Approach

The goal of treatment is to reduce gastric inflammation, relieve symptoms, and eliminate the underlying cause.[3][33] Emergence of antibiotic resistant strains of Helicobacter pylori has resulted in a variety of strategies to enhance eradication. These include the addition of a bismuth-containing salt to the antibiotic regimen, altering the duration of therapy, and use of sequential therapy, which is still considered an emerging treatment.

Helicobacter pylori gastritis

Therapy that offers the greatest likelihood of eradicating H pylori infection is used.[4] First-line treatment options include triple therapy (a proton-pump inhibitor [PPI] plus 2 antibiotics) or quadruple therapy (a PPI plus bismuth plus 2 antibiotics).[4][32] Eradication in 70% to 80% of patients is reported.[57][58] A systematic review evaluated different treatment regimens, as well as duration of treatment, and concluded that longer duration of therapy, up to 14 days compared to 7 days, is associated with better eradication of the bacteria.[59] [ Cochrane Clinical Answers logo ] Duration of therapy is usually 14 days when giving triple therapy with a PPI, clarithromycin, and amoxicillin, or substituting amoxicillin with metronidazole in penicillin-allergic patients.[4][60] In patients who have previously taken a macrolide antibiotic or metronidazole, a 7-day course of bismuth-based quadruple therapy (with tetracycline, metronidazole, and a PPI) is recommended.[4][32] This regimen can also be used in penicillin-allergic patients. The frequency of adverse effects is no greater with quadruple therapy than with triple therapy.[61]

A large, community-based, randomized controlled trial evaluated factors that impact on eradication therapy among H pylori-positive residents of Linqu County, China.[62] Gender, body mass index, change over baseline value of the 13C-urea breath test, missed medication doses, smoking, and increased alcohol intake were all independent predictors of eradication failure.[62]

An increased risk of neuropsychiatric events has been described with H pylori eradication therapy containing clarithromycin.[63]

Erosive gastritis

Reducing exposure to the associated agent is essential. For patients with nonsteroidal anti-inflammatory drug (NSAID)-associated gastritis, NSAIDs should be discontinued if possible.[31] Factors identified as placing patients at increased risk for NSAID-related gastrointestinal (GI) complications include prior history of GI event (ulcer, hemorrhage), age >60 years, high dosage of NSAID, and concurrent use of corticosteroids or anticoagulants.[22][23]

Reduction in or abstinence from alcohol use should be encouraged in patients with alcohol-associated gastritis.[21] Symptomatic therapy with either H₂ antagonists or a PPI is effective and is essential when NSAID use has to be continued.[32]H pylori eradication in patients on long-term NSAIDs may lead to a healing of gastritis despite ongoing NSAID therapy.[64]

Autoimmune gastritis

Patients with autoimmune gastritis are at risk of, or have, an established vitamin B₁₂ malabsorption state. Patients with low serum vitamin B₁₂ should be treated with intramuscular cyanocobalamin (vitamin B₁₂) for repletion, followed by monthly injections. The duration of therapy has not been established, but is likely to be long-term.[25] Oral crystalline cyanocobalamin may have a role in vitamin B₁₂ maintenance therapy in these patients, but further studies are required.

Bile reflux gastritis

For patients with primary bile reflux, or reflux following gastric or biliary surgery, symptomatic therapy with rabeprazole or sucralfate as an initial therapy is preferred to surgical intervention.[5][6][7] Addition of hydrotalcite (aluminum magnesium carbonate hydroxide hydrate) to rabeprazole may further decrease the number of reflux episodes including episodes lasting longer than 5 minutes, with no difference in endoscopic hyperemia or histologic inflammation.[65]

Surgical Roux-en-Y diversion is considered in patients with prior gastric surgery and persistent symptoms.[8] However, surgery performed after the development of severe bile-reflux gastropathy does not reverse any associated gastric atrophy or intestinal metaplasia.[8]

Phlegmonous gastritis

Phlegmonous gastritis is a rare but life-threatening infection of the gastric submucosa and muscularis propria seen in debilitated patients.[11][12][13][14] Diagnosis is difficult to make preoperatively and initial stabilization of septic patients requires vigorous fluid resuscitation and early empirical parenteral antibiotic therapy.[66] Patients should be admitted to the intensive care unit for central-line placement and volume resuscitation.[11][12][13][14][67] Intravenous fluids should replace previous losses and any electrolyte imbalance should be corrected.[67] Vasopressors are used as indicated in current guidelines. Norepinephrine (noradrenaline) is the vasopressor of choice.[67] Nasogastric decompression may provide relief and also provide fluid for culture.[11][12][13][14]

Empiric broad-spectrum intravenous antibiotics should be given against Staphylococcus aureus, streptococci, Escherichia coli, Enterobacter, other gram-negative bacteria, and Clostridium welchii.[11][12][13][14] Empiric treatment depends in part on local bacterial susceptibility patterns. Results of the gastric fluid culture and organism sensitivity will guide more specific therapy.[66] Duration of treatment depends on clinical response to therapy; once this is demonstrated, switching to oral therapy may be considered. If the disease is diagnosed in an early phase, it can be treated conservatively with antibiotics and intravenous fluid infusion.[29][68]

Although nasogastric drainage and antibiotic therapy may be sufficient, in many cases subtotal/total gastrectomy is necessary.[11][12][13][14] Indications for surgery include deterioration despite optimal medical management, involvement of a large portion of stomach, presence of gastric infarction, or perforation.[66]

Prevention of stress gastritis

Critically-ill patients are at risk of developing stress-induced GI bleeding.[9] The main risk factors are mechanical ventilation for >48 hours and coagulopathy (platelet count <50 × 10³/microliter, partial thromboplastin time >2 times the upper limit of the normal range, international normalized ratio >1.5).

For patients at risk, treatment with H₂ antagonists or a proton-pump inhibitor (PPI) is indicated. Sucralfate or misoprostol are alternatives.[9]

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