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Chronic Gastritis Treatment & Management

  • Author: Akiva J Marcus, MD, PhD; Chief Editor: BS Anand, MD  more...
 
Updated: Jun 29, 2016
 

Approach Considerations

Treatment of chronic gastritis can be aimed at a specific etiologic agent, if such an agent is known. For example, the treatment approach for H pylori infection is described in detail below. (See also American College of Gastroenterology Issues Guidelines for Treatment of Helicobacter pylori Infection.) When gastritis represents gastric involvement of a systemic disease, treatment is directed toward the primary disease.

Some entities manifested by chronic gastritis do not have well-established treatment protocols. For example, in lymphocytic gastritis, some cases of spontaneous healing have been reported. However, because the disease has a chronic course, treatment is recommended. Some studies have reported successful treatment of exudative lymphocytic gastritis with omeprazole.

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Pharmacotherapy for H pylori

At first, specific recommendations for H pylori eradication were limited to peptic ulcer disease. However, the 1997 Digestive Health Initiative (DHI) International Update Conference on H pylori broadened the recommendations for H pylori testing and treatment. H pylori testing and eradication were also recommended after resection of early gastric cancer and for low-grade mucosa-associated lymphoid tissue (MALT) lymphoma. Furthermore, it is now widely accepted that if H pylori is identified as the underlying cause of gastritis, it should be eradicated.

H pylori infection is not easily cured, and research has shown that multidrug therapy is required. As with any bacterial infection, therapy must include antimicrobial agents to which the bacterium is sensitive. Antibiotics that have proven effective against H pylori include clarithromycin, amoxicillin, metronidazole, tetracycline, and furazolidone. Cure rates with single antibiotics have been poor (0-35%). Monotherapy is associated with the rapid development of antibiotic resistance, especially to metronidazole and clarithromycin.

Five regimens are approved by the US Food and Drug Administration (FDA) for the treatment of H pylori infection. One is a version of the traditional bismuth-metronidazole-tetracycline (BMT) triple therapy, which is commercially available as Helidac (Prometheus Laboratories, San Diego, CA). The antibiotics and bismuth are provided in a convenient dose pack that is thought to enhance compliance.

Three different combinations using clarithromycin have been approved, including 2 dual therapies consisting of 500 mg of clarithromycin 3 times daily plus either omeprazole or ranitidine bismuth citrate. The cure rates reported in the packaging literature suggest that the 3 combinations are similarly effective.

Clinical experience has shown that the most effective of these regimens is BMT triple therapy, followed by ranitidine bismuth citrate plus clarithromycin and then by omeprazole plus clarithromycin.

Because higher success rates can be achieved when a third drug is added to the dual therapies, most authorities now recommend triple-drug combinations. This recommendation was confirmed by the FDA’s approval of a combination regimen comprising the proton pump inhibitor (PPI) lansoprazole, clarithromycin, and amoxicillin. The cure rate with this combination exceeds 85%. A 2-drug regimen consisting of lansoprazole plus amoxicillin was also approved, but it yields tremendously variable results and thus is a very poor choice.

The most widely used regimens for eradicating H pylori are triple therapies, which are recommended as first-line treatments; quadruple therapies[92] are recommended as second-line treatment when triple therapies fail. With either type of regimen, the best results are achieved by administering therapy for 10-14 days, though some studies have limited the duration of treatment to 7 days. The accepted definition of cure is that no evidence of H pylori exists for 4 or more weeks after ending the antimicrobial therapy.

Do not administer antibiotic therapy if the patient does not have a confirmed infection, and be sure to assess the results of the therapy carefully. Manage cases of subsequent H pylori eradication failure on a case-by-case basis, and base antibiotic selection on pretreatment antibiotic sensitivity test results.

Triple therapies (with indicated adult dosing)

Twice-daily PPI or ranitidine bismuth citrate triple therapies include the following:

  • Lansoprazole 30 mg, omeprazole 20 mg, or ranitidine bismuth citrate 400 mg orally twice daily
  • Clarithromycin 500 mg orally twice daily
  • Amoxicillin 1000 mg or metronidazole 500 mg orally twice daily

Pack kits containing triple therapies are available as a combination of lansoprazole, amoxicillin, and clarithromycin (PrevPac; Takeda Pharmaceuticals America, Deerfield, IL) or a combination of bismuth subsalicylate, tetracycline, and metronidazole (ie, Helidac).

PrevPac contains drug combinations in the dosage recommended as first-line treatment by the Maastricht 2-2000 Consensus Report in Europe.[93] The components are as follows:

  • Lansoprazole 30 mg orally twice daily
  • Clarithromycin 500 mg orally twice daily
  • Amoxicillin 1000 mg orally twice daily

The components of Helidac triple therapy are as follows:

  • Bismuth subsalicylate 525 mg (2 chewable 262.4-mg tablets) 4 times daily
  • Metronidazole 250 mg 4 times daily
  • Tetracycline hydrochloride 500 mg 4 times daily

Quadruple therapies (with indicated adult dosing)

Quadruple therapy for H pylori infection typically includes the following:

  • PPI (lansoprazole 30 mg or omeprazole 20 mg) orally twice daily
  • Tetracycline HCl 500 mg orally 4 times daily
  • Bismuth subsalicylate 120 mg orally 4 times daily
  • Metronidazole 500 mg orally 3 times daily

Treatment of H pylori infection in children

Optimal therapy for H pylori infection in childhood is not well established. Treatment has not been studied extensively, and there is no consensus as to the best regimen. However, the benefits of treating the infection in patients with duodenal ulcer are obvious, whereas the benefits of treating children who are asymptomatic remain controversial. Although the literature is replete with contrary recommendations, many authorities now recommend treating all people, adults and children, in whom H pylori infection is demonstrated.

Isolated studies have shown eradication efficiencies with triple therapies, ranging from 56-87% of the cases. In children, clarithromycin and metronidazole H pylori resistance is a problem in several countries, resulting in less efficient eradication regimens.

In a study of triple therapy with lansoprazole 0.75 mg/kg plus amoxicillin 25 mg/kg plus clarithromycin 10 mg/kg given twice daily for 7 days, the eradication rate was 87%. A similar study used the same drugs but different dosages—lansoprazole 0.45 mg/kg/day in 2 doses (maximum dose, 15 mg twice daily), amoxicillin 40 mg/kg/day in 2 doses (maximum dose, 1 g twice daily), and clarithromycin 250 mg (for age < 10 y) or 500 mg (for age >10 y) twice daily for 2 weeks. This protocol eradicated bacteria in only 56% of children.

Eradication rates in children have been reported to be as high as 96% with alternative eradication regimens that include amoxicillin, bismuth, and metronidazole.

The adverse effects of the various regimens are similar in children and adults. Bismuth toxicity is not a concern in children receiving H pylori therapy, but salicylate ingestion from the use of bismuth subsalicylate is. Inform parents of the presence of subsalicylate. Ideally, children younger than 16 years should not receive salicylate-containing compounds, because of the risk of Reye syndrome.

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Long-Term Monitoring

If a patient was treated for H pylori infection, confirm that the organism has been eradicated. Evaluate eradication at least 4 weeks after the beginning of treatment. Eradication may be assessed by means of noninvasive methods such as the urea breath test or the stool antigen test.

Follow-up may be individualized, depending on findings during endoscopy. For example, if dysplasia is found at endoscopy, increased surveillance is necessary. For patients with atrophic gastritis or dysplasia, follow-up endoscopy is recommended after 6 months.

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Contributor Information and Disclosures
Author

Akiva J Marcus, MD, PhD Attending Gastroenterologist, West Palm Hospital

Akiva J Marcus, MD, PhD 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 Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, New York Society for Gastrointestinal Endoscopy, International Society for Stem Cell Research

Disclosure: Nothing to disclose.

Coauthor(s)

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.

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.

Acknowledgements

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.

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

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.

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

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 the lamina propria.
Granulomatous chronic gastritis. Noncaseating granulomas in the lamina propria. Image courtesy of Sydney Finkelstein, MD, PhD, University of Pittsburgh.
Chronic gastritis. Mycobacterium avium-intracellulare in the gastric lamina propria macrophages. Image courtesy of Sydney Finkelstein, MD, PhD, University of Pittsburgh.
Chronic gastritis. Typical cytomegalovirus inclusions in the 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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