Gastritis — Symptoms, Causes & Treatment | MyMedicPlus

Gastritis is acute or chronic inflammation of the gastric mucosa (stomach lining), ranging from superficial histological changes to severe erosive disease with haemorrhage. The most common cause globally is Helicobacter pylori (H. pylori) infection — a gram-negative spiral bacterium that colonises the gastric antrum and body — affecting approximately 44% of the global population (over 3.5 billion people), with prevalence highest in developing countries (above 70% in parts of Africa and South America) and lower in high-income nations (25–35%). Gastritis is classified as acute (sudden onset, typically erosive) or chronic (long-standing histological inflammation classified by the Sydney System as non-atrophic, atrophic, or special forms). Type B gastritis (H. pylori-associated — most common) primarily affects the antrum; Type A gastritis (autoimmune) affects the body and fundus, destroying acid-secreting parietal cells and intrinsic factor-producing cells, leading to pernicious anaemia. The clinical importance of gastritis extends beyond symptomatic discomfort — chronic H. pylori gastritis is the principal precursor to peptic ulcer disease, gastric adenocarcinoma (H. pylori is a WHO class 1 carcinogen), and mucosa-associated lymphoid tissue (MALT) lymphoma. Early detection and H. pylori eradication can reverse pre-malignant changes in a substantial proportion of patients.

Helicobacter pylori infection accounts for approximately 80–90% of chronic gastritis cases — the bacterium evades gastric acid by producing urease, which generates an ammonia cloud neutralising the local pH; it triggers an intense mucosal inflammatory response (neutrophils, lymphocytes, IL-8 release) causing ongoing damage. NSAIDs (ibuprofen, aspirin, naproxen, diclofenac, celecoxib to a lesser degree) are the second most common cause — they inhibit cyclooxygenase-1 (COX-1) and reduce prostaglandin E2 synthesis, impairing the protective mucosal phospholipid layer and bicarbonate secretion; gastric erosions occur in 30–50% of regular NSAID users and frank ulcers in 15–25%. Alcohol causes direct mucosal injury, vasodilation, and increased vascular permeability. Autoimmune gastritis (Type A): anti-parietal cell and anti-intrinsic factor antibodies destroy acid-producing parietal cells and intrinsic factor — vitamin B12 malabsorption leads to pernicious anaemia (macrocytic megaloblastic anaemia with neurological complications). Associated autoimmune conditions include Hashimoto's thyroiditis and type 1 diabetes. Stress gastritis (acute erosive) occurs in critically ill patients (burns — Curling's ulcer; brain injury — Cushing's ulcer; mechanical ventilation) — stress-induced mucosal ischaemia causes acute erosions. Other causes include bile reflux, radiation to the gastric area, eosinophilic gastritis, Crohn's disease, cytomegalovirus (in immunocompromised patients), and ischaemia.

Most cases of chronic gastritis (particularly H. pylori gastritis) are asymptomatic — histological inflammation is present without clinical symptoms, and incidental endoscopic discovery is common. When symptomatic, gastritis causes: epigastric pain or burning (dyspepsia) — characteristically worse on empty stomach and temporarily relieved by eating or antacids in duodenal ulcer pattern, or worsened by food in gastric ulcer pattern; nausea (with or without vomiting); early satiety, bloating, and belching from impaired gastric emptying; and loss of appetite with unintentional weight loss in severe cases. Erosive or haemorrhagic gastritis: vomiting bright red blood (haematemesis) or 'coffee grounds' vomitus (partly digested blood); melaena (black, tarry, offensive stools from upper GI blood loss); iron-deficiency anaemia from chronic occult haemorrhage — presenting as fatigue, pallor, and exertional dyspnoea. Autoimmune gastritis: symptoms of vitamin B12 deficiency — fatigue, weakness, pallor, glossitis, angular cheilitis, peripheral neuropathy (subacute combined degeneration of the spinal cord — paraesthesia, loss of proprioception and vibration sense, ataxia), and neuropsychiatric features (depression, psychosis in severe cases). Achlorhydria (absent acid secretion) from parietal cell destruction increases susceptibility to enteric bacterial infections.

Upper GI endoscopy (gastroscopy/oesophagogastroduodenoscopy — OGD) is the gold standard for diagnosing gastritis, directly visualising mucosal changes (erythema, erosions, haemorrhage, atrophy, intestinal metaplasia), obtaining multiple biopsies for histology and H. pylori testing, and excluding peptic ulcer disease and gastric cancer. The Sydney System provides standardised histological scoring (inflammation grade, activity, atrophy, intestinal metaplasia, and H. pylori density). H. pylori diagnostic tests: (1) Urea breath test (UBT — 13C or 14C-labelled urea) — sensitivity 95%, specificity 96%; first-line non-invasive test; requires stopping PPIs 2 weeks and antibiotics 4 weeks before testing; also used to confirm eradication 4 weeks after treatment. (2) Stool antigen test (SAT) — similar accuracy to UBT; convenient. (3) Rapid urease test (CLO test) on endoscopic biopsy — result in 1 hour; sensitivity 90%, specificity 95%. (4) Histology — gold standard for confirming H. pylori and assessing degree of inflammation and pre-malignant changes (atrophy, intestinal metaplasia — the Correa cascade of gastric carcinogenesis). (5) H. pylori serology (IgG) — widely available but cannot distinguish active from past infection; not recommended for confirming eradication. Blood tests: full blood count (anaemia — iron-deficiency from chronic loss; macrocytic from B12 deficiency), serum B12, folate, intrinsic factor antibodies and anti-parietal cell antibodies (autoimmune gastritis).

H. pylori eradication therapy — recommended for all H. pylori-positive gastritis — significantly reduces peptic ulcer risk (70–80% reduction), gastric cancer risk (30–40% risk reduction in prospective studies), and MALT lymphoma (75–90% of low-grade MALT lymphomas remit on H. pylori eradication alone). Antibiotic resistance is a major global challenge: (1) Standard triple therapy (PPI + clarithromycin 500 mg + amoxicillin 1 g BD for 7–14 days) — eradication rates 70–85% where clarithromycin resistance is below 15%; declining due to increasing clarithromycin resistance in Europe and Americas. (2) Bismuth-based quadruple therapy (PPI + bismuth subsalicylate + tetracycline 500 mg + metronidazole 400 mg QID for 10–14 days) — eradication rates above 90%; first-line in high-resistance regions or after failed triple therapy (NICE NG238 recommends this). (3) Concomitant therapy (PPI + amoxicillin + clarithromycin + metronidazole for 10–14 days) — effective in high-resistance settings. Confirm eradication with UBT or stool antigen test at least 4 weeks after completing therapy (and 2 weeks after stopping PPI). Acid suppression: proton pump inhibitors (omeprazole 20–40 mg OD, lansoprazole 30 mg OD, esomeprazole 40 mg OD) are the cornerstone of symptom control — given 30–60 minutes before meals for optimal efficacy; typically 4–8 weeks for acute gastritis or peptic ulcer healing. NSAID-associated gastritis: discontinue NSAIDs where possible; switch to COX-2 selective inhibitor (celecoxib, etoricoxib) or add co-prescribed PPI (pantoprazole, omeprazole) if NSAIDs cannot be stopped. Autoimmune gastritis: parenteral vitamin B12 (hydroxocobalamin 1 mg IM monthly) for pernicious anaemia.

Peptic ulcer disease is the most common complication of H. pylori gastritis — the bacterium disrupts mucosal defence, allowing acid to cause discrete mucosal ulcers; gastric ulcers (Type I — lesser curve, Type II — body + duodenum, Type III — prepyloric) and duodenal ulcers develop in 10–15% of H. pylori-infected individuals. Upper gastrointestinal haemorrhage from gastric erosions or ulcers affects 0.1–0.5% of patients annually and carries significant mortality (5–10% in-hospital). Gastric adenocarcinoma: H. pylori is the most important risk factor for gastric cancer (10–20-fold increased risk) — the Correa cascade (chronic active gastritis → gastric atrophy → intestinal metaplasia → dysplasia → carcinoma) is the principal carcinogenic pathway; gastric cancer remains the 4th most common cancer globally and 3rd leading cause of cancer death. Mucosa-associated lymphoid tissue (MALT) lymphoma of the stomach is a rare B-cell lymphoma directly caused by chronic H. pylori-induced lymphoid proliferation — H. pylori eradication achieves complete remission in 75–90% of localised low-grade MALT lymphoma. Pernicious anaemia from autoimmune gastritis-associated vitamin B12 deficiency causes irreversible spinal cord damage (subacute combined degeneration) if not treated promptly with parenteral B12. Gastric atrophy and achlorhydria increase susceptibility to enteric bacterial infection and impair absorption of calcium, iron, and B12.

See a GP for: persistent upper abdominal pain or discomfort lasting more than 2-4 weeks, indigestion and bloating not responding to antacids or over-the-counter PPIs, or confirmed Helicobacter pylori infection requiring eradication treatment. Seek urgent or same-day assessment for: upper gastrointestinal bleeding (vomiting fresh blood or dark coffee-ground material — haematemesis), passing black tarry stools (melaena — indicating upper GI bleeding), or severe sudden upper abdominal pain (possible perforation). Seek urgent 2-week-wait cancer referral for: new onset dyspepsia in a person over 55 with any of the following alarming features — dysphagia (difficulty swallowing), unintentional weight loss, persistent vomiting, iron-deficiency anaemia, epigastric mass, or upper gastrointestinal bleeding (NICE NG12). These features require urgent gastroscopy to exclude gastric cancer.

Prevent H. pylori infection through good hand hygiene, safe water supply, and improved sanitation. Avoid routine NSAID use — use paracetamol (acetaminophen) for pain relief where possible. Take NSAIDs with food and add PPI prophylaxis if NSAID use is unavoidable in high-risk patients (age over 65, history of ulcer, concurrent corticosteroid or anticoagulant use). Limit alcohol consumption to within recommended guidelines. Quit smoking, which worsens gastric mucosal healing and increases H. pylori-related cancer risk. After H. pylori eradication, a return visit for urea breath test confirms successful treatment.