Medication Summary
Specific treatment is dependent on the etiology of gastritis.
According to the Centers for Disease Control and Prevention (CDC), the treatment of tuberculosis consists of a 2-month period of daily isoniazid, rifampin, and pyrazinamide, followed by 4 months of daily isoniazid along with rifampin. See Tuberculosis.
Medical management generally is ineffective in treating phlegmonous gastritis. No effective antiviral therapy exists for the treatment of human cytomegalovirus (HCMV) infection, though 2 agents (ie, ganciclovir, foscarnet) have been shown to be virostatic. See Cytomegalovirus.
The treatment of C albicans includes a variety of agents, including nystatin, oral clotrimazole, itraconazole, fluconazole, amphotericin B, and ketoconazole. See Candidiasis.
The treatment of disseminated histoplasmosis includes a variety of agents, including amphotericin B, itraconazole, and fluconazole. They have all been determined to be effective. See Histoplasmosis.
No drugs are available to treat anisakidosis. Endoscopic removal may be necessary.
Antacids
Class Summary
Used for general prophylaxis. Antacids containing aluminum and magnesium can help relieve symptoms of gastritis by neutralizing gastric acids. These agents are inexpensive and safe.
Aluminum and magnesium hydroxide, magnesia and alumina oral suspension (Rulox)
Drug combination that neutralizes gastric acidity and increases pH of the stomach and duodenal bulb. Aluminum ions inhibit smooth-muscle contraction and inhibit gastric emptying. Magnesium/aluminum antacid mixtures are used to avoid bowel function changes.
H2 blockers
Class Summary
This class includes drugs whose mechanism of action is competitive inhibition of histamine at the histamine 2 (H2) receptor. Histamine plays an important role in gastric acid secretion, thereby making H2 blockers effective suppressors of basal gastric acid output and acid output stimulated by food and the neurological system. When used alone, they are frequently used as antisecretory drugs in H pylori therapy regimens. There are different drugs with different potencies and half-lives (eg, cimetidine, ranitidine, famotidine, nizatidine). Cimetidine will be discussed below as a representative of this class of drugs.
Cimetidine (Tagamet)
Inhibits histamine at H2 receptors of gastric parietal cells, which results in reduced gastric acid secretion, gastric volume, and hydrogen concentrations.
Proton pump inhibitors
Class Summary
Proton pump inhibitors are potent inhibitors of the proton (acid) pump (ie, the enzyme H+,K+-ATPase), located in the apical secretory membrane of the gastric acid secretory cells (parietal cell). Proton pump inhibitors can completely inhibit acid secretion and have a long duration of action. They are the most effective gastric acid blockers. Omeprazole will be discussed as a representative of this class of drugs.
Omeprazole (Prilosec)
Decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATPase pump.
Antibiotics
Class Summary
Bacterial infections also can cause gastritis. The most common causative organism is H pylori. A number of therapeutic regimens are effective against H pylori. Single antimicrobial agents generally are not recommended because of the potential development of resistance.
Dual therapy includes a proton pump inhibitor plus amoxicillin (no longer recommended because eradication rates are 30-80%) or a proton pump inhibitor plus clarithromycin (eradication rate of roughly 71%). Adding a second antimicrobial agent is recommended for successful eradication.
Triple regimens are preferred in clinical practice. One drug is a proton pump inhibitor or a bismuth-based drug, the second drug is clarithromycin, and the third drug is amoxicillin or metronidazole. Quadruple therapy regimens (ie, 2 antibiotics, bismuth, antisecretory agent) generally are effective; however, because more drugs are prescribed and taken, increased adverse effects and decreased patient compliance can occur. This regimen is used in the event that triple therapy fails.
The decision of which medications to use is based on the following 4 criteria: (1) the different toxicities of the various medications, (2) the relative costs of each medication and regimen, (3) the emergence of antimicrobial-resistant bacteria, and (4) the level of patient compliance.
Amoxicillin (Amoxil, Trimox)
Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.
Tetracycline (Sumycin)
Inhibits bacterial protein synthesis by binding with 30S and possibly 50S ribosomal subunit(s).
Metronidazole (Flagyl)
Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa.
Clarithromycin (Biaxin)
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes and causing RNA-dependent protein synthesis to arrest.
Antidiarrheal agents
Class Summary
Used in combination with antibiotics and proton pump inhibitors/H2 receptor antagonists to eradicate H pylori.
Bismuth subsalicylate (Bismatrol, Pepto-Bismol)
Drug combination that treats active duodenal ulcer associated with H pylori.
Ford AC, Marwaha A, Lim A, Moayyedi P. What is the prevalence of clinically significant endoscopic findings in subjects with dyspepsia? Systematic review and meta-analysis. Clin Gastroenterol Hepatol. Oct 2010;8(10):830-7, 837.e1-2. [Medline].
Laine L, Curtis SP, Cryer B, Kaur A, Cannon CP. Risk factors for NSAID-associated upper GI clinical events in a long-term prospective study of 34 701 arthritis patients. Aliment Pharmacol Ther. Nov 2010;32(10):1240-8. [Medline].
Andersen LP. Colonization and infection by Helicobacter pylori in humans. Helicobacter. Nov 2007;12 Suppl 2:12-5. [Medline].
Beers M, Berkow R, eds. Gastritis. In: The Merck Manual of Diagnosis and Therapy. 18th ed. 2006:Section 3, Chapter 23. [Full Text].
Feldman. Sleisenger and Fordtran's Gastrointestinal and Liver Disease. 7th ed. 2002:810-823.
Ford A, Delaney B, Forman D. Eradication therapy for peptic ulcer disease in Helicobacter pylori positive patients. Cochrane Database Syst Rev. 2004;CD003840.
Gelfand DW, Ott DJ, Chen MY. Radiologic evaluation of gastritis and duodenitis. AJR Am J Roentgenol. Aug 1999;173(2):357-61. [Medline].
Gisbert JP, Pajares JM. Diagnosis of Helicobacter pylori infection by stool antigen determination: a systematic review. Am J Gastroenterol. Oct 2001;96(10):2829-38. [Medline].
Haruma K. Helicobacter heilmannii: a spiral shaped organism other than Helicobacter pylori. Intern Med. Mar 1999;38(3):217-8. [Medline].
Iwakiri Y, Kabemura T, Yasuda D, et al. A case of acute phlegmonous gastritis successfully treated with antibiotics. J Clin Gastroenterol. Mar 1999;28(2):175-7. [Medline].
Kasper DL, Braunwald E, Fauci A, et al. Gastritis. In: Harrison's Principles of Internal Medicine: Companion Handbook. 16th ed. McGraw-Hill: 2006:Part 12, Chapter 274.
Richieri JP, Pol B, Payan MJ. Acute necrotizing ischemic gastritis: clinical, endoscopic and histopathologic aspects. Gastrointest Endosc. Aug 1998;48(2):210-2. [Medline].
Soltermann A, Koetzer S, Eigenmann F, et al. Correlation of Helicobacter pylori virulence genotypes vacA and cagA with histological parameters of gastritis and patient's age. Mod Pathol. Aug 2007;20(8):878-83. [Medline]. [Full Text].
Srivastava A, Lauwers GY. Pathology of non-infective gastritis. Histopathology. Jan 2007;50(1):15-29. [Medline].
Suerbaum S, Michetti P. Helicobacter pylori infection. N Engl J Med. Oct 10 2002;347(15):1175-86. [Medline].
Yamamoto T, Matsumoto J, Shiota K, et al. Helicobacter heilmannii associated erosive gastritis. Intern Med. Mar 1999;38(3):240-3. [Medline].

