Gastritis epidemiology and demographics
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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
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]
Epidemiology and Demographics
Helicobacter pylori–associated Gastritis
H. pylori is the most common cause of gastritis worldwide and the most common chronic bacterial infection in humans.[1]
Global Prevalence and Secular Trends
- 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]
| 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% |
United States
- 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]
Age and Birth-cohort Effect
- 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]
Sex
- Globally, H. pylori prevalence is modestly higher in men (OR ~1.12; 95% CI 1.09–1.15).[1]
Immigration
- 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]
Chronic Atrophic Gastritis
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:
- 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]
Autoimmune Gastritis
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]
Eosinophilic Gastritis
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]
Areas of Uncertainty
- 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]
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 Chey WD, Howden CW, Moss SF, Morgan DR, Greer KB, Grover S, Shah SC (2024). "ACG Clinical Guideline: Treatment of Helicobacter pylori Infection". Am J Gastroenterol. 119 (9): 1730–1753. doi:10.14309/ajg.0000000000002968. PMID 39626064 Check
|pmid=value (help). - ↑ 2.0 2.1 2.2 2.3 Chen YC, Malfertheiner P, Yu HT, Kuo CL, Chang YY, Meng FT, Wu YX, Hsiao JL, Chen MJ, Lin KP, Wu CY, Lin JT, O'Morain C, Megraud F, Lee WC, El-Omar EM, Wu MS, Liou JM (2024). "Global prevalence of Helicobacter pylori infection and incidence of gastric cancer between 1980 and 2022". Gastroenterology. 166 (4): 605–619. doi:10.1053/j.gastro.2023.12.022. PMID 38176660 Check
|pmid=value (help). - ↑ 3.0 3.1 3.2 3.3 3.4 Shah SC, Halvorson AE, Lee D, Bustamante R, McBay B, Gupta R, Denton J, Dorn C, Wilson O, Peek R Jr, Gupta S, Liu L, Hung A, Greevy R, Roumie CL (2024). "Helicobacter pylori burden in the United States according to individual demographics and geography: a nationwide analysis of the Veterans Healthcare System". Clin Gastroenterol Hepatol. doi:10.1016/j.cgh.2023.05.016. PMID 37245717 Check
|pmid=value (help). - ↑ 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 4.12 4.13 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). - ↑ 5.0 5.1 5.2 5.3 5.4 Li M, Huang Y, Liang X, Lu H. Prevalence of autoimmune gastritis worldwide: a systematic review and meta-analysis. Helicobacter. 2025.
- ↑ 6.0 6.1 6.2 Jensen ET, Martin CF, Kappelman MD, Dellon ES (2016). "Prevalence of eosinophilic gastritis, gastroenteritis, and colitis: estimates from a national administrative database". J Pediatr Gastroenterol Nutr. 62 (1): 36–42. doi:10.1097/MPG.0000000000000865. PMC 4654708. PMID 25988554.
- ↑ 7.0 7.1 7.2 Li Y, Choi H, Leung K, Jiang F, Graham DY, Leung WK (2023). "Global prevalence of Helicobacter pylori infection between 1980 and 2022: a systematic review and meta-analysis". Lancet Gastroenterol Hepatol. 8 (6): 553–564. doi:10.1016/S2468-1253(23)00070-5. PMID 37086739 Check
|pmid=value (help). - ↑ 8.0 8.1 8.2 8.3 Malfertheiner P, Camargo MC, El-Omar E, et al. (2023). "Helicobacter pylori infection". Nat Rev Dis Primers. 9 (1): 19. doi:10.1038/s41572-023-00431-8. PMID 37081005 Check
|pmid=value (help). - ↑ 9.0 9.1 9.2 9.3 Nguyen Wenker T, Peng FB, Emelogu I, Mallepally N, Kanwal F, El-Serag HB, Tan MC (2023). "The predictive performance of contemporary guideline recommendations for Helicobacter pylori testing in a United States population". Clin Gastroenterol Hepatol. 21 (7): 1771–1780.
- ↑ Yin Y, Liang H, Wei N, Zheng Z (2022). "Prevalence of chronic atrophic gastritis worldwide from 2010 to 2020: an updated systematic review and meta-analysis". Ann Palliat Med. 11 (12).
- ↑ Li J, Pan J, Xiao D, Shen N, Wang R, Miao H, Pu P, Zhang H, Yv X, Xing L (2024). "Chronic atrophic gastritis and risk of incident upper gastrointestinal cancers: a systematic review and meta-analysis". J Transl Med. 22. doi:10.1186/s12967-023-04736-w. PMID 38711123 Check
|pmid=value (help). - ↑ 12.0 12.1 Burke E, Harkins P, Arumugasamy M. Gastric atrophy and gastric cancer: a meta-analytical assessment of risk and the influence of topographical distribution. Eur J Gastroenterol Hepatol. 2026.
- ↑ 13.0 13.1 Huang RJ, Balasubramanian V, Shum MV, Ji HP, Hwang JH (2025). "Incidence of non-cardia gastric cancer among commercially-insured individuals aged 18–64 with chronic atrophic gastritis". PLoS One. 20: e0315833. doi:10.1371/journal.pone.0315833.
- ↑ 14.0 14.1 14.2 14.3 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). - ↑ 15.0 15.1 Lenti MV, Miceli E, Vanoli A, Di Sabatino A. Autoimmune gastritis: emerging insights and clinical management. Nat Rev Gastroenterol Hepatol. 2026.
- ↑ 16.0 16.1 16.2 16.3 Tan MC, Caskey KN, Lee IJ, et al. (2026). "Characteristics and incidence of gastric cancer among patients with autoimmune and non-autoimmune atrophic gastritis in a U.S. population". Dig Dis Sci. doi:10.1007/s10620-026-09800-1. PMID 41781724 Check
|pmid=value (help). - ↑ 17.0 17.1 17.2 17.3 Lenti MV, Rossi CM, Dellon ES, et al. Eosinophilic gastrointestinal diseases. Nat Rev Dis Primers. 2026.
- ↑ Rothenberg ME, Chehade M, Dellon ES, et al. Eosinophilic gastritis: burden of disease, diagnostic challenges and unmet needs. Gut. 2026.
- ↑ 19.0 19.1 19.2 Chehade M, Kamboj AP, Atkins D, Gehman LT (2021). "Diagnostic delay in patients with eosinophilic gastritis and/or duodenitis: a population-based study". J Allergy Clin Immunol Pract. 9 (5): 2050–2059.e20.