Barrett Esophagus Medication

Updated: Dec 29, 2017
  • Author: Mark H Johnston, MD; Chief Editor: Praveen K Roy, MD, AGAF  more...
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Medication

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.

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.

Famotidine (Pepcid)

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

Nizatidine (Axid)

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

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.

Omeprazole (Prilosec)

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

Lansoprazole (Prevacid)

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

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.

Dexlansoprazole (Dexilant)

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

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.

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.

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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