Gastritis risk factors
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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 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
- Risk factors differ by histologic entity:
- Distinguishing these entities matters because only inflammatory gastritis (particularly corpus-predominant or atrophic forms) carries meaningful long-term neoplastic risk.[1]
Established Risk Factors
Helicobacter pylori Infection
- 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]
Autoimmunity (Autoimmune Gastritis)
- 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]
NSAIDs and Aspirin
- 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]
Critical Illness (Stress-Related Mucosal Disease)
- 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]
Probable Risk Factors and Cofactors
- 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]
Controversial or Weakly Supported Factors
- 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]
Summary of Risk Factors
| 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 | — |
References
- ↑ 1.0 1.1 Rugge M, Genta RM, Malfertheiner P, Dinis-Ribeiro M, El-Serag H, Graham DY, Kuipers EJ, Leung WK, Park JY, Rokkas T, Schulz C, El-Omar EM (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). - ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 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). - ↑ 3.0 3.1 3.2 3.3 Bjarnason I, Scarpignato C, Holmgren E, Olszewski M, Rainsford KD, Lanas A (2018). "Mechanisms of Damage to the Gastrointestinal Tract From Nonsteroidal Anti-Inflammatory Drugs". Gastroenterology. 154 (3): 500–514. doi:10.1053/j.gastro.2017.10.049. PMID 29221664.
- ↑ 4.0 4.1 4.2 Washington MK, Peek RM Jr. Gastritis and gastropathy. In: Yamada's Textbook of Gastroenterology. Wiley-Blackwell; 2022.
- ↑ 5.0 5.1 Thrift AP, Wenker TN, El-Serag HB (2023). "Global burden of gastric cancer: epidemiological trends, risk factors, screening and prevention". Nat Rev Clin Oncol. 20: 338–349.
- ↑ 6.0 6.1 6.2 Huang RJ, Balasubramanian V, Shum MV, Ji HP, Hwang JH. Incidence of non-cardia gastric cancer among commercially-insured individuals aged 18-64 with chronic atrophic gastritis. PLoS One. 2024.
- ↑ 7.0 7.1 7.2 7.3 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). - ↑ 8.0 8.1 8.2 Patel et al. Gastric cancer: a review. JAMA. 2026.
- ↑ 9.0 9.1 Vakil N (2024). "Peptic Ulcer Disease: A Review". JAMA. 332 (21): 1832–1842. doi:10.1001/jama.2024.19094. PMID 39466269 Check
|pmid=value (help). - ↑ 10.0 10.1 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). - ↑ 11.0 11.1 11.2 11.3 11.4 Rustgi SD, Bijlani P, Shah SC (2021). "Autoimmune gastritis, with or without pernicious anemia: epidemiology, risk factors, and clinical management". Therap Adv Gastroenterol. 14: 17562848211038771. doi:10.1177/17562848211038771. PMID 34484423 Check
|pmid=value (help). - ↑ 12.0 12.1 Li et al. Helicobacter. 2025.
- ↑ 13.0 13.1 Lenti MV, et al. Autoimmune gastritis: emerging insights and clinical management. Nat Rev Gastroenterol Hepatol. 2026.
- ↑ 14.0 14.1 14.2 Wilcox CM, Allison J, Benzuly K, Borum M, Cryer B, Grosser T, Hunt R, Ladabaum U, Lanas A, Paulus H, Regueiro C, Sandler RS, Simon L (2006). "Consensus development conference on the use of nonsteroidal anti-inflammatory agents, including cyclooxygenase-2 enzyme inhibitors and aspirin". Clin Gastroenterol Hepatol. 4 (9): 1082–9. doi:10.1016/j.cgh.2006.04.010. PMID 16877048.
- ↑ 15.0 15.1 McConaghy JR, Decker A, Nair S (2023). "Peptic Ulcer Disease and Helicobacter pylori Infection". Am Fam Physician. 107 (2): 165–172.
- ↑ 16.0 16.1 16.2 16.3 16.4 Bardou M, Quenot JP, Barkun A (2015). "Stress-related mucosal disease in the critically ill patient". Nat Rev Gastroenterol Hepatol. 12 (2): 98–107. doi:10.1038/nrgastro.2014.235. PMID 25560847.
- ↑ 17.0 17.1 17.2 Cook DJ, Fuller HD, Guyatt GH, Marshall JC, Leasa D, Hall R, Winton TL, Rutledge F, Todd T, Roy P (1994). "Risk factors for gastrointestinal bleeding in critically ill patients". N Engl J Med. 330 (6): 377–81. doi:10.1056/NEJM199402103300601. PMID 8272140.
- ↑ 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.
- ↑ Lee et al. Dig Dis Sci. 2017.
- ↑ 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.
- ↑ "Exploring the interactions between Helicobacter pylori (Hp) infection and other risk factors of gastric cancer: a pooled analysis in the Stomach cancer Pooling (StoP) Project". Int J Cancer. 149 (6): 1228–1238. 2021. doi:10.1002/ijc.33678. PMID 33990950 Check
|pmid=value (help). - ↑ Feyisa ZT, Woldeamanuel BT. PLoS One. 2021.