AUTHOR AND EDITOR INFORMATION

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• Workup
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• Follow-up
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INTRODUCTION

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Background

Atrophic gastritis is a histopathological 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.

The 2 main causes of atrophic gastritis result in distinct topographic types of gastritis, which can be distinguished histologically. H pylori–associated atrophic gastritis usually is a multifocal process that involves both the antrum and oxyntic mucosa of the gastric corpus and fundus, while 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 frequently is asymptomatic, but individuals with this disease are at increased risk of developing gastric carcinoma. Patients with chronic atrophic gastritis develop low gastric acid output and hypergastrinemia, which may lead to enterochromaffin-like (ECL) cell hyperplasia and carcinoid tumors.

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 Media files 1-3). The infection usually is 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. 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 simply are replaced by fibrous tissue, resulting in an expanded lamina propria. 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.

H pylori–associated chronic gastritis progresses with 2 main topographic patterns that have different clinicopathological 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 (see Media file 2, Media file 4). Autoimmune gastritis is associated with serum antiparietal and antiintrinsic 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. 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 vitamin B-12. Cell-mediated immunity also contributes to the disease. T-cell lymphocytes infiltrate the gastric mucosa and contribute to the epithelial cell destruction and resulting gastricatrophy.

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 clinicopathological complications that may develop during the course of the underlying disease.

• Similar to other individuals infected with H pylori, patients who develop atrophic gastritis may complain of dyspeptic symptoms. Individuals with either H pylori–associated atrophic gastritis or autoimmune atrophic gastritis or autoimmune atrophic gastritis carry an increased risk of developing gastric carcinoid tumors and gastric carcinoma.
• The major effects of autoimmune gastritis are consequences of the loss of parietal and chief cells and include achlorhydria, hypergastrinemia, loss of pepsin and pepsinogen, anemia, and an increased risk of gastric neoplasms.
• Autoimmune atrophic gastritis represents the most frequent cause of pernicious anemia in temperate climates. The risk of gastric adenocarcinoma appears to be at least 2.9 times higher in patients with pernicious anemia than in the general population. A recent study also reported an increased frequency of esophageal squamous carcinomas in patients with pernicious anemia.
• Autoimmune atrophic gastritis and H pylori gastritis may also have a significant role in the development of unexplained or refractory iron deficient anemia.

Race

• H pylori–associated atrophic gastritis appears to be more common among Asian and Hispanic persons than people of other races.
• In the United States, H pylori infection is more common among African Americans than white persons, a difference attributed to socioeconomic factors. However, whether higher rates of H pylori–associated atrophic gastritis are observed among African Americans has not been established.
• Autoimmune atrophic gastritis is more frequent in individuals of northern European descent and African Americans and is much less frequent in southern Europeans and Asians.

Sex

• Atrophic gastritis affects both sexes similarly.
• H pylori infection affects both sexes to the same extent.
• Autoimmune gastritis has been reported to affect both sexes, with a female-to-male ratio of 3:1.

Age

• Atrophic gastritis is detected late in life because it results from the effects of long-standing damage to the gastric mucosa.
• H pylori–associated atrophic gastritis develops gradually, but extensive multifocal atrophy usually is detected in individuals older than 50 years.
• Patients with autoimmune atrophic gastritis usually present with pernicious anemia, which typically is diagnosed in individuals aged approximately 60 years; however, pernicious anemia can be detected in children (juvenile pernicious anemia).

CLINICAL

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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.

• Acute H pylori infection usually is not detected clinically, but experimental infection results in a clinical syndrome characterized by epigastric pain, fullness, nausea, vomiting, flatulence, malaise, and, sometimes, fever. The symptoms resolve in approximately a week, regardless of whether H pylori organisms are eliminated.
• Persistence of the organism causes H pylori chronic gastritis, which usually is asymptomatic or may manifest as gastric pain and, rarely, nausea, vomiting, anorexia, or significant weight loss. Symptoms associated with complications of chronic H pylori–associated atrophic gastritis may develop, including gastric ulcers and gastric adenocarcinoma.
• Autoimmune atrophic gastritis clinical manifestations primarily are related to deficiency in cobalamin, which is not absorbed adequately because of IF deficiency resulting from severe gastric parietal cell atrophy. The disease has an insidious onset and progresses slowly. Cobalamin deficiency affects the hematological, GI, and neurologic systems.
• • Hematologic manifestations: The most significant manifestation is megaloblastic anemia, but, rarely, purpura due to thrombocytopenia may develop. Symptoms of anemia include weakness, light-headedness, vertigo and tinnitus, palpitations, angina, and symptoms of congestive failure.
  • GI manifestations: The lack of cobalamin is associated with megaloblastosis of the GI tract epithelium. Patients sometimes complain of a sore tongue. Anorexia with moderate weight loss occasionally associated with diarrhea may result from malabsorption associated with megaloblastic changes in the epithelium of the small intestine.
  • Neurologic manifestations: These result from demyelination, followed by axonal degeneration and neuronal death. The affected sites include peripheral nerves, posterior and lateral columns of the spinal cord, and the cerebrum. Signs and symptoms include numbness and paresthesias in the extremities, weakness, and ataxia. Sphincter disturbances may be present. Mental function disturbances vary from mild irritability to severe dementia or psychosis. Neurologic disease may occur in patients with normal hematocrit and normal red cell parameters.
  • Pernicious anemia: Patients with pernicious anemia have an increased frequency of gastric polyps and have a 2.9-fold increase in gastric cancer.
  • Additionally, patients with autoimmune atrophic gastritis and H pylori infection may manifest iron deficient anemia that may be refractory to oral iron treatment. H pylori eradication in combination with continued oral iron therapy was shown to result in a significant increase in hemoglobin levels.

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.

• In uncomplicated H pylori–associated atrophic gastritis, clinical findings are few and nonspecific.
• • Epigastric tenderness may be present.
  • If gastric ulcers coexist, guaiac-positive stool may result from occult blood loss.
• Findings in a patient with autoimmune atrophic gastritis result from the development of pernicious anemia and neurologic complications.
• With severe cobalamin deficiency, the patient is pale and has slightly icteric skin and eyes. The pulse is rapid, and the heart may be enlarged. Auscultation usually reveals a systolic flow murmur.

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.

• Chronic gastritis caused by H pylori infection of the stomach
• • H pylori infection of the stomach is by far the most common cause of chronic atrophic gastritis.
  • Whether H pylori infection follows the multifocal atrophic gastritis pathway or the nonatrophic antral gastritis pathway may be related to genetic susceptibility factors, environmental factors that modulate the host-bacterial interaction, or bacterial strains.
  • Although H pylori possessing the cag (cytotoxin-associated gene) pathogenicity island have been shown to have increased virulence, to cause higher levels of mucosal inflammation, and to be present more frequently in individuals infected with H pylori who develop gastric cancer, no specific virulence factors have been identified that might be useful to predict specific H pylori disease outcome.
  • Host factors or the effects of other environmental agents are likely to be the determinant elements modulating patterns of disease progression. For example, family relatives of individuals with gastric cancer develop pangastritis more frequently in response to H pylori infection and they also develop multifocal intestinal metaplasia more often, a preneoplastic lesion of the stomach and a component of H pylori–associated atrophic gastritis.
• Autoimmune atrophic gastritis
• • Autoimmune atrophic gastritis is a type of chronic atrophic gastritis limited to corpus-fundus mucosa and characterized by marked diffuse atrophy of parietal and chief cells.
  • Autoimmune gastritis is associated with serum antiparietal and anti-IF antibodies that cause IF deficiency, which, in turn, causes decreased availability of cobalamin and, eventually, pernicious anemia in some patients.
  • In some families, the disease appears to be transmitted with an autosomal dominant pattern of inheritance.

DIFFERENTIALS

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Other Problems to be Considered

Functional (nonulcer) dyspepsia

WORKUP

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Lab Studies

• The diagnosis of atrophic gastritis only can be ascertained histologically. The endoscopic findings are not helpful for diagnosis, but endoscopy is essential to perform multiple gastric biopsy sampling. Obtain at least 2 biopsy samples from the gastric antrum, 2 from the corpus and 1 from the incisure, and submit to pathology in separate vials.
• Decreased serum pepsinogen I levels and the ratio of pepsinogen I to pepsinogen II in the serum can be used to assess gastric atrophy. The finding of low pepsinogen I levels (<20 ng/mL) has a sensitivity of approximately 96.2% and a specificity of 97% for detection of fundus atrophy.
• Identifying the underlying cause of atrophic gastritis and assessing specific complications can require several laboratory tests.
• Diagnosis of H pylori–associated atrophic gastritis is as follows:
• • Histological examination of gastric biopsy with H pylori special stains: Histological identification of H pylori is the standard method to assess if the organism is the underlying cause of atrophic gastritis. Histological examination also helps evaluate the degree and distribution of atrophy, which helps identify the type of atrophic gastritis. Although histological identification of H pylori is the standard approach to identify the infection, at late stages of extensive atrophic gastritis, the number of H pylori organisms is decreased markedly because intestinal metaplasia creates an unfavorable environment for H pylori. In these cases, other tests, such as the urea breath test (ie, with nonradioactive isotope 13C or with radioactive isotope 14C), and serological evidence of infection may provide evidence for H pylori infection.
  • Rapid urease test from gastric biopsy tissue
  • Bacterial culture of gastric biopsy specimens: This usually is performed in the research setting or to assess antibiotic susceptibility in patients in whom first-line eradication therapy fails.
  • Serological detection of anti-H pylori antibodies
• Diagnosis of autoimmune gastritis is as follows:
• • Antiparietal and anti-IF antibodies in the serum
  • Achlorhydria, both basal and stimulated, and hypergastrinemia
  • Low serum cobalamin (B-12) levels ( <100 pg/mL)
  • Shilling test: Results may be abnormal and can be corrected by IF.

Procedures

• Upper GI endoscopy is essential to establish a diagnosis of atrophic gastritis.
• • Areas of intestinal metaplasia may be recognized with endoscopy; perform sampling of multiple biopsy specimens.
  • Tissue sampling from both the gastric antrum and corpus is essential to establish the topography of gastritis and to identify atrophy and intestinal metaplasia, which may be patchy.

Histologic Findings

H pylori–associated atrophic gastritis

H pylori–associated atrophic gastritis (see Media files 1-4) can display different levels of severity. 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 histological changes vary in different phases of autoimmune atrophic gastritis (Media file 2, Media file 4). 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 isspared.

TREATMENT

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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.

• Triple therapy, with indicated adult dose
• • Twice-a-day (bid) PPI or RBC triple therapies include lansoprazole (Prevacid), 30 mg PO bid; omeprazole (Prilosec), 20 mg PO bid; or RBC (Tritec), 400 mg bid. Antibiotic therapy includes clarithromycin (Biaxin), 500 mg PO bid; amoxicillin, 1000 mg PO bid; or metronidazole, 500 mg PO bid.
  • Pack kits containing combination triple therapies are available as combinations of lansoprazole, amoxicillin, and clarithromycin (PrevPac) and bismuth subsalicylate, tetracycline, and metronidazole (Helidac). PrevPac contains drug combinations in the dosage recommended as first-line treatment by the Maastricht 2-2000 Consensus report from Europe.
  • • PrevPac components include lansoprazole (Prevacid), 30 mg PO bid; clarithromycin (Biaxin), 500 mg PO bid; and amoxicillin, 1000 mg PO bid.
    • Helidac triple-therapy components include bismuth subsalicylate, 525 mg (two 262.4-mg chewable tabs) 4 times per day (qid); metronidazole, 250 mg qid; and tetracycline HCL, 500 mg qid.
• Quadruple therapy, with indicated adult dose is a PPI bid, including lansoprazole (Prevacid), 30 mg PO bid or omeprazole (Prilosec), 20 mg PO bid, and antibiotics, including tetracycline HCl, 500 mg PO qid; bismuth subsalicylate, 120 mg PO qid; and metronidazole, 500 mg PO 3 times per day (tid).
• Handle subsequent H pylori eradication failures on a case-by-case basis.

MEDICATION

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

Drug Category: Antibiotics

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

Drug Category: Proton pump inhibitors

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.

Drug Category: Bismuth compounds

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.

FOLLOW-UP

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Further Outpatient Care

• Guidelines for follow-up care for cases of atrophic gastritis are not established.
• If the patient was treated for H pylori infection, confirm eradication. Perform evaluation of eradication at least 4 weeks after the end of treatment. Eradication may be assessed by noninvasive methods, such as the urea breath test.
• Follow-up care may be individualized depending on findings during endoscopy. For example, if dysplasia is found at endoscopy, increased surveillance is necessary.

Deterrence/Prevention

• Epidemiological studies of H pylori–associated chronic gastritis show that acquisition of the infection is associated with large crowded households and lower socioeconomic status.
• Well-defined measures to prevent infection are not established.

Complications

• The multifocal atrophic gastritis that develops in some individuals with H pylori infection is associated with increased risk of the following:
• • Gastric ulcers
  • Gastric adenocarcinoma
• The corpus-restricted atrophic gastritis that develops in patients with autoimmune gastritis is associated with an increased risk of the following:
• • Pernicious anemia
  • Gastric polyps
  • Gastric adenocarcinoma

Prognosis

• Atrophic gastritis is a progressive condition with increasing loss of gastric glands and replacement by foci of intestinal metaplasia over years.
• Results from studies evaluating the evolution of atrophic gastritis after eradication of H pylori have been conflicting. Follow-up for up to several years after H pylori eradication has not shown regression of gastric atrophy in most studies, while other studies report improvement in the extent of atrophy.
• Whether H pylori eradication in a patient with atrophic gastritis reduces the risk of development of gastric cancer is another important question.
• • Available data are limited, but a prospective study in a Japanese population reported that H pylori eradication in patients with endoscopically-resected early gastric cancer resulted in decreased appearance of new early cancers, while intestinal-type gastric cancers developed in the control group without H pylori eradication.
  • These findings support an interventional approach, with eradication of H pylori if the organisms are detected in patients with atrophic gastritis, aiming at prevention of development of gastric cancer.

Patient Education

• For excellent patient education resources, visit eMedicine's Esophagus, Stomach, and Intestine Center. Also, see eMedicine's patient education article Gastritis.

MULTIMEDIA

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Media file 1:  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.
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Media file 2:  Patterns of atrophic gastritis associated with chronic Helicobacter pylori infection and autoimmune gastritis.
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Media file 3:  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.
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Media type:  Photo

Media file 4:  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.
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Media type:  Photo

Media file 5:  Marked gastric atrophy of the stomach body.
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Media file 6:  Severe gastric atrophy of the stomach antrum.
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Media type:  Photo

REFERENCES

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• 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. [Medline].
• 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. [Medline].
• 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. [Medline].
• Rugge M, Genta RM. Staging and grading of chronic gastritis. Hum Pathol. Mar 2005;36(3):228-33. [Medline].
• Sipponen P, Harkonen M, Alanko A, et al. Diagnosis of atrophic gastritis from a serum sample. Clin Lab. 2002;48(9-10):505-15. [Medline].
• 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. [Medline].
• Whittingham S, Mackay IR. Autoimmune gastritis: historical antecedents, outstanding discoveries, and unresolved problems. Int Rev Immunol. Jan-Apr 2005;24(1-2):1-29. [Medline].

Article Last Updated: Mar 22, 2006