This document discusses H. pylori and peptic ulcers. It begins by introducing H. pylori as a gram-negative bacteria that causes gastritis and is associated with peptic ulcer disease and gastric cancer. It then discusses the epidemiology, pathogenesis, diseases associated with H. pylori infection including gastritis, peptic ulcers, gastric cancer, and MALT lymphoma. The document outlines methods for diagnosing and treating H. pylori, as well as managing peptic ulcer disease through lifestyle changes, medication, and occasionally surgery for refractory cases.

1. H. PYLORI AND
PEPTIC ULCERS
Dr. NDAYISABA CORNEILLE
CEO of CHG
MBChB,DCM,BCSIT,CCNA

2. HELICOBACTER PYLORI

3. INTRODUCTION: THE BACTERIA
•Gram negative flagellate
•Slow growing
•Urease producing
•Found mainly in antral Gastric mucosa
•Discovered in 1980s
•Classified a type 1 carcinogen
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4. INTRODUCTION: THE BACTERIA
•Adheres to gastric epithelial cells in the gastric
pits
•Protected by from gastric acid by
•juxtamucosal mucous
•Ammonia produced by bacterial urease
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5. EPIDEMIOLOGY
• 80-90% of population in developing countries
• 20-50% developed countries
• On the whole, ½ of the world population is infected
• ?faecal-oral route, gastro-oral route, cats and sheep
• Acquired mainly in childhood
• Incidence decreases with age
• Prevalence of H. pylori is inversely correlated with
socioeconomic status: family income levels, hygiene, and
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6. PATHOGENESIS
H.pylori causes disease via several mechanisms
1.H.pylori adheres to adhesion molecules such as BabA
2.Causes gastritis in all infected by inducing enzyme
production and apoptosis.
3.Urease enables conversion of urea to ammonia which
is cytotoxic
4.Reduces mucosal defenses by reducing the thickness
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7. PATHOGENESIS
5. Increase gastric acid secretion by producing various
antigens, virulence factors, and soluble mediators.
6. Induces inflammation, which increases parietal-cell
mass and capacity to secrete acid.
8. Recent studies have provided evidence that H. pylori
occasionally enters epithelial cells via a zipper-like
mechanism
7. Ulcers are common is strains that express Cytotoxic-
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8. PATHOGENESIS
9. These genes are associated with a more pronounced
induction of IL-8 that potentiates gastric inflammation.
10. They also interfere with epithelial cell signalling
pathways thereby interfering with mucosal barrier and
cause phenotypic changes of gastric epithelial cells.
11. Host genetic variation are proposed such as genetic
polymorphism for IL-1β that is associated with atrophic
gastritis and cancer
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9. PATHOGENESIS: DISEASES ASSOC WITH
H.PYLORI
•Majority of infected remain asymptomatic.
•Antral gastritis
•Peptic ulcers (duodenal and gastric)
•Gastric adenocarcinoma
•Gastric mucosal-associated lymphoid tissue (MALT)
lymphoma (<1%)
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10. DISEASES ASSOC WITH
H.PYLORI
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11. PATHOGENESIS: DISEASES ASSOC WITH
H.PYLORI
Antral gastritis:
•Often asymptomatic but features of dyspepsia may
occur
•Chronic gastritis leads to hypergastrinemia due to
gastrin release from antral G cells.
•This may consequently lead to duodenal ulceration.
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12. PATHOGENESIS: DISEASES ASSOC WITH
H.PYLORI
Duodenal Ulcer:
• Prevalence of H.pylori in duodenal ulcers is 50-75% in
developed countries
• Eradication of the bacteria leads to healing and reduces
recurrence
• Only 15% with H.pylori develop Duodenal ulcers
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13. PATHOGENESIS: DISEASES ASSOC WITH
H.PYLORI
•Gastric Ulcer:
•H.pylori is thought to reduce gastric mucosa resistance
by cytokine production or alteration in gastric mucus.
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14. DIAGNOSIS OF H.PYLORI
•Indications of testing:
• Active peptic ulcer disease
• Previous peptic ulcer disease
• MALT/lymphoma
• Test and treat in those under 55 without ALARM symptoms
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15. DIAGNOSIS OF H.PYLORI
• Serological tests:
• Test for IgG
• Sensitivity (90%); specificity (83%)
• IgG titres take 1 year to fall by 50% after eradication
• Urea breath Test:
• Can be used as a screening tool
• Sensitivity (90%); specificity (96%)
• Mass spectrometer measures CO2 produced
• Best results if patient has not taken in Abcs or PPIs 4 and 2 wks
respectively
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16. DIAGNOSIS OF H.PYLORI
•Stool Antigen Test
• Sentistivity (97.6%); specificity (96%)
• Useful in both diagnosis and monitoring efficacy of eradication
• Patient should be off PPIs for atleast 2 weeks
• Biopsy urea test
• Biopsy samples from antrum are added to substrate containing urea
and phenol
• Color change occurs due to breakdown of urea to ammonia by Urease
• Test can be false negative if patient is on PPIs or Antibiotics
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17. DIAGNOSIS OF H.PYLORI
•Histology
•H.pylori can be detected on Giemsa staining of
sections of gastric mucosa
•Sensitivity affected by PPIs
•Culture
•Enables testing for antibiotic sensitivity
•Often reserved for patients with refractory H. Pylori
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18. DIAGNOSIS OF H.PYLORI
•PCR
•Done of endoscopic tissue biopsies.
•Very sensitive but prone to false positive results
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19. ERADICATION OF H.PYLORI
•All patients with DUs and GUs and H. pylori should have
eradication therapy.
•Whether all H. pylori positive patients should be treated
is controversial.
•Eradication therapies have been successful in 90%
depending on resistance patterns.
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20. ERADICATION OF H.PYLORI
•Reinfection occurs in less than 1% in developed
countries
•In developing countries reinfection is higher owing to
less compliance and metronidazole resistance.
•Common drugs used: clarithromycin, metronidazole,
bismuth chelates, amoxicillin, tetracycline.
•Quinolones (Cipro, furazolidone) and rifabutin may be
used as “rescue therapy” when standard regimens fails
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21. ERADICATION OF H.PYLORI
Examples of Regimens (7 – 14 days of Rx)
•Omeprazole (20mg) +clarithromycin (500mg) +
amoxicillin (1g) twice daily.
•Omeprazole (20mg) + Metronidazole (400mg)
+clarithromycin (500mg) twice daily.
•Eradication failure regimen:
• Bismuth chelates (120mg X 4 daily) + Metro (400mg X 3
daily) + Tetracycline (500mg X 4 daily) + PPI (20-40mg X 2
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22. ERADICATION OF H.PYLORI
•10 day and 14 day regimens are 7-9% more effective
than 7 day regimens
•Eradication should be confirmed 4-8 weeks after
treatment completion with urea breath test.
•Amoxicillin is preferred in the first line regimen
because of higher resistance patterns to metronidazole.
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23. PEPTIC ULCER DISEASE

24. INTRODUCTION
•Consists of a break in the superficial epithelial
cells penetrating down to the muscularis mucosa.
•Most Duodenal ulcers are in the duodenal cap
•Gastric ulcers are more common in the lesser
curvature near the incisura.
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25. PUD: EPIDEMIOLOGY
•Duodenal ulcers affect 10% of the population
•Duodenal ulcers are 3-4 times more common
than gastric ulcers in the west while Gus are
commoner in Asia & Japan
•DUs and GUs are common in older people
•More prevalent in developing countries due to
H.pylori
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26. PUD: EPIDEMIOLOGY
•Some studies report an increase in the non-
NSAID non-H.pylori ulcers in the US
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27. ETIOLOGIES
1) H pylori infection: (90% of DU, 70% of GU)
• Most infections acquired in child hood
• Transmission is through feco-oral or oral-oral
• Natural habitat is gastric mucosa of the antrum
• Mechanism of action is that suppresses epithelial cell immune
response and generating autoantibodies which cross-react with
the G and D cells causing atrophy/death
• There is a release of gastrin without inhibition and hence
excessive acid secretion and unlcer formation
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28. 2) DRUGS: Nsaids, Aspirin, Oral Bisphosphonates, Potassium Chloride,
Immuno Suppressors
• Causes 10% of DU and 15-30% of GU, 0.1-4% UGIB
• Mechanism of action is by inhibition of GI cyclooxynase-1 (COX 1) and most
are weak acids
3) Gastrinoma and other hyper secretory state such as Zollinger-Ellision
syndrome
4)Malignancy (5-10% GU):
• Adenocarcinoma or lymphoma
5.Psychologic stress
6.Cigarette smoking
7.Alcohol consumption
8. Age-related decline in prostaglandin levels
9. Others:
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29. PATHOPHYSIOLOGY
• Parietal cells produce acid, stimulated by i) vagus nerve/ACH, ii) Histamine, iii)
G cell/gastrin, iv) Proton pump
• Although gastric acid is needed for gastric ulcer formation most people may
not develop ulcer even with higher than normal levels except in condition
such as Zollinger Ellision syndrome.
• Normal GI hemeostatsis : balance of the defensive mechanism (Bicarb,
mucus), and aggressive factors (H.pylori, NSAIDS, acid, pepsin and smoking)
Insults:
• Exogenous(NSAIDS, Tobacco use, ETOH)
• Endogenous ,bile, acid and gastrin
Defence:
First line : Mucus and bicarb barrier
Second line: epithelial cell mechanism (intrinsic cell defense, extrusion of acid)
Third line mech: Blood-flow mediated( supply energy and removal of back-
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30. • Failure of the defences= epithelial cell injury
• First-line repair: restitution
• Second-line repair: cell replication
• Failure of repair = acute wound formation
• Third-line repair: wound healing(formation of granuloma tissue,
angiogenesis, remodeling of basement membrane)
• Failure of continuous repair = Ulcer
• Duodenal ulcer is essentially related to H. pylori causing increase in
acid and pepsin load and gastric metaplasia in the duodenal cap.
• GUs are related to NSAID use in the west.
• Both ulcers are associated with an imbalance between protective and
aggressive factors caused by inflammation
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31. DR NDAYISABA CORNEILLE

32. PUD: CLINICAL FEATURES
•Recurrent burning epigastic pain (may be absent
in the elderly)
•Pointing with one finger at the epigastrium is
strongly associated with PUD
•Association with food is variable
•Pain is relieved by anti-acids
•Pain of DU is worse on hunger
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33. PUD: CLINICAL FEATURES
•Nausea may be accompanied and/or relieved by
vomiting
•Anorexia and weight loss may occur in Gus
•Persistent severe pain may suggest penetration
into other viscera
•Back pain may indicate penetrating posterior
ulcer.
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34. PUD: CLINICAL FEATURES
•Untreated, symptoms relapse and remit
spontaneously
•Epigastric tenderness can occur but also present
in non-ulcer dyspepsia
•Perforated ulcer: rigid, board-like abdomen with
generalised rebound tenderness
•Obstruction: nausea, vomiting, early satiety,
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35. DIAGNOSTIC TEST
To detect PUD
• Esophagogastroduodenoscopy (EGD) >95% sensitive with biopsy to rule out
Gastric cancer
Test for H.pylori: Invasive (EGD with biopsy: antrum x 2, fundus x2 and angularis
x1)
• Rapid Urease/CLO (sensitivity and specificity >95%); +ve H.pylori infection >>
NH₃/CO₂ basic PH via NH₃ and color change
• Biopsy /histology to view organism
• Biopsy/culture (highly specific), but difficult and not clinically useful
Non Invasive H.pylori test
• Serology for IgG/IgA antibodies test
• Urea breath test
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36. •If under 55 years with symptoms of PUD and
positive H. pylori test, eradication therapy suffices
without further investigation.
•Older patients require endoscopy (and biopsy of
ulcers) to rule out gastric cancer
•Endoscopy is required for all patients with ALARM
symptoms (dysphagia, weight loss, vomiting,
anorexia, hematemesis/melana)
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37. MANAGEMENT
H.pylori eradication
• PPI (Omeprazole, Lansoprazole, etc) bid, &
Clarithromycin 500 bid and Amoxicillin 1g bid
(PCA), for 10-14 days (>90% success rate)
• In pts with Penicillin allergy substitute Amoxicillin
with Metronidazole 500mg bid
• Check for eradiaction with UBT or stool antigen test
after treatment
• Continue PPI in recurrent ulcer afterwards
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38. • If H.pylori negative use only PPI
• Recurrent rate is 2-10% per year with antibiotic use , >90% without
antibiotic use
Discontinue NSAIDS
• If NSAIDs must continue add PPI
Anti-secretory therapy : 8 wks for DU, 4-8wks for GU
• H₂RA: safe and can heal 90% of ulcer at 8 weeks, side effects:
impotence, gynecomastia, binds P450, dizzines, headach, caution
with elderly
• Sucralfate: promotes angiogenesis, given 30-60 mins before meal,
best binding ulcers at low PH (Aluminium based, 3%absorbed-
caution with renal failure)
• Misoprostol-stimulates mucus/bicarb (causes significant diarrhoea,
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39. • PPI:Forms irreversible complex with H+/K+ ATPase pump
• Anti-acid- binds bile and inhibits pepsin, promotes angiogenesis
in injured mucosa, atleast 30cc in needed/day to heal ulcer leading
to severe side effects; Magnesium containing agents (diarrhoea),
Aluminium containing agents (constipation), Calcium containing
agents (acid rebound)
Life style changes- disco smoking, ETOH, etc
Surgery rarely needed for cases refractory to medical therapy
• Endoscopic healing is the gold standard in evaluating healing.
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40. PUD: PREVENTION
•Co-administration of PPIs in patients on chronic NSAID
use reduces risk of PUD
•Prostaglandin analogues such as Misoprostol may have
a benefit in preventing NSAID induced PUD.
•Use of selective NSAIDs (coxibs) – concurrent use with
aspirin blunts this effect.
•New Agents: COX inhibitor-NO deliverer, 5-
lipoxygenase/COX inhibitors.
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41. PUD: COMPLICATIONS
Refractory ulcer: a symptomatic, endoscopically proven
ulcer greater than 5 mm in diameter that does not heal
after treatment with a PPI (duration of PPI therapy is 6
weeks for duodenal ulcers or 8 weeks for gastric ulcer),
or does not heal after a full dose of H2RA (within 8
weeks for duodenal ulcers or 12 weeks for gastric ulcers)
•Search for H. pylori, Zollinger-Ellison, current NSAID
use
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42. PUD: COMPLICATIONS
•Bleeding
•Perforation
•Recurrence
•Gastric cancer
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43. REFERENCES
1. Kumar & Clarke’s Clinical Medicine. 8th Edition,
Saunders 2012
2. “The Human Gastric Pathogen Helicobacter pylori
and Its Association with Gastric Cancer and Ulcer
Disease”. Bianca B. and Thomas F.M. Hindawi
Publishing Corporation Ulcers Volume 2011, Article
ID 340157, 23 pages
3. « Peptic Ulcer Disease Today » Yuhong Y., Ireneusz
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44. END
THANKS FOR LISTENING
By
DR NDAYISABA CORNEILLE
MBChB,DCM,BCSIT,CCNA
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