Medication Summary
Best results are achieved with 10- to 14-day protocols using combination therapies, with eradication in 80-95% of the cases.
Antibiotics
Class Summary
Antimicrobial activity against most H pylori strains. Rare resistant strains have been reported.
Amoxicillin (Amoxil, Trimox)
Semisynthetic penicillin, an analogue of ampicillin. Interferes with the synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.
Clarithromycin (Biaxin)
Semisynthetic macrolide antibiotic. Inhibits bacterial growth, possibly by blocking the dissociation of peptidyl t-RNA from ribosomes, causing arrest of RNA-dependent protein synthesis.
Tetracycline (Sumycin)
Active against gram-positive and gram-negative organisms and mycoplasmal, chlamydial, and rickettsial infections. Inhibits bacterial protein synthesis by binding with 30S and possibly 50S ribosomal subunit(s). Yellow, odorless, crystalline powder. Potency is affected in solutions of pH < 2.0 and is destroyed rapidly by alkali hydroxide solutions.
Metronidazole (Flagyl)
Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Used in combination with other antimicrobial agents (except for C difficile enterocolitis).
Proton pump inhibitors
Class Summary
A substituted benzimidazole (a compound that inhibits gastric acid secretion) is the active ingredient. PPIs do not exhibit anticholinergic or H2 antagonistic activities but suppress acid secretion by specific inhibition of the H+/K+ -ATPase enzyme system on the secretory surface of parietal cells.
Omeprazole (Prilosec)
Decreases gastric acid secretion by inhibiting the parietal cell H+/K+ -ATP pump.
Lansoprazole (Prevacid)
Decreases gastric acid secretion by inhibiting parietal cell H+/K+ -ATP pump.
Esomeprazole (Nexium)
S-isomer of omeprazole. Inhibits gastric acid secretion by inhibiting H+/K+-ATPase enzyme system at the secretory surface of gastric parietal cells.
Bismuth compounds
Class Summary
The components of bismuth-containing therapies, including bismuth subsalicylate, metronidazole, clarithromycin, and tetracycline, individually have demonstrated in vitro activity against most susceptible strains of H pylori.
Bismuth subsalicylate (Bismatrol, Pepto-Bismol)
Highly insoluble salt of trivalent bismuth and salicylic acid. More than 80% of salicylic acid is absorbed from oral doses of bismuth subsalicylate chewable tabs.
Ranitidine bismuth citrate (Tritec)
Combination of ranitidine (inhibits H2 receptor in gastric parietal cells, which reduces gastric acid secretion, gastric volume, and hydrogen concentrations) and bismuth citrate. Do not administer as monotherapy.
Administer 30 min prior to sucralfate.
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Atrophic gastritis. Schematic representation of Helicobacter pylori–associated patterns of gastritis. Involvement of the corpus, fundus, and gastric antrum, with progressive development of gastric atrophy as a result of the loss of gastric glands and partial replacement of gastric glands by intestinal-type epithelium, or intestinal metaplasia (represented by the blue areas in the diagram) characterize multifocal atrophic gastritis. Individuals who develop gastric carcinoma and gastric ulcers usually present with this pattern of gastritis. Inflammation mostly limited to the antrum characterizes antral-predominant gastritis. Individuals with peptic ulcers usually develop this pattern of gastritis, and it is the most frequent pattern in the Western countries.
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Patterns of atrophic gastritis associated with chronic Helicobacter pylori infection and autoimmune gastritis.
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Atrophic gastritis. Helicobacter pylori–associated chronic active gastritis (Genta stain, 20x). Multiple organisms (brown) are observed adhering to gastric surface epithelial cells. A mononuclear lymphoplasmacytic and polymorphonuclear cell infiltrate is observed in the mucosa.
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Atrophic gastritis. Intestinal metaplasia of the gastric mucosa (Genta stain, 20x). Intestinal-type epithelium with numerous goblet cells (stained blue with the Alcian blue stain) replace the gastric mucosa and represent gastric atrophy. Mild chronic inflammation is observed in the lamina propria. This pattern of atrophy is observed both in Helicobacter pylori–associated atrophic gastritis and autoimmune gastritis.
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Marked gastric atrophy of the stomach body.
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Severe gastric atrophy of the stomach antrum.