Gastritis and Helicobacter pylori infection

• Gastritis is inflammation of the gastric mucosa. It is best classified by cause and by whether it is acute or chronic, superficial or atrophic, instead of by endoscopic appearance alone.
• Helicobacter pylori infection is the commonest cause of chronic gastritis worldwide. It infects an estimated 40 to 60% of people, usually acquired in childhood, and persists for life unless treated. ^[3][1]
• The bacterium protects itself with urease, which neutralises gastric acid, and strains carrying CagA and VacA are more strongly tied to ulcer disease and cancer. ^[4][1][5]
• Chronic atrophic autoimmune gastritis of the body and fundus is a different disease: parietal cells are destroyed, acid is lost, intrinsic factor antibodies cause pernicious anaemia, and the risk of type 1 gastric neuroendocrine tumours and gastric cancer is raised. ^[6]
• H. pylori is diagnosed with tests of active infection (urea breath test, stool antigen, biopsy urease test, histology, culture or PCR) and is never confirmed by serology alone; preparation and test-of-cure timing must be observed. ^[4][1]
• Eradication clears the inflammation and halves the risk of gastric cancer. Bismuth quadruple therapy for 10 to 14 days is the standard first-line choice where clarithromycin resistance is high (above a 15% regional threshold). ^[2][8][9]
• Stress ulcers are acute gastric erosions in critically ill patients, most often seen within 72 hours of illness, and acid suppression is reserved for those with risk factors. ^[7]

By the end of this page you should be able to:

1. Define gastritis and separate true inflammation (gastritis) from mucosal injury without inflammation (gastropathy).
2. Classify acute and chronic gastritis by cause, including acute erosive or haemorrhagic, autoimmune body and fundus (type A), H. pylori antral (type B), lymphocytic, eosinophilic, granulomatous and Menetrier disease.
3. Explain the virulence of H. pylori and its epidemiology, and decide who needs testing and treatment.
4. Choose the correct diagnostic test and preparation, and interpret a test of cure.
5. Select first-line and salvage H. pylori regimens, including for penicillin allergy, and state why clarithromycin triple therapy is no longer first choice in high-resistance regions.
6. State the indications for stress ulcer prophylaxis in intensive care.
7. Describe the long-term risks of autoimmune gastritis and the principles of gastric cancer prevention.

Gastritis means inflammation of the gastric mucosa, and every sentence about it on this page rests on that distinction: gastropathy is mucosal injury without inflammation, and the two conditions can coexist. This is one of the most common histological findings in gastroenterology, yet the word is used loosely. A patient with "gastritis" on a barium meal or endoscopy report may have only reddening from bile reflux, alcohol or a swallowed tablet; only biopsy can separate true inflammation from injury. ^[4]

The most important single cause of chronic gastritis is H. pylori. Worldwide it colonises roughly 40 to 60% of people, usually in childhood, and stays for life unless eradicated. ^[3][1] The other major chronic pattern is autoimmune gastritis of the body and fundus. The acute patterns, by contrast, are diseases of situational injury: non-steroidal drugs, alcohol, ischaemia, shocked states and direct toxins such as cytotoxic chemotherapy. Understanding which mechanism is at work decides the management, from "stop the offending drug" to "treat H. pylori" to "surveil for neuroendocrine tumours".

Acute gastritis is usually acute erosive or haemorrhagic disease: focal loss of surface epithelium on a background of inflamed or congested mucosa. The causes are the causes of the injured stomach.

• NSAIDs and aspirin. These inhibit cyclo-oxygenase and deplete prostaglandins, removing mucus and bicarbonate secretion and mucosal blood flow. Susceptibility is highest in older adults and in anyone with a prior ulcer. ^[2]
• Alcohol. A direct irritant and vasodilator that produces acute haemorrhagic lesions.
• Acute stress and ischaemia. Shock, major trauma, surgery, burns and sepsis produce stress-related mucosal disease (SRMD): endoscopic lesions appear in 75 to 100% of critically ill patients within 72 hours, with clinically significant bleeding in 1 to 3%. ^[7]
• Curling ulcer is a duodenal ulcer after severe burns; Cushing ulcer follows head injury or raised intracranial pressure and can be gastric, duodenal or oesophageal. Both are stress ulcers: in Cushing ulcer direct vagal stimulation raises acid secretion. ^[7]
• Bile reflux. After gastric or biliary surgery, refluxed bile and pancreatic juice damage the gastric mucosa, producing alkaline reflux gastritis. ^[1]
• Other direct toxins. Cytotoxic chemotherapy, radiation, corrosives and swallowed foreign bodies.

Chronic gastritis is classified phenotypically by distribution (antrum-predominant, corpus-predominant, diffuse or multifocal) and etiologically by cause. The Sydney system, and its Houston update, records both. A few major patterns matter in practice.

Chronic non-atrophic H. pylori gastritis. Antral-predominant, non-atrophic inflammation with neutrophils in the superficial epithelium and lymphocytes in the lamina propria, driven entirely by the organism. This is the commonest form worldwide. ^[1][3]

Chronic atrophic autoimmune gastritis (type A). An immune attack on parietal cells of the body and fundus, mediated by autoantibodies against the H+/K+-ATPase proton pump. Fundic glands are destroyed; acid, pepsin and intrinsic factor are lost; gastrin rises; and enterochromaffin-like (ECL) cell hyperplasia sets in. Serum parietal cell antibodies (PCA, also called antiparietal cell antibodies) are present in most patients, and intrinsic factor antibodies (IFA) appear in a minority but are more specific. Loss of intrinsic factor produces pernicious anaemia. Because these patients lack acid, H. pylori is rarely found. The pattern is corpus-predominant fundic atrophy with antral sparing. ^[6]

Type B H. pylori antral gastritis. Corpus-sparing antral inflammation from H. pylori. Types A and B were historically distinguished by their natural history: type B (antral, H. pylori-driven) carries the main risk of peptic ulcer and distal gastric cancer, whereas type A (autoimmune, body and fundus) carries the risk of pernicious anaemia, ECL hyperplasia, type 1 gastric neuroendocrine (carcinoid) tumours and gastric cancer. ^[2][6]

Menetrier disease is giant hypertrophy of the gastric folds, usually in the body, with protein-losing gastropathy, hypoproteinaemia and relative achlorhydria. H. pylori may play a role in some cases and eradication can help. ^[1]

Other chronic patterns are defined by the predominant inflammatory cell:

• Lymphocytic gastritis: a dense infiltrate of intraepithelial lymphocytes, often in the body. It is associated with coeliac disease, H. pylori and, in some regions, varicella-zoster infection, and it presents with protein loss, anaemia or dyspepsia. ^[1]
• Eosinophilic gastritis (and gastroenteritis): eosinophil-rich infiltrate of the mucosa, often with peripheral eosinophilia and allergy; a different disease from the hypereosinophilic syndrome. ^[1]
• Granulomatous gastritis: non-caseating or caseating granulomas in the mucosa or wall. Sarcoidosis, Crohn disease, tuberculosis, syphilis, foreign bodies and fungal infection are the usual causes; acid-fast or fungal stains and clinical correlation are essential before a diagnosis is made. ^[1]

The simple way to remember the atrophic gastric diseases is to ask which part of the stomach is destroyed: in autoimmune disease the body and fundus; in H. pylori disease the antrum first, with progression to multifocal atrophy and intestinal metaplasia if infection persists for decades. ^[2][6]

H. pylori is a microaerophilic, gram-negative, spiral-shaped bacterium that lives in the gastric mucus layer. It infects about 50 to 60% of the world, with higher prevalence in resource-limited regions and lower prevalence in wealthy, low-transmission settings. ^[3] The Brazilian consensus estimated roughly 40% of the global population and showed the familiar gradient: prevalence is higher in developing countries, rural areas and households with poor sanitation. ^[1] Li and colleagues estimated a fall from 58.2% in the 1980s to 43.1% in 2011 to 2022 across 224 studies and nearly 3,000,000 people. ^[1]

Acquisition is usually in childhood, often before the age of 10, through close family contact in settings of crowded living and poor sanitation. ^[1][3] Person-to-person transmission within families is common in developing countries, with greatest concordance between mothers or siblings and children; the fecal-oral and oral-oral routes are the most likely, with water, food and gastro-oral routes also described. ^[1] Once established it persists for life. Reinfection after successful eradication is low in adults in developed countries (under 2% per year) but higher in developing countries (up to 5 to 10% per year) and in children. ^[1]

Autoimmune (type A) gastritis is far less common, with estimates from referral series rather than population studies. It affects middle-aged and older adults and is more common in women. It is strongly associated with other autoimmune disease, particularly autoimmune thyroid disease and type 1 diabetes, and with pernicious anaemia. ^[6]

In critical illness, endoscopic mucosal lesions appear in 75 to 100% of patients within 72 hours, but only 1.5 to 8.5% develop overt bleeding and 1 to 3% life-threatening bleeding. ^[7]

For H. pylori there is no single modifiable risk factor: infection is determined by childhood environment, sanitation and crowding, with familial sharing of strains. ^[1][3] Family-based test-and-treat strategies reduce recurrence better than treating individuals alone. ^[1]

Risk groups include people living with poor basic sanitation or in rural communities, household members of infected people, immunocompromised patients (transplant, chemotherapy, HIV), and people with chronic illness. Healthcare workers in endoscopy units historically carried a slightly raised risk, but universal disinfection has largely removed it. ^[1]

Autoimmune gastritis is an autoimmune disease of the gastric body and fundus, more frequent in people with thyroid autoimmunity and other autoimmune conditions. ^[6] Parietal cell antibodies are the serological marker; intrinsic factor antibodies are more specific but less sensitive. ^[6]

Acute erosive gastritis follows from NSAID or aspirin use (older age, prior ulcer, co-therapy with steroids or anticoagulants), alcohol, burns or critical illness (Curling and Cushing ulcers), bile reflux after surgery, and direct toxins. ^[2][7]

H. pylori is microaerophilic, spiral and motile, with flagella that drive it through gastric mucus. Three virulence traits dominate the clinical picture.

1. Urease splits urea into ammonia and carbon dioxide. The ammonia neutralises acid in the bacterial microenvironment and also damages epithelium directly; urease activity is the basis of the urea breath test and the rapid urease test. ^[4]
2. CagA (cytotoxin-associated gene A) is injected into epithelial cells via a type IV secretion system. It disrupts signalling, causes cytoskeletal changes, increases inflammation and is linked to peptic ulcer disease and distal gastric cancer. CagA-positive strains are cytotoxic. ^[1][5]
3. VacA (vacuolating cytotoxin A) forms anion-selective channels in membranes, induces vacuolation in epithelial cells, disrupts mitochondria and modulates immune responses, helping the bacterium survive in acid. Alleles s1 and m1 are linked to more severe disease. ^[5]

The result of chronic colonisation is a local mucosal immune response: neutrophils within the epithelium (active chronic gastritis) plus lamina propria lymphocytes and plasma cells, with progressive damage to gastric glands. Depending on host genetics, strain virulence and duration of infection, this may lead to atrophy, intestinal metaplasia and, over decades, gastric adenocarcinoma; or, if it remains confined to the antrum, to gastric or duodenal ulcer disease. ^[1][2]

H. pylori also alters gastric physiology. Antral gastritis raises gastrin, increases acid output and encourages duodenal ulcer disease. Corpus-predominant atrophic gastritis reduces acid, encourages intestinal metaplasia and increases cancer risk. ^[2]

Eradication removes the inflammatory stimulus, gastric histology can improve and cancer risk falls. ^[2][9]

In type A disease the immune attack destroys parietal cells in the body and fundus. Acid and pepsin fall, gastrin rises, ECL cells proliferate under chronic hypergastrinaemia and form type 1 (gastrin-driven) gastric neuroendocrine tumours; these are usually small, multiple and indolent but must be recognised. Pernicious anaemia develops when intrinsic factor is lost and vitamin B12 malabsorption follows. ^[6]

The classic teaching cascade is: loss of acid leads to hypergastrinaemia, which drives ECL hyperplasia, then dysplasia and NETs. Intrinsic factor loss drives vitamin B12 deficiency and pernicious anaemia. H. pylori does not cause this pattern and is usually absent, though past infection may have triggered the autoimmune process in some patients. ^[6]

Stress ulcers are produced by sympathetic over-activity and splanchnic hypoperfusion. Vasoconstriction reduces mucosal blood flow, gastric emptying slows so acid and pepsin stagnate, and the mucus-bicarbonate barrier fails. The stomach is injured by its own acid without needing H. pylori. ^[7]

Histology is the gold standard for the type of gastritis. Acute erosive disease shows focal epithelial loss with haemorrhage and fibrin. Chronic H. pylori gastritis shows superficial lamina propria inflammation, lymphoid follicles and, with Giemsa or immunostain, spiral organisms in the mucus. Autoimmune disease shows body and fundus atrophy with lymphocytic infiltrates, loss of oxyntic glands, pseudopyloric or intestinal metaplasia, ECL cell hyperplasia (confirmed with chromogranin A or synaptophysin stain) and spared antrum. Updated Sydney sampling takes at least two biopsies from the antrum, two from the corpus and one from the incisura; the MAPS II recommendation is two from the antrum and two from the corpus. ^[1][2]

H. pylori gastritis is often silent. When symptomatic it causes epigastric pain or burning, post-prandial fullness, early satiety, nausea and belching. Many describe "indigestion". Alarm symptoms are more common with ulcer disease than with uncomplicated gastritis: vomiting, bleeding, weight loss, dysphagia and anaemia. ^[2][3]

Autoimmune gastritis is similarly silent early. Later patients present with pernicious anaemia (macrocytic anaemia, fatigue, glossitis, subacute combined degeneration of the cord) and with dyspepsia. Neurological involvement can be severe, even with modest anaemia. ^[6]

Stress ulcer declares itself as upper gastrointestinal bleeding in someone already critically ill: haematemesis, coffee-ground vomitus, melaena, or a sudden drop in haemoglobin. It can also perforate. ^[7]

Acute erosive gastritis gives sudden epigastric pain, nausea and often haematemesis, particularly in drinkers, patients on NSAIDs, and the recently burned or critically injured. ^[2]

Most patients have a normal examination. Epigastric tenderness is common but non-specific. Signs of anaemia (pallor, koilonychia in chronic autoimmune disease) and neurological signs (impaired vibration and proprioception, spasticity) may be the clue in pernicious anaemia. Bleeding manifests as hypotension and tachycardia. ^[2][6]

The differential is broad because "dyspepsia" is a symptom, not a diagnosis.

• Peptic ulcer disease. Penetration, bleeding and pain that wakes the patient at night point more to ulcer than to uncomplicated gastritis. ^[2]
• Gastro-oesophageal reflux disease. Burning rising into the chest, worse after meals and lying down, responds to acid suppression. ^[2]
• Functional (non-ulcer) dyspepsia. Meets Rome IV criteria, with normal endoscopy. ^[2]
• Gastric or oesophageal malignancy. New dyspepsia after the age of 55, weight loss, anorexia, dysphagia, bleeding, early satiety or a mass. ^[1]
• Medication-induced injury. Bisphosphonates, iron, potassium, cytotoxic drugs, alcohol. ^[1]
• Bile reflux gastropathy, eosinophilic, lymphocytic and granulomatous gastritis as above.
• Zollinger-Ellison syndrome in severe or recurrent ulcer disease with diarrhoea: gastrin-secreting tumour, diagnosed by raised fasting gastrin.

Endoscopy separates these reliably; when endoscopy is unavailable, a treat-and-test strategy is reasonable in young patients without alarm features. ^[1]

Endoscopy is indicated for alarm symptoms, for dyspepsia in patients above the local age threshold, for suspected bleeding, and whenever risk stratification matters. Endoscopic appearances (redness, swelling, nodularity, atrophy) are not specific and do not confirm infection. Biopsies at the recommended sites allow histology, a rapid urease test, culture or PCR. ^[1][4]

Choosing the test follows the question: documenting active infection for diagnosis, or confirming success after treatment.

Preparation decides accuracy. Stop proton pump inhibitors and potassium-competitive acid blockers 14 days, H2-receptor blockers 2 hours, and antibiotics and bismuth compounds 4 weeks before diagnostic testing. Continue antacids, alginates and sucralfate without restriction. ^[1]

For a test of cure, use a urea breath test or monoclonal stool antigen test, taken at least 4 weeks after treatment is completed, and at least 6 weeks after therapy was started, with the same washout intervals observed. The Brazilian consensus states this plainly: breath or stool testing at least 6 weeks after therapy starts, 2 weeks after stopping PPIs and 4 weeks after stopping antibiotics. ^[1]

Serology for parietal cell antibodies (PCA) and intrinsic factor antibodies (IFA); serum gastrin (raised); fasting pepsinogens (low pepsinogen I in corpus atrophy); full blood count and vitamin B12 level; autoantibodies to thyroid. Endoscopy with biopsies is needed to stage atrophy and exclude dysplasia or NETs. ^[6]

Endoscopy is for alarm symptoms, for patients at or above the local age threshold for dyspepsia, for suspected bleeding, anaemia or weight loss, for high gastric cancer risk, and whenever histological staging of atrophy or metaplasia is needed. Where it is unavailable, non-invasive test-and-treat is appropriate for people under 45 without alarm symptoms, particularly in high-prevalence settings. ^[1][2]

There is no severity score for gastritis itself; classification is histological (Sydney system) and staging of premalignant change (OLGA for atrophy, OLGIM for intestinal metaplasia) guides surveillance. Autoimmune gastritis is diagnosed by histology (body and fundus atrophy with sparing of the antrum) plus autoantibodies; pernicious anaemia by macrocytic anaemia with low vitamin B12 and a positive intrinsic factor antibody. ^[6]

Eradication is indicated for H. pylori-positive chronic gastritis, peptic ulcer disease, functional dyspepsia, uninvestigated dyspepsia below the age threshold, gastric MALT lymphoma, early gastric cancer after endoscopic or surgical resection, first-degree relatives of gastric cancer patients, iron deficiency anaemia and immune thrombocytopenia of unclear cause, long-term NSAID or aspirin users, and patients with gastric precancerous conditions. ^[1][9]

MALT lymphoma (localized, low-grade, stage IE) is an established indication: removing H. pylori removes the antigen drive and can produce durable histological remission in most such tumours; concomitant lesions and response should be confirmed endoscopically. ^[1][8]

Treatment is more effective when acid is well suppressed, so a standard or high dose of a proton pump inhibitor, or a potassium-competitive acid blocker such as vonoprazan 20 mg twice daily, underpins every regimen. ^[1][2]

Bismuth quadruple therapy achieves eradication above 90% even in resistant strains and is the standard first-line empirical choice in the Maastricht VI consensus, the 2024 ACG guideline, the Korean 2025 guideline and the Brazilian consensus. ^[2][8][9] Concomitant therapy is a good alternative where susceptibility testing is not available; clarithromycin-containing regimens are limited or avoided where regional clarithromycin resistance exceeds 15% (modern Korean series report 33%). ^[2]

P-CABs such as vonoprazan produce deeper and more durable acid suppression than PPIs and raise eradication rates: in direct comparisons, vonoprazan-based regimens eradicated in 88.4% versus 79.0% for PPI-based ones. ^[2] Vonoprazan is therefore preferred when available, especially in clarithromycin, amoxicillin and levofloxacin regimens. ^[1][2]

Do not repeat a failed regimen. After failure of clarithromycin-based triple therapy, use second-line bismuth quadruple therapy or levofloxacin-based therapy; after BQT failure, use rifabutin-based triple therapy (rifabutin 150 mg twice daily, amoxicillin 1 g twice daily and a PPI, preferably 14 days) or a salvage BQT. Rifabutin resistance is extremely low (under 1%) and eradication in refractory disease is around 96%, but myelotoxicity and mycobacterial resistance must be considered. ^[2][1]

After three failures, susceptibility (genotypic or phenotypic) testing should guide the choice; even then salvage regimens achieve eradication in 80 to 90% of cases. ^[2]

In confirmed or uncertain penicillin allergy, first-line treatment is bismuth quadruple therapy for 10 to 14 days, or dual therapy with tetracycline and a P-CAB for 14 days; second-line options include an unused first-line option or clarithromycin-quinolone-PPI triple therapy for 14 days. ^[1]

This is the "test-and-treat" approach: people with uninvestigated dyspepsia under 45 without alarm symptoms, dyspepsia with alarm features requiring endoscopy, ulcer disease, a personal or family history of gastric cancer, gastric MALT lymphoma, early gastric cancer resection, and planned long-term NSAID or aspirin. ^[1] Guidelines also support testing before or during long-term PPI therapy for reflux, because acid suppression shifts H. pylori into the corpus and accelerates atrophy. ^[1]

• Always stop PPIs and P-CABs 14 days, H2-blockers 2 hours, antibiotics and bismuth 4 weeks before testing. ^[1]
• Confirm eradication 4 to 6 weeks after completing treatment, and 6 weeks or more after starting it. ^[1]
• Use the urea breath test or validated monoclonal stool antigen test as the test of cure; serology is useless for this. ^[1][4]
• Re-test, re-confirm washout, and consider susceptibility testing after failure. ^[2]

• Acute erosive gastritis: stop the offending drug (NSAID, alcohol), give a PPI, and add antiemetic and fluid support if needed. Investigate bleeding with endoscopy when alarm features exist. ^[2][7]
• Autoimmune gastritis: no anti-H. pylori treatment is needed unless the organism is present. Replace vitamin B12 (intramuscular, then maintenance) for pernicious anaemia; monitor iron; screen for other autoimmunity. ^[6]
• Menetrier disease: a trial of H. pylori eradication, nutritional support and, in severe protein loss, octreotide or gastric resection. ^[1]
• Lymphocytic, eosinophilic, granulomatous gastritis: treat the underlying cause (coeliac disease, allergy, infection, drug) rather than acid. ^[1]

After eradication, H. pylori-associated chronic gastritis settles histologically over months. Patients with intestinal metaplasia or atrophy need an endoscopic surveillance strategy based on local guidance (commonly 3 yearly for high-risk OLGA/OLGIM stages). ^[1] Autoimmune gastritis warrants structured surveillance because of NET and cancer risk; MAPS III supports endoscopic surveillance every 3 years, whereas some societies consider evidence insufficient for routine intervals. ^[6]

Refer for upper gastrointestinal bleeding, perforation, alarm symptoms, uncertain diagnosis, refractory infection, suspected or confirmed NET or cancer, and any case needing endoscopic therapy or surgery. ^[1]

• Peptic ulcer and bleeding. The commonest clinically significant consequence of chronic H. pylori gastritis. ^[2]
• Gastric adenocarcinoma. Risk rises with decades of persistent infection, atrophy and intestinal metaplasia. ^[2][9]
• Gastric MALT lymphoma. Antigen-driven; eradication can produce cure. ^[1]
• Pernicious anaemia and neurological complications in autoimmune gastritis. ^[6]
• Type 1 gastric NETs from ECL hyperplasia in autoimmune (and occasionally H. pylori) atrophy. ^[6]
• Nutrient deficiencies: iron and vitamin B12 even before frank anaemia. ^[6]
• Perforation in stress ulcer disease, mortality up to 20%. ^[7]

Uncomplicated H. pylori gastritis has an excellent prognosis after eradication: inflammation resolves and symptoms settle. Cancer risk is lowered, with cohort studies and trials showing reduced gastric cancer incidence (relative risk 0.65, 95% confidence interval 0.48 to 0.88) and cancer-related mortality when eradication is given before preneoplastic changes. ^[2] Autoimmune gastritis carries a higher long-term burden: gastric neoplasm incidence of about 2.08 per 1000 person-years for cancer, 5.35 for dysplasia and 14.56 for type 1 NETs; pernicious anaemia carries roughly a 2.7 to 2.8-fold risk of gastric cancer. ^[6] Stress ulcers in the critically ill carry high mortality when bleeding occurs (around 49% versus 9% in non-bleeding patients). ^[7]

• Primary prevention of H. pylori-related disease is, at present, impractical beyond sanitation and hygiene; family-based screen-and-treat strategies reduce reinfection. ^[1]
• Eradication prevents cancer best when given before atrophy or intestinal metaplasia develop. ^[2]
• Avoid NSAIDs and alcohol where possible; if NSAIDs are essential, use the lowest effective dose, a PPI and, where appropriate, test and treat for H. pylori. ^[1]
• Autoimmune gastritis: structured endoscopic surveillance every 3 years in high-risk disease, with NET surveillance guided by endoscopy. ^[6]
• Family history of gastric cancer: test and treat first-degree relatives. ^[1]

In regions with high H. pylori prevalence and limited endoscopy, whole-population eradication is being explored as a cancer prevention strategy; community-based eradication has reduced cancer incidence in trial settings. Where access is restricted:

• Favour non-invasive test-and-treat using validated breath or stool tests in people under 45 without alarm symptoms. ^[1]
• Use empiric bismuth quadruple therapy where resistance data are unknown, because it retains high eradication rates even for resistant strains. ^[2]
• Improve sanitation, water and crowding conditions, which matter more than case-by-case treatment for long-term prevalence reduction. ^[1]
• Ensure treatment outcomes are confirmed with breath or stool testing rather than presumed. ^[1]

• Pregnancy. Avoid routine eradication unless there is a compelling indication such as complicated ulcer disease; manage with gestation-safe regimens and specialist advice. (Specific dosing in pregnancy is beyond the scope of this page.)
• Children. Infection is usually acquired in childhood; treatment follows paediatric weight-based dosing not covered here.
• Older adults. Polypharmacy and reduced renal function make metronidazole and bismuth harder to use; interactions and pill burden reduce adherence.
• Immunocompromised patients are at raised risk of acquisition and may have more severe disease. ^[1]

• Gastritis is mucosal inflammation diagnosed histologically; endoscopic redness alone does not prove it.
• H. pylori is the commonest cause of chronic gastritis, infecting about 40 to 60% of humanity and usually acquired before the age of 10. ^[3][1]
• Urease neutralises acid and powers both the breath and rapid urease tests; CagA and VacA mark more virulent, ulcer- and cancer-associated strains. ^[4][1][5]
• Autoimmune (type A) gastritis attacks the body and fundus, destroys acid secretion, causes pernicious anaemia and raises the risk of type 1 gastric NETs and cancer. ^[6]
• Types, site and atrophy are best described by the Sydney classification; surveillance staging uses OLGA and OLGIM.
• Diagnosis of H. pylori requires a test of active infection (UBT, stool antigen, urease, histology, culture or PCR); serology cannot prove current infection or cure. ^[4][1]
• Correct preparation (PPIs and P-CABs off for 14 days, antibiotics and bismuth off for 4 weeks) and test-of-cure timing (4 to 6 weeks after treatment) are essential. ^[1]
• Treat H. pylori in all infected patients with dyspepsia or ulcer disease, gastric MALT lymphoma, early gastric cancer, atrophic gastritis, family history, long-term NSAID users and selected haematological conditions. ^[1]
• Bismuth quadruple therapy for 10 to 14 days is the standard first-line empirical choice where clarithromycin resistance exceeds 15%; concomitant therapy is a solid alternative. ^[2][8][9]
• Keep clarithromycin triple therapy for low-resistance regions or susceptibility-confirmed cases; avoid below the 80% eradication threshold. ^[2]
• MALT lymphoma (stage IE) can regress after eradication. ^[1][8]
• Stress ulcers occur in 75 to 100% of critically ill patients within 72 hours but bleed significantly in only 1 to 3%; reserve prophylaxis for high-risk patients. ^[7]
• Gastric cancer prevention depends on eradicating before atrophy and intestinal metaplasia develop. ^[2]
• Autoimmune gastritis carries a raised lifelong risk of pernicious anaemia, type 1 NETs and gastric cancer and merits structured surveillance. ^[6]

No separate linked topics are listed here; this page stands on its own.