Gastritis

Table of Contents

1. What Is Gastritis?
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. Research Papers
12. Connections
13. Featured Videos

What Is Gastritis?

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 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 NSAIDs, 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.
• NSAIDs (non-steroidal anti-inflammatory drugs) — aspirin, ibuprofen, naproxen, and ketorolac inhibit 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%. PPIs must be stopped 2 weeks before testing (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 (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) — 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: Triple Therapy

The standard first-line regimen in most guidelines is clarithromycin-based triple therapy for 14 days:

• 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 (PPI + bismuth + tetracycline + metronidazole) or concomitant therapy (adding metronidazole to standard triple) are preferred. Confirm eradication with a UBT or stool antigen test at least 4 weeks after completing antibiotics and 2 weeks after stopping PPIs.

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 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 GI symptoms appear, because parietal cell destruction reduces both intrinsic factor and acid needed for iron absorption.

Diagnosis

• Upper endoscopy (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 triple therapy 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 (PPIs) — suppress acid production; first-line for symptom relief, NSAID-associated gastritis, and as a component of H. pylori eradication. Examples: omeprazole, esomeprazole, pantoprazole, lansoprazole. PPIs are most effective when taken 30 minutes before a meal.
• H2-receptor antagonists — famotidine, ranitidine (now withdrawn due to NDMA contamination); less potent than PPIs 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 NSAIDs in high-risk patients to restore mucosal protection).
• Discontinuing causative agents — stopping NSAIDs, alcohol, and other irritants is essential. If NSAIDs cannot be stopped, switch to a COX-2 selective inhibitor (e.g., celecoxib) and add a PPI.
• 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 — IV iron may be needed if oral absorption is impaired by achlorhydria.

Dietary and Lifestyle Approaches

• Avoid NSAIDs — acetaminophen is a safer analgesic alternative for most patients with gastritis.
• Limit or eliminate alcohol — even moderate intake can perpetuate mucosal inflammation.
• Reduce coffee and carbonated beverages — stimulate acid production; limit to see if symptoms improve.
• Eat smaller, more frequent meals — reduces the load on the stomach at any one time.
• Choose low-acid, low-fat foods — oatmeal, bananas, lean proteins, cooked vegetables. Spicy foods, citrus, and tomato-based products worsen symptoms in many people.
• Don't lie down after eating — wait at least 2–3 hours to reduce reflux and bile regurgitation.
• Manage 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 GI 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.

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.

Surveillance endoscopy is recommended every 3–5 years because autoimmune gastritis carries a 3- to 6-fold increased risk of gastric neuroendocrine tumors (ECL-cell carcinoids, driven by hypergastrinemia) and a modestly elevated risk of gastric adenocarcinoma.

Complications

• Peptic ulcer disease — erosive gastritis, especially H. pylori-associated, is the direct precursor to gastric and duodenal ulcers.
• GI 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 IARC; eradication reduces cancer incidence by 33–47% in high-prevalence populations.
• 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. PMID: 6145023
2. Sipponen P, Maaroos HI. Chronic gastritis. Scand J Gastroenterol. 2015;50(6):657-667. PMID: 25901896
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. PMID: 8827022
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. PMID: 28071659
5. Rugge M, Genta RM; OLGA Group. Staging gastritis: an international proposal. Gastroenterology. 2005;129(5):1807-1808. PMID: 16285973
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. PMID: 27707777
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. PMID: 11556297
8. Lahner E, Annibale B. Pernicious anemia: new insights from a gastroenterological point of view. World J Gastroenterol. 2009;15(43):5395-5401. PMID: 19916167
9. Lanas A, Chan FKL. Peptic ulcer disease. Lancet. 2017;390(10094):613-624. PMID: 28242110
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. PMID: 27092708
11. Sonnenberg A, Genta RM. Helicobacter pylori is a risk factor for colonic neoplasms. Am J Gastroenterol. 2013;108(2):208-215. PMID: 23318483
12. Sugano K, Tack J, Kuipers EJ, et al. Kyoto global consensus report on Helicobacter pylori gastritis. Gut. 2015;64(9):1353-1367. PMID: 26187502

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Research Papers

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

• Peptic Ulcer Disease
• GERD
• Barrett's Esophagus
• Pancreatitis
• Celiac Disease
• Crohn's Disease
• Inflammatory Bowel Disease
• Fatty Liver Disease (NAFLD/MASLD)
• SIBO
• Irritable Bowel Syndrome
• Gastric Cancer
• Zinc
• Vitamin B12
• Vitamin C
• Licorice Root (DGL)

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