Gastritis, Atrophic Follow-up

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

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.
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Deterrence/Prevention

  • Epidemiologic 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.
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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
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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.
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Patient Education

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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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