Gastritis causes
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Fahad Hasan, M.D.[2] Aravind Reddy Kothagadi M.B.B.S[3]
Overview
Gastritis is 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
Causes
Life-Threatening Causes
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]
Common Causes
- H. pylori infection[5]
- Autoimmune gastritis[6]
- NSAIDs and aspirin, which cause reactive gastropathy[1]
- Bile (duodenogastric) reflux[7]
Causes by Etiologic Category
Helicobacter pylori Infection
- 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
- 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]
Reactive (Chemical) Gastropathy
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]
Other Non-Infectious Gastritides
- 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]
Non–H. pylori Infectious Gastritis
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.
- Phlegmonous gastritis is caused by Streptococcus, Escherichia coli, Enterobacter, or Proteus.
- Fungal and parasitic:[1][4]
- Fungi: Candida, mucormycosis, histoplasmosis, aspergillosis
- Parasites: anisakiasis, strongyloidiasis
- These occur mainly with immunocompromise or exposure in endemic areas.
Physical, Caustic, and Ischemic Injury
- 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.
Etiologic Cofactors
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]
Summary of Etiologic Categories
| 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 |
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 Washington MK, Peek RM (2022). "Gastritis and gastropathy". Yamada's Textbook of Gastroenterology (7th ed.).
- ↑ 2.0 2.1 Sugano K, Tack J, Kuipers EJ; et al. (2015). "Kyoto global consensus report on Helicobacter pylori gastritis". Gut. 64 (9): 1353–67. doi:10.1136/gutjnl-2015-309252. PMID 26187502.
- ↑ 3.0 3.1 Rugge M, Genta RM, Malfertheiner P; et al. (2024). "RE.GA.IN.: the Real-world Gastritis Initiative—updating the updates". Gut. 73 (3): 407–441. doi:10.1136/gutjnl-2023-331164. PMID 38383142 Check
|pmid=value (help). - ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 Panarelli NC (2021). "Infectious diseases of the upper gastrointestinal tract". Histopathology. 78 (1). PMID 33382485 Check
|pmid=value (help). - ↑ 5.0 5.1 5.2 5.3 5.4 Malfertheiner P, Camargo MC, El-Omar E, Liou JM, Peek R, Schulz C, Smith SI, Suerbaum S (2023). "Helicobacter pylori infection". Nat Rev Dis Primers. 9 (1): 19. doi:10.1038/s41572-023-00431-8. PMID 37081005 Check
|pmid=value (help). - ↑ 6.0 6.1 6.2 6.3 6.4 Lenti MV, Rugge M, Lahner E, Miceli E, Toh BH, Genta RM, De Block C, Hershko C, Di Sabatino A (2020). "Autoimmune gastritis". Nat Rev Dis Primers. 6 (1): 56. doi:10.1038/s41572-020-0187-8. PMID 32647173 Check
|pmid=value (help). - ↑ 7.0 7.1 7.2 El-Zimaity H, Choi WT, Lauwers GY, Riddell R (2018). "The differential diagnosis of Helicobacter pylori negative gastritis". Virchows Arch. 473 (5): 533–550. doi:10.1007/s00428-018-2454-8. PMID 30229307.
- ↑ Suerbaum S, Michetti P (2002). "Helicobacter pylori infection". N Engl J Med. 347 (15): 1175–86. doi:10.1056/NEJMra020542. PMID 12374879.
- ↑ 9.0 9.1 9.2 Shah SC, Piazuelo MB, Kuipers EJ, Li D (2021). "AGA Clinical Practice Update on the Diagnosis and Management of Atrophic Gastritis: Expert Review". Gastroenterology. 161 (4): 1325–1332.e7. doi:10.1053/j.gastro.2021.06.078. PMID 34454714 Check
|pmid=value (help). - ↑ 10.0 10.1 10.2 Lenti MV, Miceli E, Vanoli A, Di Sabatino A (2026). "Autoimmune gastritis: emerging insights and clinical management". Nat Rev Gastroenterol Hepatol.
- ↑ Toh BH (2017). "Pathophysiology and laboratory diagnosis of pernicious anemia". Immunol Res. 65 (1): 326–330. doi:10.1007/s12026-016-8841-7. PMID 27538411.
- ↑ 12.0 12.1 Bergamaschi G, Di Sabatino A, Corazza GR (2018). "Pathogenesis, diagnosis and treatment of anaemia in immune-mediated gastrointestinal disorders". Br J Haematol. 182 (3): 319–329. doi:10.1111/bjh.15254.
- ↑ Kishikawa H, Nakamura K, Ojiro K, Katayama T, Arahata K, Takarabe S; et al. (2022). "Relevance of pepsinogen, gastrin, and endoscopic atrophy in the diagnosis of autoimmune gastritis". Sci Rep. 12 (1): 4202. doi:10.1038/s41598-022-07947-1. PMID 35273265 Check
|pmid=value (help). - ↑ 14.0 14.1 Rugge M, Savarino E, Sbaraglia M, Bricca L, Malfertheiner P (2021). "Gastritis: the clinico-pathological spectrum". Dig Liver Dis. 53 (10): 1237–1246. doi:10.1016/j.dld.2021.03.007. PMID 33785282 Check
|pmid=value (help). - ↑ 15.0 15.1 15.2 El-Zimaity H, Riddell RH (2021). "Beyond Helicobacter: dealing with other variants of gastritis—an algorithmic approach". Histopathology.
- ↑ Maguilnik I, Neumann WL, Sonnenberg A, Genta RM (2012). "Reactive gastropathy is associated with inflammatory conditions throughout the gastrointestinal tract". Aliment Pharmacol Ther. 36 (8): 736–43. doi:10.1111/apt.12031. PMID 22928604.
- ↑ Laine L (1996). "Nonsteroidal anti-inflammatory drug gastropathy". Gastrointest Endosc Clin N Am. 6 (3): 489–504. PMID 8803564.
- ↑ Nakamura M, Haruma K, Kamada T, Mihara M, Yoshihara M, Imagawa M; et al. (2001). "Duodenogastric reflux is associated with antral metaplastic gastritis". Gastrointest Endosc. 53 (1): 53–9. doi:10.1067/mge.2001.111385. PMID 11154489.
- ↑ 19.0 19.1 Franke A, Teyssen S, Singer MV (2005). "Alcohol-related diseases of the esophagus and stomach". Dig Dis. 23 (3–4): 204–13. doi:10.1159/000090167. PMID 16508284.
- ↑ Varbanova M, Frauenschläger K, Malfertheiner P (2014). "Chronic gastritis—an update". Best Pract Res Clin Gastroenterol. 28 (6): 1031–42. doi:10.1016/j.bpg.2014.10.005. PMID 25439069.
- ↑ Nakamura M, Haruma K, Kamada T, Mihara M, Yoshihara M, Sumioka M; et al. (2002). "Cigarette smoking promotes atrophic gastritis in Helicobacter pylori-positive subjects". Dig Dis Sci. 47 (3): 675–81. PMID 11911358.