Barrett Esophagus Medication

  • Author: Mark H Johnston, MD; Chief Editor: Julian Katz, MD   more...
 
Updated: May 3, 2012
 

Medication Summary

The treatment for Barrett esophagus should be the same as that for GERD, although most authorities agree that treatment should employ a PPI instead of an H2-receptor antagonist due to the relative acid insensitivity of patients with Barrett esophagus. However, although PPIs have been found to be better than H2-receptor antagonists at reducing gastric acid secretion, the evidence remains inconclusive regarding whether PPIs induce regression of Barrett esophagus.

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H2-receptor antagonists

Class Summary

These agents are reversible competitive blockers of histamine at H2 receptors, particularly those in the gastric parietal cells, where they inhibit acid secretion. The H2 antagonists are highly selective, do not affect the H1 receptors, and are not anticholinergic agents.

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Ranitidine (Zantac)

 

Ranitidine inhibits histamine the stimulation of H2 receptors in gastric parietal cells, in this way reducing gastric acid secretion, gastric volume, and hydrogen concentrations.

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Famotidine (Pepcid)

 

Famotidine competitively inhibits histamine at H2 receptors in gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen concentrations.

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Nizatidine (Axid)

 

Nizatidine competitively inhibits histamine at H2 receptors in gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen concentrations.

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Cimetidine (Tagamet)

 

Cimetidine inhibits histamine at H2 receptors of gastric parietal cells, which results in reduced gastric acid secretion, gastric volume, and hydrogen concentrations.

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Proton pump inhibitors

Class Summary

PPIs inhibit gastric acid secretion by inhibition of the H+/K+ -adenosine triphosphatase (ATPase) enzyme system in the gastric parietal cells. These agents are used in cases of severe esophagitis and in patients who do not respond to H2-antagonist therapy.

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Omeprazole (Prilosec)

 

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

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Lansoprazole (Prevacid)

 

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

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Esomeprazole (Nexium)

 

Esomeprazole is an (S)-isomer of omeprazole. It inhibits gastric acid secretion by inhibiting the H+/K+-ATPase enzyme system at the secretory surface of the gastric parietal cells.

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Dexlansoprazole (Dexilant)

 

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

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Rabeprazole sodium (AcipHex)

 

Rabeprazole sodium suppresses gastric acid secretion by specifically inhibiting the H+/K+-ATPase enzyme system at the secretory surface of gastric parietal cells.

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Pantoprazole (Protonix)

 

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

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Photosensitizers

Class Summary

These agents are used with PDT. Upon light absorption, a photosensitizer transforms to a short-lived singlet state, followed by a transition to a reactive triplet state. When in the triplet state, the photosensitizer produces reactive free radicals in the presence of oxygen; the free radicals react with cell membranes, causing direct damage to the mitochondria, endoplasmic reticulum, and/or plasma membranes.

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Porfimer (Photofrin)

 

Porfimer is indicated to treat high-grade dysplasia in Barrett esophagus. It elicits a photosensitizing effect used in PDT.

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Contributor Information and Disclosures
Author

Mark H Johnston, MD  Associate Professor of Medicine, Uniformed Services University of the Health Sciences; Consulting Staff, Lancaster Gastroenterology, Inc

Mark H Johnston, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and Christian Medical & Dental Society

Disclosure: Nothing to disclose.

Coauthor(s)

John A Eastone, MD  Gastroenterology Fellow, Bethesda and Walter Reed Army Medical Center; Instructor, Department of Internal Medicine, F Edward Herbert School of Medicine, Uniformed Services University of the Health Sciences

John A Eastone, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

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

John A Eastone, MD Gastroenterology Fellow, Bethesda and Walter Reed Army Medical Center; Instructor, Department of Internal Medicine, F Edward Herbert School of Medicine, Uniformed Services University of the Health Sciences

John A Eastone, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Ronnie Fass, MD Chief of Gastroenterology, Southern Arizona VA Health Care System; Professor of Medicine, Division of Gastroenterology, University of Arizona School of Medicine

Ronnie Fass, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, American Motility Society, American Society for Gastrointestinal Endoscopy, and Israel Medical Association

Disclosure: Takeda Pharmaceuticals Grant/research funds Conducting research; Takeda Pharmaceuticals Consulting fee Consulting; Takeda Pharmaceuticals Honoraria Speaking and teaching; Vecta Consulting fee Consulting; XenoPort Consulting fee Consulting; Eisai Honoraria Speaking and teaching; Wyeth Pharmaceuticals Conducting research; AstraZeneca Grant/research funds Conducting research; Eisai Consulting fee Consulting

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

References

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Barrett esophagus (BE). The salmon-pink area has specialized intestinal metaplasia. The white area is squamous epithelium.
Cryoablation of esophageal lining in Barrett esophagus (BE). This is one of the newest experimental ablative therapies for the esophagus performed at the author's laboratory.
Blistering of the esophageal mucosal layer after cryoablation in Barrett esophagus (BE).
 
 
 
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