TOPIC
MECHANISM
CLINICAL PICTURE
CLUE · MANAGEMENT
Flagella move through mucus; urease → NH₃ neutralizes acid locally; adhesins bind epithelium
Acquired in childhood (fecal-oral, oral-oral); most never get symptoms
More common in low-income settings
Chronic gastritis (antral)
Inflammation of antrum → ↓ somatostatin (D cells) → ↑ gastrin → ↑ acid
Dyspepsia; may be asymptomatic
Type B gastritis (vs autoimmune type A in body/fundus)
Excess acid reaching duodenum → gastric metaplasia → H pylori colonizes it
Epigastric pain better with meals, worse 2–3 h later and at night
Strongest H pylori association
Weakened mucosal defense (H pylori, NSAIDs)
Pain worse with meals, weight loss
Biopsy to exclude cancer
Chronic pangastritis → atrophy → intestinal metaplasia → dysplasia
Weight loss, early satiety, anemia
Intestinal-type cancer · CagA ⁺ strains ↑ risk
H pylori antigens drive marginal-zone B-cell proliferation
Gastric mass or thickened folds
Low-grade lesions may regress after eradication alone
Labeled urea → bacterial urease → labeled CO₂ exhaled
Diagnosis and test of cure
Stop PPIs 2 weeks, antibiotics/bismuth 4 weeks before (false negatives)
Detects active infection
Diagnosis and test of cure
Same PPI caveat
Histology (curved rods on surface) + rapid urease test
Patients ≥ 60 or with alarm features
Alarm: bleeding, weight loss, dysphagia, anemia
IgG persists after cure
Shows past or present exposure
Can't confirm eradication
PPI + clarithromycin + amoxicillin (metronidazole if penicillin allergy)
Where clarithromycin resistance is low
Confirm cure afterward
Bismuth quadruple therapy
PPI + bismuth + metronidazole + tetracycline
First-line in many areas (clarithromycin resistance)
Bismuth → black stool and tongue