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Helicobacter Pylori Infection Medication

  • Author: Luigi Santacroce, MD; Chief Editor: BS Anand, MD  more...
 
Updated: Mar 15, 2016
 

Medication Summary

The goals of pharmacotherapy are to eradicate the microorganism, to prevent complications, and to reduce morbidity. Triple therapies are used. Worldwide, accepted treatment regimens are BMT, LAC, and OAC. BMT regimen is based on the administration of bismuth subsalicylate, metronidazole, and tetracycline. Add an H2-receptor antagonist for an additional 4 weeks. LAC regimen is based on the administration of lansoprazole, amoxicillin, and clarithromycin. OAC regimen is based on the administration of omeprazole, amoxicillin, and clarithromycin.

Increasing resistance to antibiotics has made alternative treatments necessary. In a phase 3 trial conducted by Malfertheiner et al, quadruple therapy (omeprazole plus a single 3-in-1 capsule containing bismuth subcitrate potassium, metronidazole, and tetracycline) was tested against standard therapy in adults with H pylori infection.[17] This study suggests quadruple therapy provides superior eradication with similar safety and tolerability to standard therapy.

As noted, antibiotic resistance phenomena are now observed with a certain frequency in H pylori infections; occasionally, even after the use of different eradicating protocols, H pylori is not eradicated.[18, 19]  In such cases treatment with rifabutin may be indicated.

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Antidiarrheals

Class Summary

The approved antidiarrheal for this infection is bismuth subsalicylate. It has both antisecretory and antimicrobial activity.

Bismuth subsalicylate (Bismatrol, Pepto-Bismol)

 

Has cytoprotective effect on the GI mucosa, probably due to stimulation of prostaglandin production and modulation of the immune response. In addition, it has been demonstrated that some deposits (probably bismuth salts) appear on both surfaces of the cell wall of H pylori after <1 h. Such deposits induce distortion and vacuolization of the bacterial cell and loss of adherence of H pylori from antral epithelium.

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Antibiotics

Class Summary

Use agents known to be effective against H pylori.

Metronidazole (Flagyl)

 

Reduced to its active form intracellularly only by anaerobic organisms, then disrupts helical structure of DNA and inhibits bacterial nucleic acid synthesis.

Tetracycline (Sumycin)

 

Inhibits bacterial protein synthesis by binding with 30S and possibly 50S ribosomal subunit(s).

Clarithromycin (Biaxin)

 

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing the arrest of RNA-dependent protein synthesis.

Amoxicillin (Amoxil, Trimox)

 

Inhibits the final stage of bacterial cell wall synthesis by binding to specific PBPs on the inner part of the bacterial wall, leading to bacterial lysis.

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Proton pump inhibitors

Class Summary

Bind to proton pump of parietal cell, inhibiting secretion of hydrogen ions into gastric lumen. Relieve pain and heal peptic ulcers more rapidly than H2 antagonists.

Lansoprazole (Prevacid)

 

Works by inhibiting the H+/K+ -ATPase enzyme system of the gastric parietal cells.

Omeprazole (Prilosec)

 

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

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H2 receptor blockers

Class Summary

Reversible competitive blockers of histamine at H2 receptors, particularly those in gastric parietal cells, wherein they inhibit acid secretion. H2 antagonists are highly selective, do not affect the H1 receptors, and are not anticholinergic agents. Proton pump inhibitors are usually preferred.

Ranitidine (Zantac)

 

Reduces basal and nocturnal gastric acid secretion by competitive inhibition of binding of histamine to receptors (H2 receptor) on gastric parietal cells. Although not effective as single agents for the eradication of H pylori, appears to increase systemic absorption of bismuth subsalicylate.

Famotidine (Pepcid)

 

Competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen ion concentrations.

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Contributor Information and Disclosures
Author

Luigi Santacroce, MD Assistant Professor, Medical School, State University at Bari, Italy

Disclosure: Nothing to disclose.

Coauthor(s)

Manoop S Bhutani, MD Professor, Co-Director, Center for Endoscopic Research, Training and Innovation (CERTAIN), Director, Center for Endoscopic Ultrasound, Department of Medicine, Division of Gastroenterology, University of Texas Medical Branch; Director, Endoscopic Research and Development, The University of Texas MD Anderson Cancer Center

Manoop S Bhutani, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Institute of Ultrasound in Medicine, American Society for Gastrointestinal Endoscopy

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

David Greenwald, MD Professor of Clinical Medicine, Fellowship Program Director, Department of Medicine, Division of Gastroenterology, Montefiore Medical Center, Albert Einstein College of Medicine

David Greenwald, MD is a member of the following medical societies: Alpha Omega Alpha, New York Society for Gastrointestinal Endoscopy, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

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An antral gland of the stomach with a large Giemsa-stained colony of Helicobacter pylori in the lumen (arrow) at 250X power. Courtesy of Pantaleo Bufo, University of Foggia, Italy.
Helicobacter pylori infection. Lamina propria of the stomach is shown with 2 mast cells overlapping each other. Note the upper part the degranulating process with the release of granules of inflammation mediators (Giemsa staining, 250X). Courtesy of Pantaleo Bufo, University of Foggia, Italy.
Helicobacter pylori infection. A transverse section of the gastric lamina propria is shown. In the lower part, an antral gland of the stomach is present with some Helicobacter pylori in the lumen (red-blue arrow). In the upper part, a mast cell (yellow arrow) is present (Giemsa staining, 250X). Courtesy of Pantaleo Bufo, University of Foggia, Italy.
An antral gland of the stomach is shown with a large colony of Helicobacter pylori in the lumen (Giemsa staining, 425X). Courtesy of Pantaleo Bufo, University of Foggia, Italy.
 
 
 
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