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MaagklachtenPublished by: NHGLast published: 2025

The goal of treatment is to reduce gastric inflammation, relieve symptoms, and eliminate the underlying cause.[2][40] 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.[3]​ ​

For treatment-naive patients, bismuth quadruple therapy (a proton-pump inhibitor [PPI] plus bismuth plus metronidazole plus tetracycline; preferably optimised) is recommended as the first-line option when antibiotic susceptibility is unknown. This regimen is also the recommended option for patients with penicillin allergy.[3][22]​ Rifabutin triple therapy (a PPI plus rifabutin plus amoxicillin) or potassium-competitive acid blocker (PCAB) dual therapy (vonoprazan plus amoxicillin) are other first-line options that may be considered in patients with unknown antibiotic susceptibility and no history of macrolide exposure or penicillin allergy.[3]

While UK guidelines also recommend PPI-clarithromycin triple therapy (e.g., a PPI plus amoxicillin plus either clarithromycin or metronidazole, or a PPI plus clarithromycin plus metronidazole) as a first-line option for treatment-naive patients, US guidance prefers PCAB triple therapy (vonoprazan plus amoxicillin plus clarithromycin) over PPI-clarithromycin triple therapy.[3][60]​ However, US guidance advises against using clarithromycin-containing regimens without confirmed macrolide susceptibility due to rising clarithromycin resistance rates.[3]

For treatment-experienced patients, optimised bismuth quadruple therapy and rifabutin triple therapy are equally recommended for empirical treatment, depending on what the patient has received previously.[3]​ For patients with persistent infection after treatment with optimised bismuth quadruple therapy and/or rifabutin triple therapy or those who cannot tolerate rifabutin, antibiotic susceptibility testing is recommended to guide targeted salvage therapy with clarithromycin or levofloxacin. Patients with clarithromycin-sensitive H pylori who have not received clarithromycin therapy previously may be treated with optimised PPI-clarithromycin triple therapy (e.g., a PPI plus clarithromycin plus either amoxicillin or metronidazole) or PCAB triple therapy, while patients with levofloxacin-sensitive H pylori who have not received levofloxacin therapy previously may be treated with levofloxacin triple therapy (a PPI plus levofloxacin plus amoxicillin or metronidazole).[3]

One systematic review evaluated different treatment regimens, as well as duration of treatment, and concluded that longer duration of therapy, up to 14 days compared with 7 days, is associated with better eradication of the bacteria.[61] [ Cochrane Clinical Answers logo ] ​ All regimens are recommended for 14 days.[3]

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

Systemic fluoroquinolone antibiotics, such as levofloxacin, may cause serious, disabling, and potentially long-lasting or irreversible adverse events. This includes, but is not limited to: tendinopathy/tendon rupture; peripheral neuropathy; arthropathy/arthralgia; aortic aneurysm and dissection; heart valve regurgitation; dysglycaemia; and central nervous system effects including seizures, depression, psychosis, and suicidal thoughts and behaviour.[63]

  • Prescribing restrictions apply to the use of fluoroquinolones, and these restrictions may vary between countries. In general, fluoroquinolones should be restricted for use in serious, life-threatening bacterial infections only. Some regulatory agencies may also recommend that they must only be used in situations where other antibiotics that are commonly recommended for the infection are inappropriate (e.g., resistance, contraindications, treatment failure, unavailability).

  • Consult your local guidelines and drug information source for more information on suitability, contraindications, and precautions.

An increased risk of neuropsychiatric events has been described with H pylori eradication therapy containing clarithromycin.[64]

Erosive gastritis

Reducing exposure to the associated agent is essential. For patients with non-steroidal anti-inflammatory drug (NSAID)-associated gastritis, NSAIDs should be discontinued if possible.[38] Factors identified as placing patients at increased risk for NSAID-related gastrointestinal (GI) complications include prior history of GI event (ulcer, haemorrhage), age >60 years, high dosage of NSAID, and concurrent use of corticosteroids or anticoagulants.[27][28]

Reduction in or abstinence from alcohol use should be encouraged in patients with alcohol-associated gastritis.[26] Symptomatic therapy with either an H2 antagonist or a PPI is effective and is essential when NSAID use has to be continued.[39] ​H pylori eradication in patients on long-term NSAIDs may lead to a healing of gastritis despite ongoing NSAID therapy.[65]

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.[32] 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.[4][5][6] Addition of hydrotalcite (aluminium 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 hyperaemia or histological inflammation.[66]

Surgical Roux-en-Y diversion is considered in patients with prior gastric surgery and persistent symptoms.[7] However, surgery performed after the development of severe bile-reflux gastropathy does not reverse any associated gastric atrophy or intestinal metaplasia.[7]

Phlegmonous gastritis

Phlegmonous gastritis is a rare but life-threatening infection of the gastric submucosa and muscularis propria seen in debilitated patients.[10][11][12][13]​ Diagnosis is difficult to make preoperatively and initial stabilisation of patients with sepsis requires vigorous fluid resuscitation and early empirical parenteral antibiotic therapy.[67] Patients should be admitted to the intensive care unit for central-line placement and volume resuscitation.[10][11][12][13][68]​ Intravenous fluids should replace previous losses and any electrolyte imbalance should be corrected.[68] Vasopressors are used as indicated in current guidelines. Noradrenaline (norepinephrine) is the vasopressor of choice.[68] Dopamine has been associated with higher mortality, is rarely used in the UK, and should be restricted to patients with low risk of tachyarrhythmias and bradycardia.[68][69]​ Nasogastric decompression may provide relief and also provide fluid for culture.[10][11][12][13]

Empirical broad-spectrum intravenous antibiotics should be given against Staphylococcus aureus, streptococci, Escherichia coli, Enterobacter, other gram-negative bacteria, and Clostridium welchii.[10][11][12][13] Empirical treatment depends in part on local bacterial susceptibility patterns. Results of the gastric fluid culture and organism sensitivity will guide more specific therapy.[67] 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.[36][70]

Although nasogastric drainage and antibiotic therapy may be sufficient, in many cases subtotal/total gastrectomy is necessary.[10][11][12][13] Indications for surgery include deterioration despite optimal medical management, involvement of a large portion of stomach, presence of gastric infarction, or perforation.[67]

Prevention of stress gastritis

Critically ill patients are at risk of developing stress-induced GI bleeding.[8] The main risk factors are mechanical ventilation for >48 hours and coagulopathy (platelet count <50 × 10⁹/L [50 × 10³/microlitre], partial thromboplastin time >2 times the upper limit of the normal range, international normalised ratio >1.5).[8]

For patients at risk, treatment with an H2 antagonist or a PPI is indicated. Sucralfate or misoprostol are alternatives.[8]

Potential effects of long-term PPI therapy

Retrospective analyses suggest an association between PPI use and:[71][72][73]​​​​[74][75]​​​​[76][77]​​

  • Increased mortality

  • Type 2 diabetes mellitus

  • Increased fracture risk

  • Hypergastrinaemia

  • Development of pneumonia

  • Development of enteric infections

  • Microscopic colitis

  • Dementia

  • Magnesium malabsorption

  • Drug-drug interactions

  • Multidrug-resistant organisms

However, these studies have been unable to establish a causal relationship.

PPIs should, therefore, only be prescribed for appropriate indications and should be limited to the warranted therapeutic duration.[74][75]​​[76]

As PPIs are part of first-line therapy for gastritis, judicious use is warranted and appropriate protocols should be followed.

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