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Atrophic Gastritis Medication

  • Author: Nafea Zayouna, MD; Chief Editor: BS Anand, MD  more...
Updated: Jul 06, 2016

Medication Summary

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



Class Summary

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

Amoxicillin (Amoxil, Trimox)


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)


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

Tetracycline (Sumycin)


Active against 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)


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


Proton pump inhibitors

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.

Omeprazole (Prilosec)


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

Lansoprazole (Prevacid)


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

Esomeprazole (Nexium)


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


Bismuth compounds

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.

Bismuth subsalicylate (Bismatrol, Pepto-Bismol)


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)


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.

Contributor Information and Disclosures

Nafea Zayouna, MD Fellow, Department of Internal Medicine, Division of Gastroenterology, St John Providence Hospital

Nafea Zayouna, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.


Michael H Piper, MD Clinical Assistant Professor, Department of Internal Medicine, Division of Gastroenterology, Wayne State University School of Medicine; Consulting Staff, Digestive Health Associates, PLC

Michael H Piper, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Gastroenterology, American College of Physicians, Michigan State Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Additional Contributors

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

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, Society of General Internal Medicine

Disclosure: Nothing to disclose.


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.

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

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

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: Genentech Honoraria Consulting; Leica Honoraria Consulting

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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–associated 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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