Gastritis and gastropathy

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

The word gastritis is often used loosely for upper abdominal symptoms or red mucosa, but the clinically useful task is to define mechanism. Active H. pylori gastritis, autoimmune oxyntic atrophy, lymphocytic, eosinophilic or granulomatous inflammation and rare infections have different implications. Reactive gastropathy from NSAIDs or bile may show foveolar hyperplasia with little inflammation. Critical illness can cause stress-related erosive injury, while alcohol may aggravate acute mucosal damage without explaining every chronic symptom.

Pattern matters. H. pylori often begins in the antrum and can extend proximally; multifocal atrophy and intestinal metaplasia increase adenocarcinoma risk. Autoimmune disease is corpus-predominant with relative antral sparing, hypergastrinaemia and enterochromaffin-like-cell stimulation, linking it to type 1 gastric neuroendocrine tumours as well as adenocarcinoma. Iron deficiency may precede macrocytosis or neurological B12 manifestations because acid is needed for dietary iron absorption.

Treatment is cause-specific. Eradicate active H. pylori and verify cure when risk warrants; stop or reduce NSAIDs and add gastroprotection only when benefit outweighs harm; replace iron and B12 deficits; and manage portal hypertension through hepatology. Atrophy, metaplasia or dysplasia requires high-quality endoscopic mapping and a surveillance decision based on extent, histology, family history and other risk factors rather than a blanket annual gastroscopy.

Key points

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.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Helicobacter pylori

Chronic H. pylori colonisation is a common cause of active gastritis and links ulcer disease with atrophy, metaplasia and gastric neoplasia.

Autoimmune gastritis

Immune destruction of corpus parietal cells causes achlorhydria, hypergastrinaemia, early iron deficiency and later vitamin B12 deficiency.

Reactive chemical injury

NSAIDs, aspirin, bile reflux, alcohol and chemical exposure injure surface epithelium with relatively little inflammation, producing reactive gastropathy.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Barrier disruption
Infection or chemical injury weakens mucus, bicarbonate and epithelial repair, increasing exposure of the mucosa to acid and luminal irritants.
2
Chronic inflammatory remodelling
Persistent immune activation causes gland loss and replacement by metaplastic epithelium in susceptible gastric regions and alters acid secretion.
3
Functional and neoplastic consequences
Achlorhydria alters iron and vitamin absorption and raises gastrin, while metaplastic fields accumulate dysplasia and cancer risk.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Non-specific dyspepsia

Epigastric discomfort, nausea, bloating and early satiety may accompany gastritis but also functional dyspepsia, ulcer, reflux, gastroparesis, biliary disease and cancer. Symptoms cannot supply histology.

Erosive bleedingRed flag

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.

Autoimmune deficiency pattern

Refractory iron deficiency, B12 deficiency, glossitis, neuropathy or another autoimmune condition can signal corpus atrophy. Macrocytosis may disappear when iron deficiency coexists.

Premalignant histology

Gastric atrophy, intestinal metaplasia or dysplasia on a biopsy changes the problem from symptom control to topographical staging, H. pylori treatment and cancer-risk planning.

Systemic inflammatory clue

Marked eosinophilia, Crohn's disease, sarcoidosis, immunosuppression or unusual infection exposure may support a less common inflammatory gastritis and should guide extra sampling and multidisciplinary review.

Phlegmonous or caustic dangerRed flag

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.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
High-quality upper-GI endoscopyFirst step
Why
Inspect mucosa, exclude ulcer or cancer and direct systematic biopsy.
Interpretation and limitations
Describe erosions, nodularity, atrophy, vascular pattern, bile and focal lesions using landmarks and images. Normal-looking mucosa can still have autoimmune or H. pylori gastritis; erythema alone is not diagnostic.
02
Topographical gastric biopsies
Why
Determine inflammatory type, distribution, atrophy, metaplasia and dysplasia.
Interpretation and limitations
Separate antral and corpus samples and target visible abnormalities according to current BSG, AUGIS and RCPath guidance. Correct labelling allows the pathologist to distinguish multifocal H. pylori injury from corpus-predominant autoimmune disease.
03
Active H. pylori assessment
Why
Find a treatable carcinogenic and ulcerogenic infection.
Interpretation and limitations
Use histology or urease testing at endoscopy, or properly prepared breath or stool antigen testing. Suppressive medicines and atrophy can reduce organism density, so reconcile results and repeat when discordant.
04
FBC, ferritin, B12 and folate
Why
Detect haematological consequences of bleeding, achlorhydria and intrinsic-factor loss.
Interpretation and limitations
Low ferritin may appear years before B12 deficiency in autoimmune gastritis. Neurological B12 deficiency can occur without anaemia or macrocytosis, so treat the person and biochemical evidence promptly.
05
Anti-intrinsic-factor antibody
Why
Support autoimmune gastritis as the cause of vitamin B12 deficiency.
Interpretation and limitations
A positive result is strongly supportive; a negative result does not exclude the diagnosis. NICE recommends further specialist testing when suspicion persists, potentially including parietal-cell antibodies, gastrin and endoscopic biopsy.
06
Cancer-risk staging
Why
Define whether atrophy or metaplasia is limited or extensive and identify dysplasia.
Interpretation and limitations
Disease involving antrum and body carries higher risk than antral-only change. Dysplasia should be confirmed by expert pathology and linked to careful repeat examination or resection rather than routine symptom follow-up.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Functional dyspepsia

Symptoms without histological inflammation or structural explanation support functional disease; mild endoscopic erythema alone does not prove gastritis.

Peptic ulcer or cancer

A discrete mucosal break, irregular mass, weight loss or anaemia requires adequate biopsy and follow-up beyond the descriptive label gastropathy.

Portal hypertensive gastropathy

Cirrhosis with a mosaic or snakeskin vascular pattern favours congestive portal disease rather than primary inflammatory gastritis.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01DefineName the gastric mechanismFirst stepEndoscopy, anaemia, B12 deficiency or persistent upper-GI symptoms raises concern for mucosal disease.

1Review H. pylori, NSAIDs, aspirin, alcohol, bile-reflux surgery, portal hypertension, autoimmune history and immunosuppression rather than accepting a previous non-specific gastritis label.
2Use 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.
3Integrate pathology with active-infection testing, FBC, ferritin, B12 and autoimmune studies, referring unexplained or discordant patterns for specialist review.

02CorrectTreat cause and deficiencyA specific infectious, autoimmune, chemical or portal-hypertensive mechanism has been established.

1Eradicate confirmed H. pylori using current resistance-aware therapy and check cure where ulcer, premalignant change or treatment failure makes this important.
2Withdraw or minimise damaging NSAIDs and chemical exposure, manage portal hypertension through hepatology, and use acid suppression only for a defined erosive, ulcer or gastroprotection indication.
3Replace iron and vitamin B12 according to measured deficit and NICE guidance, explaining that autoimmune gastritis commonly requires lifelong B12 replacement even after symptoms improve.

03StratifyManage premalignant changeBiopsy identifies gastric atrophy, intestinal metaplasia or epithelial dysplasia.

1Confirm topographical extent with high-quality inspection and mapping if the original examination was incomplete, and ask pathology to review uncertain dysplasia.
2Offer H. pylori eradication and address smoking and family history, then apply BSG surveillance criteria rather than enrolling every focal antral finding automatically.
3Refer visible dysplasia or early neoplasia to an expert endoscopy MDT for en-bloc resection assessment, while non-visible dysplasia requires prompt repeat enhanced examination.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Corrects haematological and neurological consequences of impaired intrinsic-factor-mediated absorption.

Vitamin B12 replacement for autoimmune gastritis

Use 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.

Supports healing or gastroprotection in acid-related and drug-related injury but does not eradicate H. pylori or reverse autoimmune atrophy.

Cause-specific acid suppression

Choose 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.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Ulceration and bleeding

Erosive chemical injury or H. pylori-associated mucosal damage can cause occult loss, haematemesis or clinically important anaemia.

Iron and vitamin B12 deficiency

Hypochlorhydria impairs iron handling, while loss of intrinsic factor eventually causes vitamin B12 deficiency, neuropathy and megaloblastic anaemia.

Premalignant mucosal change

Atrophy and intestinal metaplasia increase gastric adenocarcinoma risk, while autoimmune hypergastrinaemia promotes gastric neuroendocrine tumours through enterochromaffin-like-cell stimulation.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Track dyspepsia, bleeding, weight, intake and medicine exposure while recognising that symptoms correlate poorly with microscopic activity.
Repeat FBC, ferritin and B12 response after replacement, assessing neurological recovery and searching for another source if deficiency fails to correct.
Confirm H. pylori eradication under valid test conditions when ulcer, atrophy, metaplasia or later-line treatment makes residual infection consequential.
For autoimmune gastritis, maintain lifelong B12 ownership and investigate new upper-GI symptoms promptly because adenocarcinoma and neuroendocrine tumour risk is increased.
Record the topographical extent and surveillance interval for premalignant mucosa, with a recall system rather than relying on the patient to request repeat endoscopy.
Review continued NSAID, aspirin, alcohol and PPI exposure and remove medicines that no longer have a defined benefit.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Red is not histology

Endoscopic erythema is common and non-specific; inflammation, reactive injury and normal variation can look similar without appropriately labelled biopsies.

Iron may fall first

Loss of gastric acid in autoimmune gastritis impairs non-haem iron absorption, so iron deficiency can precede intrinsic-factor-related B12 deficiency.

Macrocytosis can vanish

Concurrent iron deficiency may normalise or lower mean cell volume, meaning a normal MCV cannot safely exclude clinically important B12 deficiency.

Distribution explains mechanism

Relative antral sparing with corpus atrophy supports autoimmune disease, while multifocal antral and body change often reflects longstanding H. pylori injury.

Eradication is not erasure

Removing H. pylori reduces future injury, but extensive established metaplasia or dysplasia still needs its own risk and surveillance plan.

11Common pitfallsFrequent interpretation and management errors.

01
Using gastritis as a synonym for any epigastric discomfort without tissue or a defined mechanism.
02
Treating endoscopic erythema with indefinite PPI while ignoring H. pylori and NSAID exposure.
03
Excluding autoimmune gastritis because intrinsic-factor antibodies are negative.
04
Waiting for macrocytic anaemia before considering neurological vitamin B12 deficiency.
05
Placing focal antral metaplasia and extensive antrum-plus-body disease into the same surveillance category.
06
Replacing B12 but failing to address iron deficiency, gastric neoplasia risk and lifelong treatment ownership.