Medical Care
Once atrophic gastritis is diagnosed, treatment can be directed (1) to eliminate the causal agent, which is a possibility in cases of H pylori–associated atrophic gastritis; (2) to correct complications of the disease, especially in patients with autoimmune atrophic gastritis who develop pernicious anemia (in whom vitamin B-12 replacement therapy is indicated); or (3) to attempt to reverse the atrophic process.
No consensus from different studies exists regarding the reversibility of atrophic gastritis; however, removal of H pylori from the already atrophic stomach may block further progression of the disease. Until recently, specific recommendations for H pylori eradication were limited to peptic ulcer disease. At the Digestive Health Initiative International Update Conference on H pylori held in the United States, the recommendations for H pylori testing and treatment were broadened. H pylori testing and eradication of the infection also were recommended after resection of early gastric cancer and for low-grade mucosa-associated lymphoid tissue lymphoma.
If H pylori is identified as the underlying cause of gastritis, subsequent eradication now is almost generally an accepted practice. Protocols for H pylori eradication require a combination of antimicrobial agents and antisecretory agents, such as a proton pump inhibitors (PPIs), ranitidine bismuth citrate (RBC), or bismuth subsalicylate. Despite the combinatorial effect of drugs in regimens used to treat H pylori infection, cure rates remain, at best, 80-95%.
Lack of patient compliance and antimicrobial resistance are the most important factors influencing poor outcome. Currently, the most widely used and efficient therapies to eradicate H pylori are triple therapies (recommended as first-line treatments) and quadruple therapies (recommended as second-line treatment when triple therapies fail to eradicate H pylori). In both cases, the best results are achieved by administering therapy for 10-14 days, although some studies have recommended the duration of treatment of 7 days. The accepted definition of cure is no evidence of H pylori 4 or more weeks after ending the antimicrobial therapy.
Triple therapy, with indicated adult dose
Twice-a-day (bid) PPI or RBC triple therapies include lansoprazole (Prevacid), 30 mg PO bid; omeprazole (Prilosec), 20 mg PO bid; or RBC (Tritec), 400 mg bid. Antibiotic therapy includes clarithromycin (Biaxin), 500 mg PO bid; amoxicillin, 1000 mg PO bid; or metronidazole, 500 mg PO bid.
Pack kits containing combination triple therapies are available as combinations of lansoprazole, amoxicillin, and clarithromycin (PrevPac) and bismuth subsalicylate, tetracycline, and metronidazole (Helidac). PrevPac contains drug combinations in the dosage recommended as first-line treatment by the Maastricht 2-2000 Consensus report from Europe. Note the following:
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PrevPac components include lansoprazole (Prevacid), 30 mg PO bid; clarithromycin (Biaxin), 500 mg PO bid; and amoxicillin, 1000 mg PO bid.
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Helidac triple-therapy components include bismuth subsalicylate, 525 mg (two 262.4-mg chewable tabs) 4 times per day (qid); metronidazole, 250 mg qid; and tetracycline HCL, 500 mg qid.
Quadruple therapy, with indicated adult dose
Quadruple therapy, with indicated adult dose is a PPI bid, including lansoprazole (Prevacid), 30 mg PO bid or omeprazole (Prilosec), 20 mg PO bid, and antibiotics, including tetracycline HCl, 500 mg PO qid; bismuth subsalicylate, 120 mg PO qid; and metronidazole, 500 mg PO 3 times per day (tid).
Handle subsequent H pylori eradication failures on a case-by-case basis.
Prevention
Epidemiologic studies of H pylori–associated chronic gastritis show that acquisition of the infection is associated with large crowded households and lower socioeconomic status.
Well-defined measures to prevent infection are not established.
Long-Term Monitoring
Guidelines for follow-up care for cases of atrophic gastritis are not established.
If the patient was treated for H pylori infection, confirm eradication. Perform evaluation of eradication at least 4 weeks after the end of treatment. Eradication may be assessed by noninvasive methods, such as the urea breath test.
Follow-up care may be individualized depending on the findings during endoscopy. For example, if dysplasia is found at endoscopy, increased surveillance is necessary.
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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.
