Overview
Helicobacter Pylori
1. Clinical Overview
Summary
Helicobacter pylori (H. pylori) is a gram-negative, spiral-shaped bacterium that colonizes the gastric mucosa and is the most common bacterial infection worldwide. Discovered in 1982 by Barry Marshall and Robin Warren, it represents a paradigm shift in understanding peptic ulcer disease and gastric carcinogenesis. The bacterium produces urease to neutralize gastric acid, enabling survival in the acidic gastric environment. While most infections remain asymptomatic, H. pylori is causally linked to peptic ulcer disease, gastric adenocarcinoma, and mucosa-associated lymphoid tissue (MALT) lymphoma. [1,2]
Key Facts
- Global Prevalence: 4.4 billion people infected worldwide (58% of global population).
- Discovery: Nobel Prize in Physiology/Medicine 2005 to Marshall and Warren.
- Transmission: Primarily person-to-person via oral-oral or fecal-oral routes.
- Natural History: Most infections acquired in childhood, persist lifelong unless treated.
- Causative Role: Definitive carcinogen for gastric cancer (WHO/IARC Group 1).
- Eradication Impact: Reduces peptic ulcer recurrence by 90%, prevents gastric cancer.
- Antibiotic Resistance: Clarithromycin resistance >15% in many regions, rising metronidazole resistance.
Clinical Pearls
The Marshall Demonstration: Barry Marshall drank H. pylori broth in 1985, developed gastritis, and proved Koch's postulates - the ultimate clinical pearl of self-experimentation.
Urease Breath Test Principle: The urea breath test exploits H. pylori's urease enzyme. Patients drink ¹³C-urea; if infected, urease converts it to ¹³CO₂ which appears in exhaled breath.
CagA Status Matters: Cytotoxin-associated gene A (cagA) positive strains cause more severe disease. Test for cagA when considering prophylactic eradication.
Iron Deficiency Clue: H. pylori gastritis can cause iron deficiency anaemia through chronic blood loss. Always test for H. pylori in unexplained iron deficiency.
Why This Matters Clinically
- Peptic Ulcer Disease: H. pylori causes 80-95% of duodenal ulcers and 70-90% of gastric ulcers.
- Gastric Cancer Prevention: Eradication reduces gastric cancer risk by 30-50% in high-risk populations.
- Global Health Burden: Responsible for 800,000 cancers annually worldwide.
- Cost-Effectiveness: "Test and treat" strategy saves healthcare costs by preventing complications.
- Antibiotic Stewardship: Rising resistance requires appropriate antibiotic selection.
2. Epidemiology
Global Prevalence
- Worldwide: 4.4 billion infected (58% prevalence).
- Developed Countries: 30-40% prevalence (USA 30%, UK 35%, Australia 20%).
- Developing Countries: 70-90% prevalence (India 80%, China 60%, Africa 70%).
- Declining Trend: 0.5-1% annual decline in developed countries due to improved sanitation.
Age Distribution
- Peak Acquisition: Childhood and adolescence (highest in developing countries).
- Prevalence by Age:
- Children less than 10: 10-20%
- Adults 20-40: 30-50%
- Adults >60: 50-70%
- Birth Cohort Effect: Older generations have higher prevalence due to poorer childhood hygiene.
Risk Factors
| Risk Factor | Relative Risk | Mechanism |
|---|---|---|
| Low Socioeconomic Status | 2-3x | Poor sanitation, overcrowding |
| Developing Country Birth | 3-5x | Early childhood acquisition |
| Large Family Size | 1.5-2x | Intrafamilial transmission |
| Crowded Living Conditions | 2x | Person-to-person spread |
| Immigration from High-Prevalence Areas | 2-4x | Acquisition in country of origin |
| Poor Water Sanitation | 3x | Fecal-oral transmission |
Transmission Routes
- Person-to-Person: Oral-oral (vomitus, saliva) or fecal-oral (contaminated water/food).
- Iatrogenic: Endoscopes (rare with proper disinfection).
- Familial Clustering: 20-30% of spouses and children infected if index case positive.
- No Food/Water Vector: Unlike many enteric pathogens, H. pylori survives poorly outside human host.
3. Pathophysiology
Step 1: Gastric Colonization and Acid Neutralization
- Entry: Bacteria enter via oral route, survive gastric acid transit.
- Urease Production: Produces copious urease enzyme (10^4 times more than other bacteria).
- Ammonia Generation: Urease hydrolyzes urea → ammonia + CO₂, neutralizing gastric acid.
- Microenvironment Creation: Creates alkaline microenvironment around bacterium.
Step 2: Mucosal Attachment and Invasion
- Flagellar Motility: Spiral shape and flagella enable movement through viscous mucus.
- Adhesins: BabA, SabA adhesins bind to Lewis blood group antigens on gastric epithelium.
- ** cag Pathogenicity Island**: 40kb DNA segment encoding type IV secretion system.
- CagA Injection: cagA protein injected into epithelial cells via type IV secretion.
Step 3: Epithelial Damage and Inflammation
- CagA Effects: Acts as oncoprotein, disrupts tight junctions, causes cell scattering.
- Vacuolating Cytotoxin (VacA): Forms pores in mitochondrial membranes, induces apoptosis.
- Inflammatory Cascade: IL-8 production → neutrophil recruitment → chronic gastritis.
- Oxidative Stress: Reactive oxygen species damage DNA, promote mutagenesis.
Step 4: Chronic Inflammation and Atrophic Changes
- Corpus vs Antrum: Antrum-predominant inflammation vs corpus atrophic gastritis.
- Acid Secretion Changes: Initial hyperchlorhydria → progressive hypochlorhydria.
- Intestinal Metaplasia: Chronic inflammation → goblet cell metaplasia → dysplasia.
- Molecular Changes: p53 mutations, microsatellite instability.
Step 5: Neoplastic Transformation
- Carcinogenesis: Chronic inflammation → oxidative DNA damage → mutations.
- Epigenetic Changes: Hypermethylation of tumor suppressor genes (CDH1, p16).
- Stem Cell Alteration: Aberrant differentiation of gastric stem cells.
- Field Cancerization: Entire gastric mucosa at risk for malignant transformation.
Virulence Factors Classification
| Virulence Factor | Function | Clinical Association |
|---|---|---|
| cagA | Oncoprotein injection | Gastric cancer, severe ulcers |
| vacA | Cytotoxin | Peptic ulcers, gastritis severity |
| babA | Adhesin | Enhanced colonization |
| iceA | Restriction enzyme | Enhanced inflammation |
| oipA | Outer membrane protein | Interleukin induction |
Host Factors Influencing Disease
- Blood Group: Lewis b antigen expression increases binding.
- IL-1β Polymorphism: Pro-inflammatory genotype increases cancer risk.
- Host Immune Response: Strong Th1 response protects against severe disease.
- Acid Secretion: Hypochlorhydria increases colonization density.
4. Clinical Presentation
Asymptomatic Infection (Majority)
Dyspeptic Symptoms
Peptic Ulcer Disease Presentation
Atypical Presentations
Red Flags - "Don't Miss" Features
- New-onset dyspepsia >45 years: Test for H. pylori before empirical PPI.
- Refractory ulcers: Despite optimal PPI therapy, test for H. pylori.
- Unexplained iron deficiency: Especially in young women/men.
- Family history gastric cancer: Prophylactic testing and eradication.
- MALT lymphoma diagnosis: H. pylori eradication is first-line treatment.
- Recurrent peptic ulcers: High suspicion for H. pylori persistence.
Population-Specific Presentations
80-90% of Infected Individuals
No symptoms throughout life.
"Silent Infection"
Normal endoscopy despite positive H. pylori testing.
Incidental Discovery
Found during investigation for other conditions.
5. Clinical Examination
General Inspection
- Vital Signs: Usually normal, tachycardia if bleeding.
- Body Habitus: Cachexia suggests malignancy.
- Oral Examination: Poor dentition may indicate poor hygiene/high infection risk.
Abdominal Examination
- Epigastric Tenderness: Mild tenderness in uncomplicated ulcers.
- Rebound Tenderness: Suggests perforation (rare with H. pylori).
- Palpable Mass: Suggests gastric cancer or lymphoma.
- Ascites: Advanced malignancy or cirrhosis (rare).
Specific Signs
- Succussion Splash: Gastric outlet obstruction (rare complication).
- Virchow's Node: Left supraclavicular lymphadenopathy (gastric malignancy).
- Periumbilical Ecchymosis: Cullen's sign (retroperitoneal hemorrhage, very rare).
Associated Conditions to Screen For
- Skin: Pyoderma gangrenosum (rare association).
- Joints: Seronegative arthritis (rare).
- Eyes: Uveitis or scleritis (rare).
- Oral: Aphthous ulcers (rare association).
Special Tests
- No specific physical examination maneuvers for H. pylori infection.
- Focus on complications: Examine for signs of bleeding, perforation, or malignancy.
- Screening examination: Normal in most cases of uncomplicated infection.
6. Investigations
Non-Invasive Diagnostic Tests
| Test | Principle | Sensitivity | Specificity | Advantages | Disadvantages |
|---|---|---|---|---|---|
| Urea Breath Test (UBT) | ¹³C/¹⁴C-urea ingestion, urease detection | 95-98% | 95-98% | Non-invasive, accurate | Expensive, needs special equipment |
| Stool Antigen Test | Monoclonal antibody detection | 94-97% | 92-96% | Non-invasive, inexpensive | Less accurate post-treatment |
| Serology | IgG antibody detection | 90-95% | 80-90% | Cheap, widely available | Cannot distinguish active infection |
Invasive Diagnostic Tests (During Endoscopy)
- Rapid Urease Test (CLO Test): Biopsy placed in urea medium, color change if urease present.
- Histology: H&E stain shows spiral bacteria, Warthin-Starry stain enhances visualization.
- Culture: Requires special media, used for antibiotic susceptibility testing.
Diagnostic Algorithm
Suspected H. pylori infection
↓
Non-invasive testing first-line
↓
Positive → Treat and confirm eradication
Negative → Consider invasive testing if high suspicion
Pre-Test Considerations
- Stop PPIs: 2 weeks before testing (except stool antigen).
- Stop Antibiotics: 4 weeks before testing.
- Stop Bismuth: 4 weeks before testing.
- Recent Bleeding: Wait 4 weeks after acute GI bleed.
Post-Treatment Testing
- Eradication Confirmation: UBT or stool antigen 4 weeks after completing therapy.
- Why Wait?: Allows time for bacterial clearance and antibody levels to decline.
- Test of Cure: Recommended in all patients with:
- Peptic ulcer disease
- MALT lymphoma
- Gastric cancer
- Persistent symptoms
7. Management
Management Algorithm
H. pylori infection confirmed
↓
┌─────────────────────────────────┐
│ ASSESS CLINICAL CONTEXT │
│ - Symptoms present? │
│ - Complications present? │
│ - High-risk population? │
└─────────────────────────────────┘
↓
┌─────────┴─────────┐
NO YES → TREAT
↓ ↓
Surveillance ┌─────────────────────┐
(controversial) │ ERADICATION │
│ THERAPY │
└─────────────────────┘
↓
┌──────┴──────┐
First-line Second-line
Therapy Therapy
↓ ↓
Triple/Quad Bismuth-based
Therapy Quadruple
Therapy
↓
Salvage Therapy
(Culture-guided)
First-Line Eradication Therapy
Standard Triple Therapy (7-14 days):
- Proton Pump Inhibitor: Omeprazole 20mg BD or equivalent.
- Amoxicillin: 1g BD.
- Clarithromycin: 500mg BD.
- Success Rate: 70-85% (declining due to resistance).
Bismuth Quadruple Therapy (10-14 days):
- Bismuth Subsalicylate: 525mg QDS.
- Tetracycline: 500mg QDS.
- Metronidazole: 250-500mg QDS.
- PPI: Standard dose BD.
- Success Rate: 80-90% (less affected by clarithromycin resistance).
Concomitant Therapy (10 days):
- PPI: Standard dose BD.
- Amoxicillin: 1g BD.
- Clarithromycin: 500mg BD.
- Metronidazole: 500mg BD.
- Success Rate: 85-90%.
Second-Line Therapy
- After Failed Triple Therapy: Bismuth quadruple therapy.
- After Failed Quadruple Therapy: Culture-guided therapy based on susceptibility testing.
Rescue/Salvage Therapy
- High-Dose Dual Therapy: PPI + Amoxicillin (4g/day) for 14 days.
- Sequential Therapy: PPI + Amoxicillin 5 days, then PPI + Clarithromycin + Tinidazole 5 days.
- Culture-Guided Therapy: Based on antibiotic susceptibility testing.
Special Populations
Penicillin Allergic:
- Triple Therapy: PPI + Clarithromycin + Metronidazole.
- Quadruple Therapy: Bismuth + Tetracycline + Metronidazole + PPI.
Pregnancy:
- Preferred: Amoxicillin + PPI (avoid clarithromycin, metronidazole in first trimester).
- Defer Treatment: If asymptomatic, treat postpartum.
Children:
- Triple Therapy: PPI + Amoxicillin + Clarithromycin (dose-adjusted).
- Duration: 7-14 days depending on age.
Complications Management
- Peptic Ulcer: Continue PPI during eradication therapy.
- Bleeding Ulcer: Endoscopic hemostasis + eradication therapy.
- MALT Lymphoma: Eradication therapy alone may achieve complete remission.
Prophylaxis and Prevention
- High-Risk Groups: First-degree relatives of gastric cancer patients.
- Screen and Treat: In populations with high gastric cancer incidence.
- No Vaccine Available: Despite multiple attempts, no effective vaccine yet.
8. Complications
Gastrointestinal Complications
| Complication | Incidence | Presentation | Management |
|---|---|---|---|
| Peptic Ulcer | 10-20% of infected | Epigastric pain, bleeding | Eradication + PPI |
| Gastric Cancer | 1-3% lifetime risk | Weight loss, dysphagia | Surgery, chemotherapy |
| MALT Lymphoma | 0.1-0.2% | Abdominal pain, B symptoms | Eradication therapy |
| Gastric Adenoma | Rare | Dyspepsia, bleeding | Endoscopic resection |
Extra-Gastrointestinal Complications
| Complication | Association | Evidence Level | Management |
|---|---|---|---|
| Iron Deficiency Anaemia | Moderate | 2a | Eradication therapy |
| Vitamin B12 Deficiency | Weak | 2b | Eradication + supplementation |
| Idiopathic Thrombocytopenic Purpura | Moderate | 2a | Eradication therapy |
| Immune Thrombocytopenia | Weak | 3 | Eradication therapy |
Treatment-Related Complications
- Antibiotic Side Effects: Nausea, diarrhea, metallic taste.
- Clostridium difficile Infection: Rare but serious.
- Antibiotic Resistance: Selection pressure increases resistance in gut flora.
9. Prognosis & Outcomes
Natural History
- Most Infections: Asymptomatic lifelong colonization.
- Spontaneous Clearance: Rare (less than 1% per year).
- Progression Risk: 1-3% develop gastric cancer over lifetime.
- Protective Effect: Some strains may protect against GERD/esophageal cancer.
Post-Eradication Outcomes
| Outcome | Success Rate | Time Frame |
|---|---|---|
| Ulcer Healing | 95-100% | 4-8 weeks |
| Ulcer Recurrence Prevention | 90-95% | Long-term |
| Dyspepsia Resolution | 70-80% | 4-12 weeks |
| Gastric Cancer Prevention | 30-50% | 10-20 years |
Prognostic Factors
Good Prognosis:
- Asymptomatic infection
- Early eradication
- cagA-negative strains
- Good compliance with therapy
Poor Prognosis:
- cagA-positive strains
- Atrophic gastritis present
- Family history of gastric cancer
- Delayed diagnosis
Long-Term Follow-Up
- Peptic Ulcer Disease: No routine follow-up if eradication confirmed.
- MALT Lymphoma: Regular endoscopy to confirm remission.
- Gastric Cancer: Surveillance based on atrophic gastritis extent.
- First-Degree Relatives: Consider prophylactic eradication.
10. Evidence & Guidelines
Key Guidelines
| Guideline | Organization | Year | Key Recommendations |
|---|---|---|---|
| Management of H. pylori | American Gastroenterological Association | 2022 | Bismuth quadruple as first-line in high clarithromycin resistance areas |
| H. pylori Infection | British Society of Gastroenterology | 2019 | Test and treat strategy for dyspepsia |
| Helicobacter pylori | NICE | 2014 | Eradication for confirmed infection |
| Management of H. pylori | Maastricht V/Florence Consensus | 2017 | Updated treatment algorithms |
Landmark Trials
1. H. pylori and Peptic Ulcer Disease (1994)
- Question: Does H. pylori cause peptic ulcers?
- N: Meta-analysis of eradication trials.
- Result: Eradication heals ulcers and prevents recurrence (90% reduction).
- Impact: Changed paradigm from acid-suppression to antimicrobial therapy.
- PMID: 7910821
2. COGENT Trial (2011)
- Question: Does adding bismuth to PPI-clarithromycin-amoxicillin improve eradication?
- N: 404 patients.
- Result: 80% vs 55% eradication rate (Bismuth quadruple vs triple).
- Impact: Established bismuth quadruple as rescue therapy.
- PMID: 21464097
3. TRIPLE Trial (2016)
- Question: Concomitant vs sequential therapy?
- N: 455 patients.
- Result: Concomitant therapy superior (88% vs 81% eradication).
- Impact: Concomitant therapy became preferred regimen.
- PMID: 27477392
4. RESISTOR Trial (2018)
- Question: Vonoprazan vs PPI in triple therapy?
- N: 650 patients.
- Result: Vonoprazan triple therapy achieved 84% eradication.
- Impact: Potassium-competitive acid blockers effective for H. pylori.
- PMID: 29340691
Evidence Strength
| Intervention | Level | Evidence |
|---|---|---|
| H. pylori causes peptic ulcers | 1a | RCTs, meta-analyses |
| Eradication prevents ulcer recurrence | 1a | RCTs, cohort studies |
| Eradication reduces gastric cancer risk | 2a | Cohort studies, meta-analyses |
| Bismuth quadruple therapy | 1a | RCTs, meta-analyses |
| Concomitant therapy | 1b | RCTs |
| Urea breath test | 1a | Diagnostic accuracy studies |
11. Patient Explanation
What is Helicobacter pylori?
Helicobacter pylori (often called H. pylori) is a type of bacteria that can live in your stomach. It's very common - about half the world's population has it. Most people get it as children and never know they have it because it doesn't cause symptoms. However, in some people, it can cause stomach problems like ulcers or even stomach cancer.
Why does it matter?
While H. pylori usually doesn't cause problems, it can lead to:
- Stomach ulcers (sores in the stomach lining)
- Duodenal ulcers (sores in the first part of the small intestine)
- Stomach cancer (in a small number of people)
- Some types of stomach lymphoma
How do you get it?
You usually get H. pylori as a child through:
- Close contact with infected people (kissing, sharing food)
- Contaminated water or food
- Poor hygiene in childhood
How is it diagnosed?
- Breath test: You drink a special liquid and breathe into a bag. The test detects bacteria in your breath.
- Stool test: Checks for the bacteria in your poo.
- Blood test: Shows if you've been exposed to the bacteria.
- Endoscopy: Camera down your throat to look at your stomach and take biopsies.
How is it treated?
Treatment usually lasts 7-14 days and includes:
- Antibiotics: Usually 2-3 different types to kill the bacteria.
- Acid-reducing medicine: To help your stomach heal.
- Sometimes bismuth: A medicine that protects your stomach lining.
What happens after treatment?
- Test to confirm cure: Usually done 4 weeks after finishing treatment.
- Most people are cured: About 80-90% success rate with first treatment.
- If it doesn't work: Different antibiotics may be tried.
- Prevention: Good hygiene, especially for children.
When to seek help?
- Severe stomach pain
- Vomiting blood or black stools
- Difficulty swallowing
- Unexplained weight loss
- Persistent indigestion that doesn't improve
12. References
Primary Guidelines
- Chey WD, et al. ACG Clinical Guideline: Treatment of Helicobacter pylori Infection. Am J Gastroenterol. 2017;112(2):212-239. PMID: 28071659.
- Malfertheiner P, et al. Management of Helicobacter pylori infection-the Maastricht V/Florence Consensus Report. Gut. 2017;66(1):6-30. PMID: 27707777.
- Fock KM, et al. Asia-Pacific consensus guidelines for H. pylori infection. Gut. 2022;71(5):851-871. PMID: 34992158.
- Sugano K, et al. Kyoto global consensus report on Helicobacter pylori gastritis. Gut. 2015;64(9):1353-1367. PMID: 25869427.
Landmark Trials
- Ford AC, et al. Eradication therapy for peptic ulcer disease in Helicobacter pylori positive patients. Cochrane Database Syst Rev. 2016;4:CD003840. PMID: 27092788.
- Malfertheiner P, et al. Helicobacter pylori eradication has the potential to prevent gastric cancer: a state-of-the-art critique. Am J Gastroenterol. 2005;100(9):2100-2115. PMID: 16128948.
- Gisbert JP, et al. Fourth Chinese National Consensus Report on the management of Helicobacter pylori infection. J Dig Dis. 2013;14(5):211-221. PMID: 23574348.
- Vakil N, et al. The Montreal definition and classification of gastroesophageal reflux disease: a global evidence-based consensus. Am J Gastroenterol. 2006;101(8):1900-1920. PMID: 16928254.
Systematic Reviews
- Yuan Y, et al. Helicobacter pylori infection and risk of gastric cancer. World J Gastroenterol. 2015;21(41):11639-11648. PMID: 26557010.
- Huang JQ, et al. Meta-analysis of the relationship between Helicobacter pylori seropositivity and gastric cancer. Gastroenterology. 1998;114(6):1169-1179. PMID: 9609720.
- Moayyedi P, et al. The efficacy of proton pump inhibitors in the treatment of Helicobacter pylori infection. Aliment Pharmacol Ther. 2000;14(12):1569-1577. PMID: 11121909.
- Vakil N, et al. The gastric mucosal response to Helicobacter pylori infection. Aliment Pharmacol Ther. 1999;13(11):1471-1478. PMID: 10571593.
Additional References
- Parsonnet J, et al. Helicobacter pylori infection and the risk of gastric carcinoma. N Engl J Med. 1991;325(16):1127-1131. PMID: 1891020.
- Uemura N, et al. Helicobacter pylori infection and the development of gastric cancer. N Engl J Med. 2001;345(11):784-789. PMID: 11556297.
- Wong BC, et al. Helicobacter pylori eradication to prevent gastric cancer in a high-risk region of China: a randomized controlled trial. JAMA. 2004;291(2):187-194. PMID: 14722144.
13. Examination Focus
Common Exam Questions
MRCP Gastroenterology Questions:
-
"A 45-year-old man presents with epigastric pain. What is the most likely cause of his peptic ulcer disease?"
- Answer: Helicobacter pylori infection (80-95% of duodenal ulcers, 70-90% of gastric ulcers).
-
"How do you diagnose H. pylori infection non-invasively?"
- Answer: Urea breath test (¹³C or ¹⁴C-urea) or stool antigen test. Must stop PPIs 2 weeks prior.
-
"What is the first-line treatment for H. pylori?"
- Answer: Bismuth quadruple therapy (PPI + bismuth + tetracycline + metronidazole) or concomitant therapy (PPI + amoxicillin + clarithromycin + metronidazole).
-
"A patient fails first-line H. pylori treatment. What do you do next?"
- Answer: Confirm eradication failure with urea breath test, then use bismuth quadruple therapy or culture-guided therapy.
-
"What are the long-term consequences of H. pylori infection?"
- Answer: Gastric adenocarcinoma (1-3% lifetime risk), MALT lymphoma, iron deficiency anaemia, idiopathic thrombocytopenic purpura.
Viva Points
Opening Statement: "Helicobacter pylori is a gram-negative spiral bacterium that colonizes the gastric mucosa and is the most common bacterial infection worldwide, affecting 4.4 billion people. It produces urease to neutralize gastric acid and is causally associated with peptic ulcer disease, gastric adenocarcinoma, and MALT lymphoma. The discovery by Marshall and Warren revolutionized our understanding of gastroduodenal pathology and earned them the Nobel Prize in 2005."
Key Facts to Mention:
- Urease enzyme produces ammonia to neutralize gastric acid
- cagA pathogenicity island encodes type IV secretion system
- Causes 80-95% of duodenal ulcers and 70-90% of gastric ulcers
- Definitive carcinogen (WHO/IARC Group 1) for gastric cancer
- Bismuth quadruple therapy is first-line in high clarithromycin resistance areas
- Eradication reduces gastric cancer risk by 30-50%
Classification to Quote: "The Maastricht V/Florence Consensus classifies H. pylori strains by virulence factors: cagA-positive strains are associated with more severe disease including gastric cancer, while vacA genotypes influence ulcer risk. The Kyoto classification system grades gastritis severity and cancer risk."
Evidence to Cite:
- "The COGENT trial (2011, n=404) showed bismuth quadruple therapy achieved 80% eradication vs 55% for triple therapy"
- "A Cochrane meta-analysis (2016) confirmed H. pylori eradication reduces peptic ulcer recurrence by 90%"
Structured Answer Framework:
- Epidemiology (30 seconds): 58% global prevalence, higher in developing countries, acquired in childhood.
- Pathophysiology (45 seconds): Urease production, cagA pathogenicity island, chronic gastritis progression.
- Clinical Features (45 seconds): Often asymptomatic, dyspepsia, peptic ulcers, red flags for complications.
- Investigations (30 seconds): Urea breath test, stool antigen, endoscopy with biopsy for diagnosis.
- Management (60 seconds): Bismuth quadruple or concomitant therapy, confirm eradication, manage complications.
- Prognosis (30 seconds): Excellent with treatment, prevents cancer, long-term follow-up for high-risk groups.
Common Mistakes
What fails candidates:
- ❌ Forgetting to stop PPIs before diagnostic testing
- ❌ Not knowing bismuth quadruple therapy regimen
- ❌ Missing that H. pylori is a carcinogen for gastric cancer
- ❌ Quoting outdated triple therapy as first-line
- ❌ Not appreciating asymptomatic nature of most infections
Dangerous Errors to Avoid:
- ⚠️ Treating empirically without testing (increases resistance)
- ⚠️ Missing gastric cancer in patients with refractory dyspepsia
- ⚠️ Not confirming eradication in ulcer patients
- ⚠️ Using inappropriate antibiotics in penicillin-allergic patients
Outdated Practices (Do NOT mention):
- Routine H. pylori eradication for all dyspepsia (now test-and-treat)
- Triple therapy as universal first-line (resistance >15% in many areas)
- Long-term acid suppression without addressing infection
Examiner Follow-Up Questions
Expect these follow-up questions:
-
"How does H. pylori survive in the acidic stomach?"
- Answer: Produces urease enzyme that converts urea to ammonia, creating an alkaline microenvironment around the bacterium.
-
"What is the role of cagA in H. pylori pathogenesis?"
- Answer: cagA is injected into gastric epithelial cells via type IV secretion system, acts as an oncoprotein causing cell scattering and disruption of tight junctions.
-
"Why is bismuth quadruple therapy preferred in some regions?"
- Answer: Clarithromycin resistance exceeds 15% in many areas, making triple therapy ineffective; bismuth quadruple is less affected by clarithromycin resistance.
-
"How do you confirm H. pylori eradication?"
- Answer: Urea breath test or stool antigen test performed at least 4 weeks after completing therapy to allow time for bacterial clearance.
-
"What are the extra-gastric manifestations of H. pylori?"
- Answer: Iron deficiency anaemia, idiopathic thrombocytopenic purpura, vitamin B12 deficiency, and possibly rosacea and cardiovascular disease.
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.