Gastritis, Atrophic Workup

  • Author: Sandeep Mukherjee, MB, BCh, MPH, FRCPC; Chief Editor: Julian Katz, MD   more...
 
Updated: Jan 3, 2010
 

Laboratory 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:
    • Histologic examination of gastric biopsy with H pylori special stains: Histologic identification of H pylori is the standard method to assess if the organism is the underlying cause of atrophic gastritis. Histologic examination also helps evaluate the degree and distribution of atrophy, which helps identify the type of atrophic gastritis. Although histologic 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 serologic 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.
    • Serologic 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.
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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.
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Histologic Findings

H pylori–associated atrophic gastritis

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

Atrophic gastritis. Schematic representation of HeAtrophic 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 chrPatterns of atrophic gastritis associated with chronic Helicobacter pylori infection and autoimmune gastritis. Atrophic gastritis. Helicobacter pylori chronic acAtrophic 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 gAtrophic 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.

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).

Patterns of atrophic gastritis associated with chrPatterns of atrophic gastritis associated with chronic Helicobacter pylori infection and autoimmune gastritis. Atrophic gastritis. Intestinal metaplasia of the gAtrophic 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.

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.

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Contributor Information and Disclosures
Author

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

Sandeep Mukherjee, MB, BCh, MPH, FRCPC is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

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

Coauthor(s)

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

Antonia R Sepulveda, MD, PhD is a member of the following medical societies: American Association for Cancer Research, American Gastroenterological Association, American Society for Investigative Pathology, College of American Pathologists, and United States and Canadian Academy of Pathology

Disclosure: Nothing to disclose.

Specialty Editor Board

Gregory William Rutecki, MD  Associate Professor, Program Director, Department of Internal Medicine, Feinberg School of Medicine, Northwestern University

Gregory William Rutecki, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Nephrology, National Kidney Foundation, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine 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

Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD  Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law, Medicine & Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

References

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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.
 
 
 
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