Gastritis and H. pylori — Testing, Eradication and Confirmation

TL;DR — Gastritis is inflammation of the stomach lining; H. pylori is the bacterium that causes most cases of clinically significant gastritis worldwide. H. pylori is the most common chronic bacterial infection in humans. It causes most peptic ulcers, increases the risk of stomach cancer, and is treated with a 7–14 day combination of acid-suppressing medication plus two antibiotics. Diagnosis is by stool antigen, urea breath test, or gastroscopy with biopsy. Dr Goutham performs diagnostic gastroscopy and post-treatment confirmation across Brisbane, Redland and Logan.

What are gastritis and H. pylori?

Gastritis is inflammation of the stomach lining. It has many causes — H. pylori infection (by far the most common globally), NSAID use, alcohol, autoimmune attack on parietal cells, bile reflux, severe stress, and viral infection. Helicobacter pylori is a gram-negative spiral-shaped bacterium that lives in the mucus layer of the stomach. It is acquired in childhood, persists for life if untreated, and causes chronic active gastritis, peptic ulcers, gastric MALT lymphoma, and an increased risk of gastric cancer.

Symptoms

Most people with H. pylori have no symptoms. When symptoms occur:

• Upper abdominal pain or burning (dyspepsia), often relieved by food or antacids
• Nausea
• Early satiety, bloating
• Loss of appetite, weight loss
• Symptoms of a peptic ulcer — gnawing epigastric pain, sometimes radiating to the back
• Vomiting blood (haematemesis) or passing black tarry stool (melaena) if a bleeding ulcer develops — seek urgent care

Risk factors and complications

• Birth in or family origin from regions with high H. pylori prevalence (most of Asia, the Middle East, South America, Eastern Europe, Indigenous Australian communities)
• Overcrowded household in childhood
• Long-term NSAID or aspirin use (independent risk for gastritis and ulcer)
• Smoking, heavy alcohol intake
• Complications: peptic ulcer disease, GI bleeding, gastric outlet obstruction, gastric MALT lymphoma, gastric cancer (the strongest known modifiable risk factor for gastric cancer)

How are gastritis and H. pylori diagnosed?

• Stool antigen test — non-invasive, accurate, and the first-line test in most uncomplicated cases
• Urea breath test (UBT) — non-invasive, equally accurate
• Gastroscopy with biopsy — the test of choice when an ulcer is suspected, in patients over 50 with new dyspepsia, in patients with alarm features (weight loss, anaemia, dysphagia, vomiting, family history of gastric cancer), or to assess for atrophic change or premalignant lesions
• Serology (blood antibody test) — not recommended in Australia because it cannot distinguish current from past infection

Important: stool antigen and breath tests both require you to be off PPI (proton-pump inhibitor) medication for at least 2 weeks beforehand and off antibiotics for at least 4 weeks, otherwise the tests can be falsely negative.

How are gastritis and H. pylori treated?

For confirmed H. pylori infection, current Australian first-line treatment is 7–14 day triple or quadruple therapy:

• Triple therapy: esomeprazole or pantoprazole twice daily + amoxicillin 1 g twice daily + clarithromycin 500 mg twice daily — 14 days
• Penicillin allergy / clarithromycin resistance: bismuth-based quadruple therapy (PPI + bismuth + tetracycline + metronidazole)
• Other regimens (sequential, levofloxacin-based) for treatment failures

Eradication must be confirmed at least 4 weeks after completing antibiotics and 2 weeks after stopping any PPI, using stool antigen or urea breath test. Symptoms alone do not confirm eradication. Resistance to clarithromycin is rising globally, and some regions now favour bismuth-based regimens as first line.

For NSAID gastritis — stop the NSAID if possible; if not, co-prescribe a PPI; use the lowest effective dose. For autoimmune gastritis — B12 replacement and surveillance for gastric neuroendocrine tumours; gastric cancer surveillance in selected cases.

When to see a specialist

• New upper abdominal pain in someone over 50
• Any alarm feature: weight loss, anaemia, melaena or haematemesis, vomiting, difficulty swallowing, palpable mass
• Family history of gastric cancer
• Symptoms not responding to a standard PPI trial
• Failed first-line H. pylori eradication
• Atrophic gastritis or intestinal metaplasia on biopsy — for surveillance planning

What to expect at your appointment with Dr Goutham

Dr Goutham will review your symptoms, prior test results, family history, and medication. If gastroscopy is appropriate (alarm features, age > 50, failed PPI trial, suspected ulcer), it is arranged. The procedure takes 10 minutes under sedation; biopsies are taken for H. pylori testing (CLO / rapid urease test plus histology). Pathology results take 7–14 days. If H. pylori is confirmed, eradication therapy is prescribed by Dr Goutham or your GP; post-treatment confirmation is arranged at 4–6 weeks.

Frequently asked questions

Did I catch H. pylori from food or water?

H. pylori is acquired in childhood, usually within the household. Adult transmission is uncommon. It does not spread the way food poisoning does. If you have H. pylori, it does not mean a current dietary or hygiene issue — it almost certainly reflects childhood exposure decades ago.

If I have H. pylori, do my family members need testing?

Routine family testing is not currently recommended in Australia. However, household members with persistent dyspepsia, a family history of gastric cancer, or other risk factors should discuss testing with their GP.

Why do I need a follow-up test if my symptoms resolved?

Because symptom resolution does not confirm eradication. Treatment failure rates of 10–20% are not uncommon, particularly where there is clarithromycin resistance. Confirming eradication ensures the bacterium has been cleared and reduces the long-term risk of ulcer and gastric cancer.

Book a consultation

Phone 07 3733 1551 or send a referral via the contact form. See about Dr Goutham or the cost page.