Gastritis — H. pylori, Causes, Symptoms & Treatment Guide — Symptoms, Causes & Treatment | MyMedicPlus

Gastritis is inflammation of the gastric mucosa (stomach lining), which may be acute or chronic, focal or diffuse. It represents a spectrum from mild mucosal erythema to erosive gastritis with ulceration and haemorrhage. The most important clinical distinction is between erosive gastritis (associated with bleeding, H. pylori, NSAIDs, alcohol, and physiological stress) and non-erosive gastritis (often asymptomatic, detected incidentally or associated with autoimmune atrophic gastritis). Helicobacter pylori infection is the most common cause worldwide, affecting approximately 44% of the global population, with highest prevalence in developing countries. Chronic atrophic gastritis from H. pylori or autoimmune causes (Type A gastritis — destroying parietal cells, causing achlorhydria and vitamin B12 malabsorption/pernicious anaemia) is a precursor to gastric cancer — the third leading cause of cancer death globally.

Infectious: Helicobacter pylori (the most common cause globally — a gram-negative spiral bacterium colonising the gastric mucosa, persisting for life if untreated, causing chronic active gastritis, peptic ulcer disease, and increasing gastric cancer risk 3-6 fold). Less common infectious causes: CMV, EBV, Candida (in immunocompromised patients), Anisakis (fish parasite). Medications: NSAIDs (ibuprofen, naproxen, aspirin — inhibit prostaglandin synthesis, reducing mucosal protective factors; up to 30% of regular users develop gastritis or erosions); corticosteroids (combined with NSAIDs, the risk of peptic ulceration increases 15-fold). Alcohol: direct mucosal toxic effect — acute haemorrhagic gastritis. Stress: stress-related mucosal disease (SRMD) in critically ill patients — ICU, major surgery, burns (Curling's ulcers), head injury (Cushing's ulcers). Autoimmune (Type A): antibodies against parietal cells and intrinsic factor destroy acid-secreting parietal cells — causing chronic atrophic gastritis, achlorhydria, and pernicious anaemia (vitamin B12 malabsorption). Bile reflux, radiation, and ischaemia are rarer causes.

Many patients with gastritis (particularly H. pylori-associated) are asymptomatic — the condition is discovered on endoscopy performed for other indications. Symptomatic gastritis typically causes: epigastric pain or burning (above the navel, below the breastbone), nausea and vomiting, bloating and early satiety (feeling full after only a small amount of food), belching, and loss of appetite. Symptoms may worsen with food (most common) or be relieved by eating (in duodenal ulcer-pattern dyspepsia). Erosive gastritis and peptic ulceration may cause haematemesis (vomiting blood — may be bright red or coffee-ground coloured) or melaena (black, tarry stools from upper GI bleeding) — a medical emergency. Autoimmune atrophic gastritis additionally causes symptoms of vitamin B12 deficiency: fatigue, glossitis, paraesthesia, and neurological features.

Upper GI endoscopy (OGD — oesophagogastroduodenoscopy) is the gold standard: directly visualises the gastric mucosa, grades the degree of inflammation and erosion, takes biopsies for histology (including Sydney system grading of gastritis, H. pylori detection, and intestinal metaplasia assessment). Rapid urease test (CLO test) on endoscopic biopsy: detects H. pylori in the biopsy tissue. Non-endoscopic H. pylori testing: 13C-urea breath test (UBT — most accurate non-invasive test, excellent for confirmation after treatment; must stop PPIs for 2 weeks and antibiotics for 4 weeks before testing); H. pylori stool antigen test (HpSA — comparable accuracy to UBT, useful for primary testing and post-treatment confirmation); serology (IgG antibodies — cannot distinguish active from past infection; not recommended for routine testing). Blood tests: FBC (anaemia from blood loss or B12 deficiency), intrinsic factor antibodies and anti-parietal cell antibodies (autoimmune gastritis), serum B12 and folate, and serum gastrin (elevated in atrophic gastritis).

H. pylori eradication: standard first-line therapy is 14-day triple therapy — proton pump inhibitor (omeprazole 20 mg or lansoprazole 30 mg BD) plus two antibiotics (amoxicillin 1 g BD plus clarithromycin 500 mg BD). Eradication rates have fallen to 70-80% in many countries due to clarithromycin resistance; bismuth quadruple therapy (bismuth subcitrate, tetracycline, metronidazole, PPI — 14 days) achieves above 90% eradication and is recommended where clarithromycin resistance exceeds 15% or as second-line therapy. Confirm eradication with UBT or stool antigen 4-8 weeks after completing treatment (with PPI stopped 2 weeks before testing). NSAID-induced gastritis: stop or reduce the NSAID dose; switch to selective COX-2 inhibitor (celecoxib) if NSAID must continue; add PPI (omeprazole 20 mg or pantoprazole 40 mg daily) for gastroprotection in high-risk patients. PPI therapy: for acute symptom relief (antacids — calcium carbonate, magnesium hydroxide — for immediate relief); H2 blockers (famotidine, ranitidine) for mild gastritis. Autoimmune gastritis: 3-monthly vitamin B12 injections (hydroxocobalamin 1 mg IM) for life to treat pernicious anaemia; endoscopic surveillance every 3-5 years for gastric cancer risk.

Untreated gastritis — particularly from H. pylori infection — can progress to serious complications over years to decades. H. pylori-associated gastritis increases the lifetime risk of peptic ulcer disease (duodenal ulcer in 10-20%, gastric ulcer in 2-5%); peptic ulcers may bleed (haematemesis, melaena), perforate causing peritonitis (surgical emergency), or produce gastric outlet obstruction from pyloric scarring. Chronic H. pylori atrophic gastritis with intestinal metaplasia follows the Correa cascade — progressing to gastric adenocarcinoma; H. pylori is classified as a definitive human carcinogen (IARC Group 1), increasing gastric cancer risk 3-6 fold. Gastric MALT lymphoma (mucosa-associated lymphoid tissue lymphoma) is caused by chronic H. pylori infection — eradication therapy alone achieves remission in 70-80% of early-stage disease. Autoimmune atrophic gastritis destroys parietal cells, causing pernicious anaemia from intrinsic factor deficiency and vitamin B12 malabsorption, with associated subacute combined degeneration of the spinal cord. Erosive gastritis causing chronic blood loss results in iron-deficiency anaemia requiring investigation and treatment. H. pylori eradication before intestinal metaplasia develops significantly reduces future gastric cancer risk.

H. pylori transmission is via the faecal-oral route — good hand hygiene, safe water supply, and food safety reduce transmission risk. H. pylori vaccines are under development but not yet available. NSAID gastroprotection: always use the lowest effective NSAID dose for the shortest duration; patients over 65, with previous peptic ulcer, taking aspirin or anticoagulants, or with comorbidities should take a PPI concurrently with any NSAID. Alcohol: limit alcohol intake (no more than 14 units per week for adults) as alcohol is directly toxic to the gastric mucosa. Dietary habits: eat regular meals, avoid very spicy foods if symptomatic, limit coffee and carbonated drinks which increase gastric acid secretion. Stress reduction: chronic psychological stress impairs gastric mucosal defence and exacerbates gastritis symptoms.

Seek emergency care immediately for: vomiting blood (haematemesis — even a small amount); passing black, tarry, or maroon stools (melaena — upper GI bleeding); sudden severe upper abdominal pain (possible peptic ulcer perforation); or dizziness and faintness with abdominal pain (haemorrhagic shock). See a GP promptly (within 2 weeks) for: persistent epigastric pain lasting more than 2 weeks; unexplained weight loss with dyspepsia; difficulty swallowing; persistent nausea or vomiting; dyspepsia in any patient over 55 (requires urgent endoscopy referral to exclude gastric cancer per NICE NG12). Patients with confirmed H. pylori infection should have eradication confirmed by breath test 4-8 weeks after completing antibiotic therapy.