Chronic Gastritis Medication

  • Author: Sandeep Mukherjee, MB, BCh, MPH, FRCPC; Chief Editor: Julian Katz, MD   more...
 
Updated: Mar 29, 2012
 

Medication Summary

The most widely used and most efficient regimens for eradicating Helicobacter pylori are triple therapies (recommended as first-line treatment) and quadruple therapies (recommended as second-line treatment).

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Antibiotics

Class Summary

The antibiotics selected have antimicrobial activity against most H pylori strains. Rare resistant strains have been reported.

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Amoxicillin (Moxatag)

 

Amoxicillin is an acid-stable semisynthetic penicillin. Its antimicrobial activity is pH-dependent, with the minimal inhibitory concentration (MIC) decreasing as the pH increases.

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Clarithromycin (Biaxin)

 

Clarithromycin is a macrolide that binds to bacterial ribosomes and disrupts protein synthesis, leading to bacterial cell death. It is the most acid-stable of the macrolides and has the lowest MIC. Its major metabolite also is active against H pylori.

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Tetracycline

 

Tetracycline treats infections with gram-positive and gram-negative organisms, as well as mycoplasmal, chlamydial, and rickettsial infections. It inhibits bacterial protein synthesis by binding with 30S and possibly 50S ribosomal subunit(s). Its potency is affected in solutions whose pH is less than 2, and it is rapidly destroyed by alkali hydroxide solutions.

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Metronidazole (Flagyl)

 

Metronidazole is an imidazole ring-based antibiotic that is active against various anaerobic bacteria and protozoa. It is used in combination with other antimicrobial agents. Because the activity of metronidazole is pH-independent, it is theoretically an ideal drug for the gastric environment.

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Proton Pump Inhibitors

Class Summary

A substituted benzimidazole (a compound that inhibits gastric acid secretion) is the active ingredient of proton pump inhibitors (PPIs). PPIs do not exhibit anticholinergic or H2 antagonistic activities but suppress acid secretion by specific inhibition of the H+/K+ –adenosine triphosphatase (ATPase) enzyme system on the secretory surface of parietal cells.

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Omeprazole (Prilosec)

 

Omeprazole decreases gastric acid secretion by inhibiting the parietal cell H+/K+-adenosine triphosphate (ATP) pump at the secretory surface of gastric parietal cells.

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Lansoprazole (Prevacid)

 

Lansoprazole decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATP pump at the secretory surface of gastric parietal cells.

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Rabeprazole (AcipHex)

 

Rabeprazole decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATP pump at the secretory surface of gastric parietal cells.

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Pantoprazole (Protonix)

 

Pantoprazole decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATP pump at the secretory surface of gastric parietal cells.

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Esomeprazole (Nexium)

 

Esomeprazole inhibits gastric acid secretion by inhibiting the H+/K+-ATPase enzyme system at the secretory surface of gastric parietal cells at the secretory surface of gastric parietal cells.

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Gastrointestinal Agents, Other

Class Summary

The components of bismuth-containing therapies have demonstrated in vitro activity against most susceptible strains of H pylori.

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Bismuth subsalicylate (Pepto-Bismol, Bismatrol, Diotame)

 

This agent exerts antisecretory and antimicrobial effects. It may also provide anti-inflammatory action.

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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  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

Chief Editor

Julian Katz, MD  Clinical Professor of Medicine, Drexel University College of Medicine

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.

Additional Contributors

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.

Franco Bazzoli, MD Professor, Department of Internal Medicine and Gastroenterology, University of Bologna, Italy

Franco Bazzoli, MD is a member of the following medical societies: American Gastroenterological Association

Disclosure: Nothing to disclose.

Maria P Dore, MD Associate Professor, Department of Medicine, Institute of Internal Medicine, University of Sassari, Italy

Maria P Dore, MD is a member of the following medical societies: American Gastroenterological Association

Disclosure: Nothing to disclose.

Tushar Patel, MB, ChB Professor of Medicine, Ohio State University Medical Center

Tushar Patel, MB, ChB is a member of the following medical societies: American Association for the Study of Liver Diseases and American Gastroenterological Association

Disclosure: Nothing to disclose.

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

Disclosure: Medscape Reference Salary Employment

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Helicobacter pylori–caused chronic active gastritis. Genta stain (×20). Multiple organisms (brown) are visibly adherent to gastric surface epithelial cells.
Chronic gastritis associated with Helicobacter pylori infection. Numerous plasma cells in lamina propria.
Granulomatous chronic gastritis. Noncaseating granulomas in lamina propria. Image courtesy of Sydney Finkelstein, MD, PhD, University of Pittsburgh.
Chronic gastritis. Mycobacterium avium-intracellulare in gastric lamina propria macrophages. Image courtesy of Sydney Finkelstein, MD, PhD, University of Pittsburgh.
Chronic gastritis. Typical cytomegalovirus inclusions in lamina propria capillary endothelial cells. Image courtesy of Sydney Finkelstein, MD, PhD, University of Pittsburgh.
Chronic gastritis. Chemical gastropathy. Image courtesy of Sydney Finkelstein, MD, PhD, University of Pittsburgh.
Lymphocytic chronic gastritis. Gastric epithelium is studded with numerous lymphocytes (left). Intraepithelial lymphocytes are T-cell lymphocytes shown by immunoreactivity to CD3 (brown stain, right).
 
 
 
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