Gastritis and gastropathy — Rapid

Synopsis

Distinguish histological gastritis from reactive gastric injury, identify infectious, autoimmune, chemical and vascular mechanisms, treat the cause rather than the endoscopic adjective, and recognise anaemia and premalignant mucosal change.

Gastritis is a histological diagnosis of gastric mucosal inflammation, whereas gastropathy describes epithelial injury and regeneration with relatively little inflammation; dyspepsia alone proves neither.
H. pylori is the commonest chronic infectious cause and can progress through atrophy and intestinal metaplasia toward gastric adenocarcinoma in a subset of patients.
Autoimmune gastritis targets corpus and fundus parietal cells, producing achlorhydria, iron deficiency, later vitamin B12 deficiency and increased gastric neoplasia risk.
Reactive gastropathy is associated with NSAIDs, aspirin, bile reflux and chemical exposure; remove or modify the driver before committing to indefinite symptom suppression.
Portal hypertensive gastropathy has a mosaic or snakeskin appearance in portal hypertension and is managed through portal-pressure and bleeding pathways, not ordinary dyspepsia treatment.
Endoscopic erythema is non-specific and correlates imperfectly with microscopic inflammation, so targeted and mapping biopsies should answer a defined diagnostic or risk-staging question.
Extensive gastric atrophy or intestinal metaplasia carries greater cancer risk than limited antral disease and may justify scheduled surveillance under BSG criteria.
A negative intrinsic-factor antibody does not exclude autoimmune gastritis; interpret B12, iron, antibodies, gastrin and histological distribution together with specialist input.

Key red flags

Erosive bleeding

Coffee-ground vomiting, melaena or falling haemoglobin can arise from diffuse erosions, particularly with NSAIDs, alcohol, critical illness or portal hypertension, and requires formal bleeding-risk assessment.

Phlegmonous or caustic danger

Severe pain, fever, toxicity, haemodynamic instability or a caustic history can indicate transmural infection or necrotic injury rather than benign mucosal irritation and needs immediate specialist care.

Investigation priorities

High-quality upper-GI endoscopyFirst step

Inspect mucosa, exclude ulcer or cancer and direct systematic biopsy.

Management branches

DefineName the gastric mechanism

Endoscopy, anaemia, B12 deficiency or persistent upper-GI symptoms raises concern for mucosal disease.

Review H. pylori, NSAIDs, aspirin, alcohol, bile-reflux surgery, portal hypertension, autoimmune history and immunosuppression rather than accepting a previous non-specific gastritis label.
Use endoscopy when alarm or risk features justify it and obtain correctly sited biopsies so histology can distinguish active inflammation, reactive injury, atrophy, metaplasia and neoplasia.
Integrate pathology with active-infection testing, FBC, ferritin, B12 and autoimmune studies, referring unexplained or discordant patterns for specialist review.

Key medicines

Vitamin B12 replacement for autoimmune gastritisUse the NICE NG239 replacement route and locally agreed hydroxocobalamin or oral regimen for the clinical severity; autoimmune gastritis usually needs lifelong treatment with response-based follow-up.Do not delay treatment for neurological symptoms while awaiting every antibody result. Check folate and iron without giving folate alone in untreated B12 deficiency, and recognise that replacement does not remove gastric cancer risk.

Cause-specific acid suppressionChoose a licensed PPI and product-specific dose only when erosive injury, ulcer or continuing high-risk NSAID exposure provides a clear indication; define the review and step-down date.Avoid indefinite therapy for histological gastritis alone. Review interactions and long-term adverse effects, and stop for two weeks before active H. pylori testing when clinically safe.

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