Gastritis, Atrophic Treatment & Management

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

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.
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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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