Atrophic Gastritis

Back

Background

Atrophic gastritis is a histopathologic entity characterized by chronic inflammation of the gastric mucosa with loss of gastric glandular cells and replacement by intestinal-type epithelium, pyloric-type glands, and fibrous tissue. Atrophy of the gastric mucosa is the endpoint of chronic processes, such as chronic gastritis associated with Helicobacter pylori infection, other unidentified environmental factors, and autoimmunity directed against gastric glandular cells. See the images below.


View Image

Atrophic gastritis. Helicobacter pylori chronic active gastritis (Genta stain, 20X). Multiple organisms (brown) are observed adhering to gastric surfa....


View Image

Atrophic gastritis. Intestinal metaplasia of the gastric mucosa (Genta stain, 20X). Intestinal-type epithelium with numerous goblet cells (stained blu....

The 2 main causes of atrophic gastritis result in distinct topographic types of gastritis, which can be distinguished histologically. H pylori- associated atrophic gastritis is usually a multifocal process that involves both the antrum and oxyntic mucosa of the gastric corpus and fundus, whereas autoimmune gastritis essentially is restricted to the gastric corpus and fundus. Individuals with autoimmune gastritis may develop pernicious anemia because of extensive loss of parietal cell mass and anti-intrinsic factor antibodies.

H pylori- associated atrophic gastritis is frequently asymptomatic, but individuals with this disease are at increased risk of developing gastric carcinoma, which may decrease following H pylori eradication.[1] Patients with chronic atrophic gastritis develop low gastric acid output and hypergastrinemia, which may lead to enterochromaffin-like (ECL) cell hyperplasia and carcinoid tumors.[2]

Pathophysiology

H pylori–associated atrophic gastritis

H pylori are gram-negative bacteria that colonize and infect the stomach. The bacteria lodge within the mucous layer of the stomach along the gastric surface epithelium and the upper portions of the gastric foveolae and rarely are present in the deeper glands (see the 3 images below).


View Image

Atrophic gastritis. Schematic representation of Helicobacter pylori–associated patterns of gastritis. Involvement of the corpus, fundus, and gastric a....


View Image

Patterns of atrophic gastritis associated with chronic Helicobacter pylori infection and autoimmune gastritis.


View Image

Atrophic gastritis. Helicobacter pylori chronic active gastritis (Genta stain, 20X). Multiple organisms (brown) are observed adhering to gastric surfa....

The infection is usually acquired during childhood and progresses over the lifespan of the individual if left untreated. The host response to the presence of H pylori is composed of a T-lymphocytic and B-lymphocytic response, followed by infiltration of the lamina propria and gastric epithelium by polymorphonuclear leukocytes (PMNs) that eventually phagocytize the bacteria.

Significant damage associated with the release of bacterial and inflammatory toxic products is inflicted on the gastric epithelial cells, resulting in increasing cell loss or gastric atrophy over time. Weck published a study supporting their hypothesis that the association between H pylori and chronic atrophic gastritis was greatly underestimated due to clearance of the infection in advanced stages of the disease.[3] These results suggest that the association is much stronger than estimated by most epidemiologic studies to date. Another study also reported that mannan-binding lectin allele (MBL2 codon 54 B) is associated with a higher risk of developing more severe gastric mucosal atrophy in H pylori -infected Japanese patients.[4]

During gastric mucosal atrophy, some glandular units develop an intestinal-type epithelium, and intestinal metaplasia eventually occurs in multiple foci throughout the gastric mucosa when atrophic gastritis is established. Other glands are simply replaced by fibrous tissue, resulting in an expanded lamina propria.[5] Loss of gastric glands in the corpus, or corpus atrophy, reduces parietal cell number, which results in significant functional changes with decreased levels of acid secretion and increased gastric pH. Recent studies have also reported that moderate alcohol consumption may be associated with atrophic gastritis by facilitating H pylori clearance.[6]

H pylori- associated chronic gastritis progresses with 2 main topographic patterns that have different clinicopathologic consequences.

The first is antral predominant gastritis. Inflammation that is mostly limited to the antrum characterizes antral predominant gastritis. Individuals with peptic ulcers usually develop this pattern of gastritis, and it is the most frequently observed pattern in Western countries.

The second is multifocal atrophic gastritis. Involvement of the corpus, fundus, and gastric antrum with progressive development of gastric atrophy (ie, loss of gastric glands) and partial replacement of gastric glands by intestinal-type epithelium (intestinal metaplasia) characterize multifocal atrophic gastritis. Individuals who develop gastric carcinoma and gastric ulcers usually have this pattern of gastritis. This pattern is observed more often in developing countries and in Asia.

Autoimmune atrophic gastritis

The development of chronic atrophic gastritis limited to corpus-fundus mucosa and marked diffuse atrophy of parietal and chief cells characterize autoimmune atrophic gastritis, as shown in the 2 following images.


View Image

Patterns of atrophic gastritis associated with chronic Helicobacter pylori infection and autoimmune gastritis.


View Image

Atrophic gastritis. Intestinal metaplasia of the gastric mucosa (Genta stain, 20X). Intestinal-type epithelium with numerous goblet cells (stained blu....

Autoimmune gastritis is associated with serum antiparietal and anti-intrinsic factor antibodies that cause intrinsic factor (IF) deficiency, which, in turn, causes decreased availability of cobalamin (vitamin B-12) and, eventually, pernicious anemia in some patients.

Palladino reported that methylenetetrahydrofolate reductase (MTHFR) polymorphisms may be associated with B12 deficiency and autoimmune atrophic gastritis.[7] Autoantibodies are directed against at least 3 antigens, including IF, cytoplasmic (microsomal-canalicular), and plasma membrane antigens. Two types of IF antibodies are detected (types I and II). Type I IF antibodies block the IF-cobalamin binding site, thus preventing the uptake of vitaminB-12. Cell-mediated immunity also contributes to the disease.[8]

T-cell lymphocytes infiltrate the gastric mucosa and contribute to the epithelial cell destruction and resulting gastric atrophy. Stummvoll reported that Th17 cells induced the most destructive disease with cellular infiltrates composed primarily of eosinophils accompanied by high levels of serum IgE.[9] Polyclonal Treg also suppresses the capacity of Th1 cells and moderately suppresses Th2 cells, but it can suppress Th17-induced disease only at early time points.

The major effect of Treg was to inhibit the expansion of the effector T cells. However, effector cells isolated from protected animals were not anergic and were fully competent to proliferate and produce effector cytokines ex vivo.[9] The strong inhibitory effect of polyclonal Treg on the capacity of some types of differentiated effector cells to induce disease provides an experimental basis for the clinical use of polyclonal Treg in the treatment of autoimmune disease in humans.

The above findings led to an interesting study by Huter et al, who reported that antigen-specific-induced Treg are potent suppressors of autoimmune gastritis induced by both fully differentiated Th1 and Th17 effector cells. The investigators analyzed the suppressive capacity of different types of Treg to suppress Th1- and Th17-mediated autoimmune gastritis by comparing nTreg with polyclonal TGFbeta-induced WT Treg (iTreg) or TGFbeta-induced antigen-specific TxA23 iTreg in cotransfer experiments with Th1 or Th17 TxA23 effector T cells.[10] Th1-mediated disease was prevented by cotransfer of nTreg and also antigen-specific iTreg, whereas WT iTreg did not show an effect. However, Th17-mediated disease was only suppressed by antigen-specific iTreg. Preactivation of nTreg in vitro before the transfer did not increase their suppressive activity in Th17-mediated gastritis, supporting the investigators' hypothesis.[10]

Epidemiology

Frequency

United States

The frequency of atrophic gastritis is not known because chronic gastritis frequently is asymptomatic; however, prevalence parallels the 2 main causes of gastric atrophy, chronic H pylori infection (when the infection follows a course of multifocal atrophic gastritis) and autoimmune gastritis. In both conditions, atrophic gastritis develops over many years and is found later in life. The frequency of H pylori infection in the United States is similar to that found in other Western countries. In the United States, H pylori infection affects approximately 20% of persons younger than 40 years and 50% of those older than 60 years. However, subgroups of different ethnic backgrounds show different frequencies for the infection, which is more common in Asian, Hispanic, and African American persons.

International

An estimated 50% of the world's population is infected with H pylori, and, therefore, chronic gastritis is extremely common. H pylori infection is highly prevalent in Asia and in developing countries, and multifocal atrophic gastritis is more prevalent in these areas of the world. Autoimmune gastritis is a relatively rare disease, most frequently observed in individuals of northern European descent and in African Americans. The prevalence of pernicious anemia resulting from autoimmune gastritis has been estimated as 127 cases per 100,000 members of the population in the United Kingdom, Denmark, and Sweden. The incidence of pernicious anemia is increased in patients with other immunological diseases, including Graves disease, myxedema, thyroiditis, and hypoparathyroidism.

Mortality/Morbidity

Mortality and morbidity associated with atrophic gastritis are related to specific clinicopathologic complications that may develop during the course of the underlying disease.

Race

Sex

Age

History

Atrophic gastritis represents the end stage of chronic gastritis, both infectious and autoimmune. In both cases, the clinical manifestations of atrophic gastritis are those of chronic gastritis, but pernicious anemia is observed specifically in patients with autoimmune gastritis and not in those with H pylori– associated atrophic gastritis.

Physical

Physical examination is of little contributory value in atrophic gastritis; however, some findings are associated specifically with the complications of H pylori– associated atrophic gastritis and autoimmune atrophic gastritis.

Causes

Atrophic gastritis usually is associated with either chronic H pylori infection or with autoimmune gastritis. The environmental subtype of atrophic gastritis corresponds mostly with H pylori– associated atrophic gastritis, although other unidentified environmental factors may play a role in the development of gastric atrophy. Yagi et al used magnifying endoscopy to distinguish atrophic gastritis caused by H pylori from autoimmune gastritis.[11]

Laboratory Studies

Procedures

Histologic Findings

H pylori–associated atrophic gastritis

H pylori –associated atrophic gastritis can display different levels of severity, as demonstrated in the following images.


View Image

Atrophic gastritis. Schematic representation of Helicobacter pylori–associated patterns of gastritis. Involvement of the corpus, fundus, and gastric a....


View Image

Patterns of atrophic gastritis associated with chronic Helicobacter pylori infection and autoimmune gastritis.


View Image

Atrophic gastritis. Helicobacter pylori chronic active gastritis (Genta stain, 20X). Multiple organisms (brown) are observed adhering to gastric surfa....


View Image

Atrophic gastritis. Intestinal metaplasia of the gastric mucosa (Genta stain, 20X). Intestinal-type epithelium with numerous goblet cells (stained blu....

H pylori organisms are found within the gastric mucous layer and frequently accumulate in groups of bacteria at the apical side of gastric surface cells, occasionally in the lower portions of the gastric foveolae, and rarely within the deeper areas of the mucosa in association with glandular cells.

Patients with typical infection initially develop chronic active gastritis, in which H pylori organisms are observed in both the antrum and corpus (usually more numerous in the antrum). PMNs infiltrate the lamina propria, glands, surface, and foveolar epithelium, occasionally spilling into the lumen and forming small microabscesses. Lymphoid aggregates and occasional well-developed lymphoid follicles are observed expanding the lamina propria of the mucosa, and occasional lymphocytes permeate the epithelium.

In disease of longer duration, significant loss of gastric glands is observed, which is known as gastric atrophy. Gastric atrophy may result from the loss of gastric epithelial cells that were not replaced by appropriate cell proliferation or from replacement of the epithelium by intestinal-type epithelium (intestinal metaplasia). In advanced stages of atrophy associated with chronic H pylori infection, both the corpus and antrum display extensive replacement by intestinal metaplasia, which is associated with the development of hypochlorhydria. With the expansion of intestinal metaplasia, the numbers of H pylori detectable in the stomach decrease because H pylori are excluded from areas of metaplastic epithelium. This end stage is known as atrophic gastritis.

Autoimmune atrophic gastritis

The histologic changes vary in different phases of autoimmune atrophic gastritis (see the 2 images below).


View Image

Patterns of atrophic gastritis associated with chronic Helicobacter pylori infection and autoimmune gastritis.


View Image

Atrophic gastritis. Intestinal metaplasia of the gastric mucosa (Genta stain, 20X). Intestinal-type epithelium with numerous goblet cells (stained blu....

During the early phase, multifocal diffuse infiltration of the lamina propria by mononuclear cells and eosinophils occurs, as does focal T-cell infiltration of oxyntic glands with glandular destruction. Focal mucous neck cell hyperplasia (ie, pseudopyloric metaplasia) and hypertrophic changes of parietal cells also are observed.

During the florid phase of the disease, increased lymphocytic inflammation, oxyntic gland atrophy, and focal intestinal metaplasia occur. Diffuse involvement of the gastric corpus and fundus by chronic atrophic gastritis associated with intestinal metaplasia characterizes the end stage. Some patients present with gastric polyps, mostly nonneoplastic hyperplastic polyps and polypoid areas of preserved islands of relatively normal oxyntic mucosa that may appear polypoid endoscopically. The antrum is spared.

Medical Care

Once atrophic gastritis is diagnosed, treatment can be directed (1) to eliminate the causal agent, which is a possibility in cases of H pylori– associated atrophic gastritis; (2) to correct complications of the disease, especially in patients with autoimmune atrophic gastritis who develop pernicious anemia (in whom vitamin B-12 replacement therapy is indicated); or (3) to attempt to revert the atrophic process.

No consensus from different studies exists regarding the reversibility of atrophic gastritis; however, removal of H pylori from the already atrophic stomach may block further progression of the disease. Until recently, specific recommendations for H pylori eradication were limited to peptic ulcer disease. At the Digestive Health Initiative International Update Conference on H pylori held in the United States, the recommendations for H pylori testing and treatment were broadened. H pylori testing and eradication of the infection also were recommended after resection of early gastric cancer and for low-grade mucosa-associated lymphoid tissue lymphoma.

If H pylori is identified as the underlying cause of gastritis, subsequent eradication now is almost generally accepted practice. Protocols for H pylori eradication require a combination of antimicrobial agents and antisecretory agents, such as a proton pump inhibitors (PPIs), ranitidine bismuth citrate (RBC), or bismuth subsalicylate. Despite the combinatorial effect of drugs in regimens used to treat H pylori infection, cure rates remain, at best, 80-95%.

Lack of patient compliance and antimicrobial resistance are the most important factors influencing poor outcome. Currently, the most widely used and efficient therapies to eradicate H pylori are triple therapies (recommend as first-line treatments) and quadruple therapies (recommended as second-line treatment when triple therapies fail to eradicate H pylori). In both cases, best results are achieved by administering therapy for 10-14 days, although some studies have limited the duration of treatment to 7 days. The accepted definition of cure is no evidence of H pylori 4 or more weeks after ending the antimicrobial therapy.

Medication Summary

Best results are achieved with 10- to 14-day protocols using combination therapies, with eradication in 80-95% of the cases.

Amoxicillin (Amoxil, Trimox)

Clinical Context:  Semisynthetic penicillin, an analogue of ampicillin. Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.

Clarithromycin (Biaxin)

Clinical Context:  Semisynthetic macrolide antibiotic. Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Tetracycline (Sumycin)

Clinical Context:  Treats gram-positive and gram-negative organisms and mycoplasmal, chlamydial, and rickettsial infections. Inhibits bacterial protein synthesis by binding with 30S and possibly 50S ribosomal subunit(s). Yellow, odorless, crystalline powder. Potency is affected in solutions of pH < 2.0 and is destroyed rapidly by alkali hydroxide solutions.

Metronidazole (Flagyl)

Clinical Context:  Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Used in combination with other antimicrobial agents (except for C difficile enterocolitis).

Class Summary

Antimicrobial activity against most H pylori strains. Rare resistant strains have been reported.

Omeprazole (Prilosec)

Clinical Context:  Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ -ATP pump.

Lansoprazole (Prevacid)

Clinical Context:  Decreases gastric acid secretion by inhibiting parietal cell H+/K+ -ATP pump.

Esomeprazole (Nexium)

Clinical Context:  S-isomer of omeprazole. Inhibits gastric acid secretion by inhibiting H+/K+-ATPase enzyme system at secretory surface of gastric parietal cells.

Class Summary

A substituted benzimidazole (a compound that inhibits gastric acid secretion) is the active ingredient. PPIs do not exhibit anticholinergic or H2 antagonistic activities but suppress acid secretion by specific inhibition of the H+/K+ -ATPase enzyme system on the secretory surface of parietal cells.

Bismuth subsalicylate (Bismatrol, Pepto-Bismol)

Clinical Context:  Highly insoluble salt of trivalent bismuth and salicylic acid. More than 80% of salicylic acid is absorbed from oral doses of bismuth subsalicylate chewable tabs.

Ranitidine bismuth citrate (Tritec)

Clinical Context:  Combination of ranitidine (inhibits H2 receptor in gastric parietal cells, which reduces gastric acid secretion, gastric volume, and hydrogen concentrations) and bismuth citrate. Do not administer as monotherapy.

Administer 30 min prior to sucralfate.

Class Summary

The components of bismuth-containing therapies, including bismuth subsalicylate, metronidazole, clarithromycin, and tetracycline, individually have demonstrated in vitro activity against most susceptible strains of H pylori.

Further Outpatient Care

Deterrence/Prevention

Complications

Prognosis

Author

Antonia R Sepulveda, MD, PhD, Professor of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine; Director of Surgical Pathology, Department of Pathology and Laboratory Medicine, Hospital of the University of Pennsylvania

Disclosure: Genentech Honoraria Consulting; Leica Honoraria Consulting

Coauthor(s)

Sandeep Mukherjee, MB, BCh, MPH, FRCPC, Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center

Disclosure: Merck Honoraria Speaking and teaching; Ikaria Pharmaceuticals Honoraria Board membership

Specialty Editors

Gregory William Rutecki, MD, Professor of Medicine, Fellow of The Center for Bioethics and Human Dignity, University of South Alabama College of Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Simmy Bank, MD, Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine

Disclosure: Nothing to disclose.

Alex J Mechaber, MD, FACP, Senior Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine

Disclosure: Nothing to disclose.

References

  1. Yanaoka K, Oka M, Ohata H, et al. Eradication of Helicobacter pylori prevents cancer development in subjects with mild gastric atrophy identified by serum pepsinogen levels. Int J Cancer. Dec 1 2009;125(11):2697-703. [View Abstract]
  2. Vannella L, Lahner E, Annibale B. Risk for gastric neoplasias in patients with chronic atrophic gastritis: a critical reappraisal. World J Gastroenterol. Mar 28 2012;18(12):1279-85. [View Abstract]
  3. Weck MN, Gao L, Brenner H. Helicobacter pylori infection and chronic atrophic gastritis: associations according to severity of disease. Epidemiology. Jul 2009;20(4):569-74. [View Abstract]
  4. Tahara T, Shibata T, Wang FY, et al. Mannan-binding lectin B allele is associated with a risk of developing more severe gastric mucosal atrophy in Helicobacter pylori-infected Japanese patients. Eur J Gastroenterol Hepatol. Jul 2009;21(7):781-6. [View Abstract]
  5. Gao L, Weck MN, Nieters A, Brenner H. Inverse association between a pro-inflammatory genetic profile and Helicobacter pylori seropositivity among patients with chronic atrophic gastritis: Enhanced elimination of the infection during disease progression?. Eur J Cancer. May 7 2009;[View Abstract]
  6. Gao L, Weck MN, Stegmaier C, Rothenbacher D, Brenner H. Alcohol consumption and chronic atrophic gastritis: Population-based study among 9,444 older adults from Germany. Int J Cancer. Jun 2 2009;[View Abstract]
  7. Palladino M, Chiusolo P, Reddiconto G, et al. MTHFR polymorphisms involved in vitamin B12 deficiency associated with atrophic gastritis. Biochem Genet. Oct 2009;47(9-10):645-50. [View Abstract]
  8. Lahner E, Norman GL, Severi C, et al. Reassessment of intrinsic factor and parietal cell autoantibodies in atrophic gastritis with respect to cobalamin deficiency. Am J Gastroenterol. Aug 2009;104(8):2071-9. [View Abstract]
  9. Stummvoll GH, DiPaolo RJ, Huter EN, et al. Th1, Th2, and Th17 effector T cell-induced autoimmune gastritis differs in pathological pattern and in susceptibility to suppression by regulatory T cells. J Immunol. Aug 1 2008;181(3):1908-16. [View Abstract]
  10. Huter EN, Stummvoll GH, DiPaolo RJ, Glass DD, Shevach EM. Pre-differentiated Th1 and Th17 effector T cells in autoimmune gastritis: Ag-specific regulatory T cells are more potent suppressors than polyclonal regulatory T cells. Int Immunopharmacol. May 2009;9(5):540-5. [View Abstract]
  11. Yagi K, Nakamura A, Sekine A, Graham D. Features of the atrophic corpus mucosa in three cases of autoimmune gastritis revealed by magnifying endoscopy. Case Report Med. 2012;2012:368160. [View Abstract]
  12. Capella C, Fiocca R, Cornaggia M. Autoimmune gastritis. In: Graham DY, Genta RM, Dixon MF, eds. Gastritis. Philadelphia, Pa: Lippincott Williams; 1999:79-96.
  13. Correa P. Human gastric carcinogenesis: a multistep and multifactorial process-- First American Cancer Society Award Lecture on Cancer Epidemiology and Prevention. Cancer Res. Dec 15 1992;52(24):6735-40. [View Abstract]
  14. Dixon MF, Genta RM, Yardley JH. Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. Am J Surg Pathol. Oct 1996;20(10):1161-81. [View Abstract]
  15. Dore MP, Leandro G, Realdi G, Sepulveda AR, Graham DY. Effect of pretreatment antibiotic resistance to metronidazole and clarithromycin on outcome of Helicobacter pylori therapy: a meta-analytical approach. Dig Dis Sci. Jan 2000;45(1):68-76. [View Abstract]
  16. Franceschi F, Genta RM, Sepulveda AR. Gastric mucosa: long-term outcome after cure of Helicobacter pylori infection. J Gastroenterol. 2002;37 Suppl 13:17-23. [View Abstract]
  17. Gao L, Weck MN, Raum E, et al. Sibship size, Helicobacter pylori infection and chronic atrophic gastritis: a population-based study among 9444 older adults from Germany. Int J Epidemiol. Jul 13 2009;epub ahead of print. [View Abstract]
  18. Graham DY. Therapy of Helicobacter pylori: current status and issues. Gastroenterology. Feb 2000;118(2 Suppl 1):S2-8. [View Abstract]
  19. Graham DY, Belson G, Abudayyeh S, et al. Twice daily (mid-day and evening) quadruple therapy for H. pylori infection in the United States. Dig Liver Dis. Jun 2004;36(6):384-7. [View Abstract]
  20. Hershko C, Hoffbrand AV, Keret D, et al. Role of autoimmune gastritis, Helicobacter pylori and celiac disease in refractory or unexplained iron deficiency anemia. Haematologica. May 2005;90(5):585-95. [View Abstract]
  21. Inoue T, Uedo N, Ishihara R, et al. Autofluorescence imaging videoendoscopy in the diagnosis of chronic atrophic fundal gastritis. J Gastroenterol. Oct 30 2009;epub ahead of print. [View Abstract]
  22. Konturek PC, Konturek SJ, Brzozowski T. Helicobacter pylori infection in gastric cancerogenesis. J Physiol Pharmacol. Sep 2009;60(3):3-21. [View Abstract]
  23. Krasinskas AM, Abraham SC, Metz DC, et al. Oxyntic mucosa pseudopolyps: a presentation of atrophic autoimmune gastritis. Am J Surg Pathol. Feb 2003;27(2):236-41. [View Abstract]
  24. Laiyemo AO, Kamangar F, Marcus PM, et al. Atrophic gastritis and the risk of incident colorectal cancer. Cancer Causes Control. Oct 17 2009;epub ahead of print. [View Abstract]
  25. Leung WK, Kim JJ, Kim JG. Microsatellite instability in gastric intestinal metaplasia in patients with and without gastric cancer. Am J Pathol. Feb 2000;156(2):537-43. [View Abstract]
  26. Malfertheiner P, Megraud F, O'Morain C, et al. Current concepts in the management of Helicobacter pylori infection--the Maastricht 2-2000 Consensus Report. Aliment Pharmacol Ther. Feb 2002;16(2):167-80. [View Abstract]
  27. Rugge M, Genta RM. Staging and grading of chronic gastritis. Hum Pathol. Mar 2005;36(3):228-33. [View Abstract]
  28. Shin CM, Kim N, Lee HS, et al. Validation of diagnostic tests for Helicobacter pylori with regard to grade of atrophic gastritis and/or intestinal metaplasia. Helicobacter. Dec 2009;14(6):512-9. [View Abstract]
  29. Sipponen P, Harkonen M, Alanko A, et al. Diagnosis of atrophic gastritis from a serum sample. Clin Lab. 2002;48(9-10):505-15. [View Abstract]
  30. Vaananen H, Vauhkonen M, Helske T, et al. Non-endoscopic diagnosis of atrophic gastritis with a blood test. Correlation between gastric histology and serum levels of gastrin-17 and pepsinogen I: a multicentre study. Eur J Gastroenterol Hepatol. Aug 2003;15(8):885-91. [View Abstract]
  31. Whittingham S, Mackay IR. Autoimmune gastritis: historical antecedents, outstanding discoveries, and unresolved problems. Int Rev Immunol. Jan-Apr 2005;24(1-2):1-29. [View Abstract]

Atrophic gastritis. Helicobacter pylori chronic active gastritis (Genta stain, 20X). Multiple organisms (brown) are observed adhering to gastric surface epithelial cells. A mononuclear lymphoplasmacytic and polymorphonuclear cell infiltrate is observed in the mucosa.

Atrophic gastritis. Intestinal metaplasia of the gastric mucosa (Genta stain, 20X). Intestinal-type epithelium with numerous goblet cells (stained blue with the Alcian blue stain) replace the gastric mucosa and represent gastric atrophy. Mild chronic inflammation is observed in the lamina propria. This pattern of atrophy is observed both in Helicobacter pylori–associated atrophic gastritis and autoimmune gastritis.

Atrophic gastritis. Schematic representation of Helicobacter pylori–associated patterns of gastritis. Involvement of the corpus, fundus, and gastric antrum, with progressive development of gastric atrophy as a result of loss of gastric glands and partial replacement of gastric glands by intestinal-type epithelium, or intestinal metaplasia (represented by the blue areas in the diagram) characterize multifocal atrophic gastritis. Individuals who develop gastric carcinoma and gastric ulcers usually present with this pattern of gastritis. Inflammation mostly limited to the antrum characterizes antral-predominant gastritis. Individuals with peptic ulcers usually develop this pattern of gastritis, and it is the most frequent pattern in Western countries.

Patterns of atrophic gastritis associated with chronic Helicobacter pylori infection and autoimmune gastritis.

Atrophic gastritis. Helicobacter pylori chronic active gastritis (Genta stain, 20X). Multiple organisms (brown) are observed adhering to gastric surface epithelial cells. A mononuclear lymphoplasmacytic and polymorphonuclear cell infiltrate is observed in the mucosa.

Patterns of atrophic gastritis associated with chronic Helicobacter pylori infection and autoimmune gastritis.

Atrophic gastritis. Intestinal metaplasia of the gastric mucosa (Genta stain, 20X). Intestinal-type epithelium with numerous goblet cells (stained blue with the Alcian blue stain) replace the gastric mucosa and represent gastric atrophy. Mild chronic inflammation is observed in the lamina propria. This pattern of atrophy is observed both in Helicobacter pylori–associated atrophic gastritis and autoimmune gastritis.

Atrophic gastritis. Schematic representation of Helicobacter pylori–associated patterns of gastritis. Involvement of the corpus, fundus, and gastric antrum, with progressive development of gastric atrophy as a result of loss of gastric glands and partial replacement of gastric glands by intestinal-type epithelium, or intestinal metaplasia (represented by the blue areas in the diagram) characterize multifocal atrophic gastritis. Individuals who develop gastric carcinoma and gastric ulcers usually present with this pattern of gastritis. Inflammation mostly limited to the antrum characterizes antral-predominant gastritis. Individuals with peptic ulcers usually develop this pattern of gastritis, and it is the most frequent pattern in Western countries.

Patterns of atrophic gastritis associated with chronic Helicobacter pylori infection and autoimmune gastritis.

Atrophic gastritis. Helicobacter pylori chronic active gastritis (Genta stain, 20X). Multiple organisms (brown) are observed adhering to gastric surface epithelial cells. A mononuclear lymphoplasmacytic and polymorphonuclear cell infiltrate is observed in the mucosa.

Atrophic gastritis. Intestinal metaplasia of the gastric mucosa (Genta stain, 20X). Intestinal-type epithelium with numerous goblet cells (stained blue with the Alcian blue stain) replace the gastric mucosa and represent gastric atrophy. Mild chronic inflammation is observed in the lamina propria. This pattern of atrophy is observed both in Helicobacter pylori–associated atrophic gastritis and autoimmune gastritis.

Patterns of atrophic gastritis associated with chronic Helicobacter pylori infection and autoimmune gastritis.

Atrophic gastritis. Intestinal metaplasia of the gastric mucosa (Genta stain, 20X). Intestinal-type epithelium with numerous goblet cells (stained blue with the Alcian blue stain) replace the gastric mucosa and represent gastric atrophy. Mild chronic inflammation is observed in the lamina propria. This pattern of atrophy is observed both in Helicobacter pylori–associated atrophic gastritis and autoimmune gastritis.

Atrophic gastritis. Schematic representation of Helicobacter pylori–associated patterns of gastritis. Involvement of the corpus, fundus, and gastric antrum, with progressive development of gastric atrophy as a result of loss of gastric glands and partial replacement of gastric glands by intestinal-type epithelium, or intestinal metaplasia (represented by the blue areas in the diagram) characterize multifocal atrophic gastritis. Individuals who develop gastric carcinoma and gastric ulcers usually present with this pattern of gastritis. Inflammation mostly limited to the antrum characterizes antral-predominant gastritis. Individuals with peptic ulcers usually develop this pattern of gastritis, and it is the most frequent pattern in Western countries.

Patterns of atrophic gastritis associated with chronic Helicobacter pylori infection and autoimmune gastritis.

Atrophic gastritis. Helicobacter pylori chronic active gastritis (Genta stain, 20X). Multiple organisms (brown) are observed adhering to gastric surface epithelial cells. A mononuclear lymphoplasmacytic and polymorphonuclear cell infiltrate is observed in the mucosa.

Atrophic gastritis. Intestinal metaplasia of the gastric mucosa (Genta stain, 20X). Intestinal-type epithelium with numerous goblet cells (stained blue with the Alcian blue stain) replace the gastric mucosa and represent gastric atrophy. Mild chronic inflammation is observed in the lamina propria. This pattern of atrophy is observed both in Helicobacter pylori–associated atrophic gastritis and autoimmune gastritis.

Marked gastric atrophy of the stomach body.

Severe gastric atrophy of the stomach antrum.