis is associated with other autoimmune conditions — particularly autoimmune thyroid disease (Hashimoto's thyroiditis), type 1 diabetes, and vitiligo.

Autoimmune gastritis carries a 3- to 6-fold increased risk of gastric neuroendocrine tumors (enterochromaffin-like (ECL) cell carcinoids, driven by hypergastrinemia) and a raised risk of gastric adenocarcinoma: a 2013 pooled analysis of 27 studies put stomach cancer risk in pernicious anaemia at about 6.8 times normal (0.27% per person per year), and its authors called for better studies to confirm it.

The 2021 American Gastroenterological Association (AGA) clinical practice update states that the best surveillance interval for autoimmune gastritis is unclear and should be decided person by person. It advises upper endoscopy to screen for type 1 gastric neuroendocrine tumors, endoscopy every 1–2 years after small tumors are removed, checking for iron and vitamin B12 deficiency, and screening for autoimmune thyroid disease, which commonly occurs alongside it.

Complications

• Peptic ulcer disease — erosive gastritis, especially H. pylori-associated, is the direct precursor to gastric and duodenal ulcers.
• Gastrointestinal bleeding — from erosions or ulcers; presents as melena or hematemesis; may require endoscopic hemostasis.
• Gastric atrophy and intestinal metaplasia — stepwise changes that increase gastric cancer risk following the Correa cascade.
• Gastric adenocarcinoma — H. pylori is classified as a Group 1 carcinogen by International Agency for Research on Cancer (IARC); a 2025 meta-analysis of 11 randomized trials and 13 observational studies found that eradication lowered gastric cancer in healthy carriers (relative risk 0.64, 8 trials) and in people treated endoscopically for early stomach neoplasia (relative risk 0.52, 3 trials), and lowered deaths from gastric cancer (relative risk 0.78, 5 trials).
• Gastric neuroendocrine tumors (Type 1 ECL carcinoids) — arise in the setting of chronic atrophic gastritis and hypergastrinemia; usually small and indolent but require surveillance.
• Pernicious anemia — the defining complication of autoimmune gastritis; easily treated with B12 but historically fatal before injectable B12 was available.
• Iron deficiency anemia — due to reduced acid (impairs non-heme iron reduction) or bleeding from erosions.

Key Research Papers

1. Marshall BJ, Warren JR. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet. 1984;1(8390):1311-1315. — PubMed PMID: 6145023 · doi:10.1016/S0140-6736(84)91816-6
2. Sipponen P, Maaroos HI. Chronic gastritis. Scand J Gastroenterol. 2015;50(6):657-667. — PubMed PMID: 25901896 · doi:10.3109/00365521.2015.1019918
3. Dixon MF, Genta RM, Yardley JH, Correa P. Classification and grading of gastritis: the updated Sydney System. Am J Surg Pathol. 1996;20(10):1161-1181. — PubMed PMID: 8827022 · doi:10.1097/00000478-199610000-00001
4. Chey WD, Leontiadis GI, Howden CW, Moss SF. ACG Clinical Guideline: Treatment of Helicobacter pylori Infection. Am J Gastroenterol. 2017;112(2):212-239. — PubMed PMID: 28071659 · doi:10.1038/ajg.2016.563
5. Rugge M, Genta RM; OLGA Group. Staging gastritis: an international proposal. Gastroenterology. 2005;129(5):1807-1808. — Search PubMed · doi:10.1053/j.gastro.2005.09.056
6. Malfertheiner P, Megraud F, O'Morain CA, et al. Management of Helicobacter pylori infection — the Maastricht V/Florence Consensus Report. Gut. 2017;66(1):6-30. — PubMed PMID: 27707777 · doi:10.1136/gutjnl-2016-312288
7. Uemura N, Okamoto S, Yamamoto S, et al. Helicobacter pylori infection and the development of gastric cancer. N Engl J Med. 2001;345(11):784-789. — PubMed PMID: 11556297 · doi:10.1056/NEJMoa001999
8. Lahner E, Annibale B. Pernicious anemia: new insights from a gastroenterological point of view. World J Gastroenterol. 2009;15(41):5121-5128. — PubMed PMID: 19891010 · doi:10.3748/wjg.15.5121
9. Lanas A, Chan FKL. Peptic ulcer disease. Lancet. 2017;390(10094):613-624. — PubMed PMID: 28242110 · doi:10.1016/s0140-6736(16)32404-7
10. Ford AC, Gurusamy KS, Delaney B, et al. Eradication therapy for peptic ulcer disease in Helicobacter pylori-positive people. Cochrane Database Syst Rev. 2016;4:CD003840. — PubMed PMID: 27092708 · doi:10.1002/14651858.CD003840.pub5
11. Sonnenberg A, Genta RM. Helicobacter pylori is a risk factor for colonic neoplasms. Am J Gastroenterol. 2013;108(2):208-215. — Search PubMed · doi:10.1038/ajg.2012.407
12. Sugano K, Tack J, Kuipers EJ, et al. Kyoto global consensus report on Helicobacter pylori gastritis. Gut. 2015;64(9):1353-1367. — PubMed PMID: 26187502 · doi:10.1136/gutjnl-2015-309252
13. Chey WD, Howden CW, Moss SF, Morgan DR, Greer KB, Grover S, Shah SC. ACG Clinical Guideline: Treatment of Helicobacter pylori Infection. Am J Gastroenterol. 2024;119(9):1730-1753. — PubMed PMID: 39626064 · doi:10.14309/ajg.0000000000002968
14. Malfertheiner P, Megraud F, Rokkas T, et al. Management of Helicobacter pylori infection: the Maastricht VI/Florence consensus report. Gut. 2022;71(9):1724-1762. — PubMed PMID: 35944925 · doi:10.1136/gutjnl-2022-327745
15. Shah SC, Piazuelo MB, Kuipers EJ, Li D. AGA Clinical Practice Update on the Diagnosis and Management of Atrophic Gastritis: Expert Review. Gastroenterology. 2021;161(4):1325-1332.e7. — PubMed PMID: 34454714 · doi:10.1053/j.gastro.2021.06.078
16. Vannella L, Lahner E, Osborn J, Annibale B. Systematic review: gastric cancer incidence in pernicious anaemia. Aliment Pharmacol Ther. 2013;37(4):375-382. — PubMed PMID: 23216458 · doi:10.1111/apt.12177
17. Ford AC, Yuan Y, Park JY, Forman D, Moayyedi P. Eradication Therapy to Prevent Gastric Cancer in Helicobacter pylori-Positive Individuals: Systematic Review and Meta-Analysis of Randomized Controlled Trials and Observational Studies. Gastroenterology. 2025;169(2):261-276. — PubMed PMID: 39824392 · doi:10.1053/j.gastro.2024.12.033

PubMed Topic Searches

Curated PubMed topic searches of peer-reviewed literature on gastritis. Each link opens a live PubMed query so you always see the most current studies.

1. PubMed: H. pylori gastritis eradication
2. PubMed: NSAID gastritis mucosal protection
3. PubMed: Autoimmune gastritis pernicious anemia
4. PubMed: Gastric intestinal metaplasia cancer risk
5. PubMed: OLGA/OLGIM staging gastritis
6. PubMed: PPI gastritis healing
7. PubMed: Urea breath test H. pylori
8. PubMed: Triple therapy peptic ulcer
9. PubMed: Correa cascade gastric cancer
10. PubMed: Stress gastritis critically ill

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Connections

• Gastroenterology
• Stomach Acid, pH & the Proton Pump Inhibitor Trade-off — interactive animation
• Digestion — interactive animation
• Peptic Ulcer Disease
• H. pylori: Ulcers and Gastritis
• Gastroesophageal Reflux Disease
• Barrett's Esophagus
• Pancreatitis
• Celiac Disease
• Crohn's Disease
• Inflammatory Bowel Disease
• Fatty Liver Disease (Non-Alcoholic Fatty Liver Disease/Metabolic Dysfunction-Associated Steatotic Liver Disease)
• Small Intestinal Bacterial Overgrowth
• Irritable Bowel Syndrome
• Gastric Cancer
• Zinc
• Vitamin B12
• Vitamin C
• Licorice Root (DGL)
• Herbs covered on this site that discuss this condition: Meadowsweet · Marshmallow Root · Black Pepper · Blessed Thistle · Horehound · Betel Leaf (Piper betle)

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