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MaagklachtenPublished by: NHGLast published: 2025Gastritis is defined as histological evidence of inflammation of the gastric mucosa. The broader term gastropathy encompasses lesions characterised by minimal or no inflammation.[1][2]
Patients may present with generalised dyspepsia or epigastric discomfort. However, these features are often non-specific.[2][40] Diagnosis is based upon clinical and relevant medical history and exclusion of benign and malignant gastrointestinal ulcerations as the cause of the symptoms.[40] Clinical guidelines have been established to aid the evaluation of patients with dyspepsia, and these should be applied to patients with suspected gastritis.[39][40] A histological diagnosis of gastritis is commonly made in patients without gastrointestinal symptoms.
History and physical examination
Patients may be asymptomatic or present with generalised dyspepsia or epigastric discomfort. Other symptoms may include nausea, vomiting, and loss of appetite. However, these are often non-specific.[40]
A full medical history, including a review of all drugs and use of alcohol, is essential:
This should include recent use of non-steroidal anti-inflammatory drugs (NSAIDs) or alcohol misuse, because these are common causes of erosive gastritis. Up to 10% to 20% of patients taking NSAIDs report symptoms of dyspepsia, although the prevalence may range from 5% to 50%.[17][18] Factors identified as placing patients at increased risk for NSAID-related GI complications include prior history of a GI event (peptic ulcer, haemorrhage), age >60 years, high dosage of NSAIDs, and concurrent use of corticosteroids or anticoagulants.[27][28] Phlegmonous gastritis is also associated with recent intake of large quantities of alcohol. Emphysematous gastritis is a rare infection of the stomach wall caused by gas-producing organisms such as Clostridium welchii.[10][11][12][13] Risk factors for emphysematous gastritis include gastric surgery, corticosteroid use, use of NSAIDs, ingestion of corrosive agents, stress, diabetes mellitus, immunodeficiency, high alcohol consumption, malnutrition, and renal failure.[30]
Any history of previous gastric or abdominal surgery should be obtained; gastric surgery or biliary surgery, including cholecystectomy, are recognised causes of bile-reflux gastritis.[4][5][6]
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]
Autoimmune disorders associated with increased risk of autoimmune gastritis include thyroid disease, idiopathic adrenocortical insufficiency, vitiligo, type 1 diabetes mellitus, and hypoparathyroidism.[20][31] Patients may have signs and symptoms consistent with clinical vitamin B12 deficiency and pernicious anaemia (e.g., abnormal neurological examination, presence of cognitive impairment, angular cheilitis, atrophic glossitis).[2][29][31] Patients often have Northern European or Scandinavian ancestry.[9]
Acute upper abdominal pain, fever, significant vomiting, and clinical evidence of sepsis may be present in patients with phlegmonous gastritis.[10][11][12][13]
Investigations
Endoscopy
Endoscopy allows assessment of the gastric mucosa for presence of gastritis or alternative pathology. Biopsies are performed for histological assessment and testing for Helicobacter pylori infection.[2][40][41]
Findings of intestinal metaplasia on histology almost always point towards a finding of atrophic gastritis. Thus, documenting the extent is important. On oesophagogastroduodenoscopy (OGD) findings of pale mucosa, loss of gastric folds, thinning of mucosa, and/or metaplastic changes should be noted. Biopsies should be taken from these regions to determine the extent and severity of disease.[42]
The American College of Gastroenterology (ACG) and the Canadian Association of Gastroenterology (CAG) guidelines on dyspepsia recommend endoscopy for patients aged 60 years or older presenting with dyspepsia, and only on a case-by-case basis in younger patients with dyspepsia who have alarm features (weight loss, anaemia, dysphagia and persistent vomiting).[40]
The National Institute for Health and Care Excellence recommends same day referral to a specialist for any patient presenting with dyspepsia and significant gastrointestinal bleeding.[39]
Any patient with a family history of GI cancer, previous oesophago-gastric malignancy, lymphadenopathy, or an abdominal mass should undergo OGD.[40]
Endoscopy should be considered to exclude an alternative aetiology in patients unresponsive to therapy.[39][43]
Proton-pump inhibitors (PPIs) and possibly potassium-competitive acid blockers (PCABs), bismuth, and antibiotics can interfere with this test.[3]
Testing for H pylori
Guidelines recommend that patients with uninvestigated dyspepsia aged <60 years without alarm features suggestive of upper GI malignancy should undergo non-invasive testing for H pylori, with subsequent therapy as appropriate ('test-and-treat' strategy).[3][39]
Tests such as faecal antigen assay, urea breath test, rapid urease test, and histology of a biopsy specimen can confirm the diagnosis of H pylori infection.[22][44]
Both the urea breath test and the faecal antigen test are highly sensitive and specific assays for active H pylori infection. They can also be used to monitor response to therapy.[3] PPIs, bismuth, antibiotics, and PCABs can interfere with these tests.[3][45] It is generally recommended that, in the post-treatment setting, PPIs and PCABs are withheld for 7-14 days and antibiotics and bismuth withheld for at least 28 days prior to use of the urea breath test to assess H pylori eradication.[3]
H pylori urea breath test has >90% sensitivity and 96% specificity for presence of active infection.[44][46][47]
H pylori faecal antigen test identifies H pylori antigen in the stool to diagnose active infection. Both monoclonal and polyclonal assays are available, each with >90% sensitivity and specificity; monoclonal assay has a sensitivity of 96% and a specificity of 97%.[48][49]
Mucosal biopsy specimens can be tested for H pylori infection (using tissue rapid urease testing and direct culture or molecular studies).[2][3][41] Use of Warthin-Starry silver stain has 93% sensitivity and 99% specificity for H pylori.[46]H pylori rapid urease test can be performed on a single biopsy specimen from the antrum and a single biopsy specimen from the posterior corpus.[44] The tissue is placed in an agar gel or on a reaction strip containing urea, a buffer, and a pH-sensitive indicator. In the presence of H pylori urease, the urea is metabolised to ammonia and bicarbonate and detected as a colour change. This test has a 90% sensitivity and 100% specificity, as long as the patient does not have an acute GI bleed and is not taking a PPI or an antibiotic.[46][47][50] If the patient does have an acute GI bleed or is taking a PPI or an antibiotic, histological confirmation is recommended.[51] Overall, these tests may also be of value to determine H pylori eradication in patients currently receiving therapy with PPIs, bismuth, and antibiotics.[3]
Patients with findings of atrophic gastritis should be tested for H pylori.[42]
NSAID or alcohol-associated gastritis
If the initial non-invasive testing for H pylori is negative, and NSAID- or alcohol-associated gastritis is suspected on clinical grounds, then reduction/discontinuation of agent exposure and symptomatic therapy should be initiated.[2][40]
In patients unresponsive to such therapy, endoscopy should be considered to exclude an alternative aetiology.[39][40]
Autoimmune gastritis
If autoimmune gastritis is suspected, serum vitamin B12 and autoantibody studies should be ordered.[2][29][31][52] Vitamin B12 deficiency is associated with the loss of parietal cell mass and associated loss of acid and intrinsic factor. It is seen most commonly in older patients.[53] Patients with confirmed pernicious anaemia should undergo endoscopy to evaluate for any associated gastric malignancy.[41]
A full blood count may be appropriate to evaluate for any evidence of anaemia.[2]
Intrinsic factor antibodies are highly sensitive for pernicious anaemia; parietal cell antibodies are present in about 90% of patients with atrophic gastritis.[29]
Assessment for H pylori infection with a non-serological test, eradication treatment if positive, and post-treatment testing to confirm eradication is recommended for patients with autoimmune gastritis. A personalised surveillance approach may be considered.[54]
Phlegmonous gastritis
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