Laboratory tests - Helicobacter pylori testing

Organism and test-and-treat

Gram-negative, microaerophilic, urease-producing spiral bacillus colonising gastric mucus
Test only if you intend to treat ("test-and-treat") - there is no role for testing without an indication

Test	Use	Caveat
Urea breath test (13C)	Diagnosis AND confirmation of eradication	Needs prep (below); not MBS-rebated in Australia for initial diagnosis in some settings
Faecal antigen	Diagnosis and eradication check	Same prep requirements
Serology (IgG)	Almost never useful	Stays positive after eradication - cannot confirm cure; may be the only test unaffected by PPI/antibiotics or recent bleeding
Rapid urease test (CLO) on biopsy	At endoscopy	False negative with PPI, bleeding, atrophy
Histology (antrum + body)	At endoscopy; detects atrophy/metaplasia/MALT	The reference standard
Culture / molecular susceptibility testing	After 2 failed eradication attempts	Guides salvage therapy

Global prevalence ~40-50%; Australia ~15-20%, falling with each birth cohort
Much higher in migrant, Aboriginal and Torres Strait Islander, and older Australians
Causes ~90% of duodenal ulcers and ~70-80% of gastric ulcers
Clarithromycin resistance in Australia ~15-20% and rising; metronidazole resistance ~40-50%
- This is why clarithromycin-based triple therapy is no longer automatically first-line

Urease -> urea to ammonia -> neutralises gastric acid locally -> survival
- This is the basis of both the urea breath test and the CLO test
Flagellar motility + adhesins (BabA) -> colonisation of gastric mucus
CagA and VacA virulence factors -> more inflammation, more ulcer and cancer risk
Two divergent phenotypes:
- Antral-predominant gastritis -> inc gastrin -> inc acid -> DUODENAL ULCER
- Corpus-predominant/pancorporeal gastritis -> atrophy -> dec acid -> GASTRIC ULCER and ADENOCARCINOMA
Correa cascade: gastritis -> atrophic gastritis -> intestinal metaplasia -> dysplasia -> gastric adenocarcinoma
WHO class I carcinogen

Active or past peptic ulcer disease (unless eradication already documented)
Low-grade gastric MALT lymphoma, or after endoscopic resection of early gastric cancer
Uninvestigated dyspepsia
- <60 and no alarm features -> non-invasive test-and-treat
- >=60, OR any alarm feature -> ENDOSCOPY first (weight loss, severe abdominal pain, dysphagia, vomiting, GI bleeding, anaemia)
Long-term aspirin or NSAID use (especially before starting)
Immune thrombocytopenic purpura - eradication raises the platelet count in a substantial minority
Unexplained iron deficiency anaemia, after other causes excluded
Family history of gastric cancer; considered before long-term PPI
Not indicated: asymptomatic people, GORD alone (eradication does not treat reflux)

*Stop antibiotics AND bismuth for 4 weeks*
*Stop PPI for at least 1-2 weeks* (H2 blocker or antacid may be substituted)
Failure to do this causes FALSE NEGATIVES - acid suppression reduces bacterial load and urease activity
Recent upper GI bleeding also causes false negatives - retest later, or use serology in that window

Regimen	Components
Bismuth quadruple (preferred where clarithromycin resistance >15%, or any prior macrolide use)	PPI bd + bismuth subcitrate + metronidazole + tetracycline, 14 days
Clarithromycin triple (only if no prior macrolide exposure and low local resistance)	Esomeprazole 20 mg bd + amoxicillin 1 g bd + clarithromycin 500 mg bd, 14 days
Concomitant (non-bismuth quadruple)	PPI + amoxicillin + clarithromycin + metronidazole (or tinidazole), 14 days

Penicillin allergy -> bismuth quadruple (contains no amoxicillin)
14 days beats 7 days - the shorter Australian courses of the past are now discouraged
Vonoprazan-based regimens (potassium-competitive acid blocker) are superior internationally but vonoprazan is not widely available in Australia

*Never repeat an antibiotic the patient has already failed* (especially clarithromycin)
Second line: bismuth quadruple if triple failed; or levofloxacin-based (PPI + amoxicillin + levofloxacin)
After 2 failures -> endoscopy with culture and susceptibility testing, or molecular resistance testing
Check adherence and smoking (smoking reduces eradication rates)

Duodenal ulcer: stop PPI once eradication confirmed - no maintenance needed
Gastric ulcer: repeat endoscopy at 6-8 weeks to confirm healing and exclude malignancy
MALT lymphoma: eradication alone cures *~70-80% of localised, H. pylori-positive, t(11;18)-negative disease*
- t(11;18) translocation predicts failure to respond
Bleeding ulcer: eradication markedly reduces rebleeding - the single most effective secondary prevention

Peptic ulcer disease - duodenal (~90%) and gastric (~70-80%)
Gastric adenocarcinoma (intestinal type) and gastric MALT lymphoma
Atrophic gastritis, intestinal metaplasia, pernicious anaemia
Iron deficiency anaemia (unexplained) and B12 deficiency
Immune thrombocytopenic purpura
Functional dyspepsia - modest benefit from eradication (NNT ~14)
Inverse associations: GORD, Barrett's oesophagus, oesophageal adenocarcinoma, and possibly asthma
Household crowding, migration from high-prevalence regions

Untreated infection is lifelong without antibiotics
Only ~10-15% develop ulcers and ~1-2% gastric cancer - most are asymptomatic carriers
Eradication reduces gastric cancer risk, and most in those treated before atrophy/intestinal metaplasia develops
- Once extensive intestinal metaplasia is established, surveillance endoscopy is still required despite eradication
Reinfection in Australia is rare (<1-2%/yr) - a positive test after confirmed eradication is usually treatment failure, not reinfection
Untreated after a bleeding ulcer -> high rebleeding rate

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