Link between H.pylori and diseases

1. From may 2000 to may 2006
• 1704 upper GI endoscopies were done
at RNH endoscopy unit, Riyadh, KSA

2. 0
200
400
600
800
1000
1200
1400
Males
Femles
• Males 1210
( 71%)
• Females 494
( 29%)

3. INDICATIONS

4. INDICATIONS
0
100
200
300
400
500
600
700
800
900
1000
• Dyspep 903 (53%)
• Reflux 443 (26%)
• Haemat 145 (8.5%)
• Melaena 58 (3.4%)
• Both 43 (2.5%)
• Vomiting 58 (3.4%)
• Dysphag 29 (1.7%)
• Anaemia 15 (0.9%)
• Wt loss 5 (0.3%)
• Diarrhoea 5 (0.3%)

5. FINDINGS

6. Gastritis 699 (41%)
GERD 238 (14%)
NERD 208 (12.2%)
Duodenitis 199 (11.7%)
BRG 177 (10.4%)
DU 116 (6.8%)
Gastr erosions 106 (6.2%)
Bleed DU 68 (4%)
GERD/H hernia 65 (3.8%)

7. Varices 49 (2.9%)
GU 44 (2.6%)
NERD/H hernia 43 (2.5%)
Mallory-Weiss 22 (1.3%)
Bleed GU 15 (0.9%)
Ca stomach 5 (0.3%)
G Lymphoma 5 (0.3%)
Ca oesophagus 7 (0.4%)
Gastric polyp 3 (0.2%)
Oesophageal eros 3 (0.2%)
Villous atrophy 3 (0.2%)

8. Lieomyoma 1 (0.1%)
Zollinger-Ellison 1 (0.1%)
FB 3 (0.2%)
Achalasia 1 (0.1%)
Dieulafoy lesion 1 (0.1%)

9. # Gastritis is the commonest finding, 41%
followed by GERD and or NERD in 32.5%.
# About 50% of patients with reflux symptoms
had no oesophagitis but NERD.
# Hiatus hernia present in only 19.4% of
patients with GERD/ or NERD.
# BRG is a common cause of dyspepsia and
reflux symptoms(>10%) specially post-
cholecystectomy.

10. # Peptic ulcer (DU or GU), is present in
about 27% of patients presented with
dyspepsia.
# DU is about three times more common
than GU .
# Bleeding DU is more common than
bleeding GU .

11. • # The 3 cases of esophageal erosions were
drug induced ( Tabucine and Fosamax).
• # The 3 cases of gastric polyps were treated
with polypectomy and both were benign.
• # The 3 cases of villous atrophy were due to
celiac disease in 2 and giardiasis infection in
one patient.

12. # 1635 (96%) patients had biopsies for H.
pylori testing, either by rapid urease test
(CLO) or by histopathology
# 69 (4%) patients did not have biopsies
(coagulopathy)

13. FINDINGS……continue
0
200
400
600
800
1000
1200
H. pyl pos
H. pyl neg
• H. pylori positive
1170 (71.6%)
• H. pylori negative
465(28.4%)

14. # More than 97% of patients with DU are
H. pylori positive.
# About 70% of patients with GU are H.
pylori positive.
# 4 of the 10 patients with gastric
malignancy tested positive
# Positive males were 73%
# Positive females were 67%

15. FINDINGS………continue
0
20
40
60
80
100
120
140
160
180
Pos DU
Neg DU
Pos GU
Neg GU
• H. pylori positive
DU 179 ( 97% )
• H. pylori negative
DU 5 ( 3% )
• H.pylori positive
GU 41 ( 70% )
• H. pylori negative
GU 18 ( 30% )

16. DISTRIBUTION OF PEPTIC ULCER
0
10
20
30
40
50
60
70
80
90
SA
Jord
Ind
yem
Egy
Flip
Sud
Turk
• SA 85 (35%)
• Jord 39 (16%)
• Ind 39 (16%)
• Yem 29 (12%)
• Egy 17 (7%)
• Flip 17 (7%)
• Sud 15 (6%)
• Turk 2 (1%)

17. AGE DISTRIBUTION in 1704 patients
10 - 19 years 48
20 - 29 371
30 - 39 489
40 - 49 426
50 - 59 189
60 - 69 81
70 - 79 62
80 and over 38

18. TREATMENT OF H.pylori
• Different regimens for H. pylori eradication
were used in 1170 patients and these were
chosen from the literature:

19. # 350 patients received (OCA);
Omeprazole 20 mg +
Clarithromycin 500 mg +
Amoxil 1000 mg, both twice daily for 1 week

20. # 475 patients received (PCA);
Pantoprazole 40 mg +
Clarithromycin 500 mg +
Amoxil 1000 mg, both twice daily for 1 week

21. # 185 patients received (LCA);
Lansoprazole 30 mg +
Clarithromycin 500 mg +
Amoxil 1000 mg, both twice daily for 1 week

22. # 35 patients received (OMA);
Omeprazole 20 mg +
Metronidazole 500 mg +
Amoxil 1000 mg, both twice daily for 1 week

23. # 125 patients received (EAL);
The most recent regimen;
Esomeprazole (Nexium) 20 mg +
Azithromycin (Zithromax) 500 mg+
Levofloxacin (Tavanic) 500 mg, both once
daily for 1 week

24. RESULTS OF TREATMENT
• We were using 13
C-UBT/ 14
C-UBT or
HpSAg to confirm H.pylori eradication 4
weeks after completing the course of the
triple therapy in 850 patients
• The eradication rate was as follow:
• LCA regimen…………………….88%

25. • OCA regimen…………………….87%
• EAL regimen (once daily)……..87%
• PCA regimen……………………. 75%
• OMA regimen…………………….28.5%

26. This rate of eradication is similar to that
seen in most studies (80-90%), although
the eradication rate for metronidazole
based regimens was much lower than
other studies(28.5%).
This could be explained by higher
H.pylori resistance to metronidazole in
our locality due to abuse of
metronidazole.

27. 246 out of the 1704 gastroscopy
(14.5%) were done as emergency procedures
for acute upper GI bleeding ( haematemesis
and/or melaena).

28. 0
10
20
30
40
50
60
70
80
DU 28%
G/D eros 26%
Varices 20%
MW tear 8%
GU 6%
GERD 6%
Ca stom 2%
Leiomyo 0.8%
ZE synd 0.8%
Dieulafoy 0.5%
Causes of haematemesis and/or melaena in
246 patients

29. OUTCOME IN THE 246 PATIENTS
8 patients were referred for surgery, ( 6 for bleeding
DU, 1 for leiomyoma, 1 for Dieulafoy leison), one of
these ulcer patients developed cardiac arrest before
surgical intervention and this is the only patient who
died representing mortality of 0.4% ( was referred for
endoscopy 3 days after haematemesis)!!!.

30. OUTCOME IN 246 PATIENTS cont…
17patients with Ca stomach and Ca oesophagus
were referred to specialist centers
# The other 221patients(90%) were treated
successively medically with sclerotherapy, adrenaline
injection, heat coagulation, Sengstaken tube and
drugs.

31. • How does gastric H. pylori colonization increase
risk for DU? One explanation is that antral H. pylori
colonization diminishes the number of somatostatin-
producing cells; somatostatin-mediated inhibition of
gastrin release leads to hypergastrinemia.
Individuals with antral-predominant gastritis (and
thus a normally functioning acid-producing gastric
corpus) develop increased acid secretion, which
may increase the risk of DU per se or may induce
gastric metaplasia in the duodenum, which becomes
colonized by H. pylori, then inflamed, and finally
ulcerated. After eradication of H. pylori from
patients with DU disease, the level of acid secretion
often falls.

44. Eradication of H. pylori eliminates DU
recurrence
0
10
20
30
40
50
60
70
80
90
100
months 0 6 12 18 24
H. pylori -
H. pyolri +
Huang et al, Am J Gastroenterol 1996;91(9):125

46. • The effect of H. pylori eradication on
24 H esophageal acid secretion is
variable, but most treatment trials with
PPI do not find that H. pylori status
adversely affects symptom relief or
healing of GERD in the majority of
patients.

47. Relationship between H. pylori and extra-
gastric gastrointestinal malignancies
• H. pylori role in extra-gastric gastrointestinal
malignancies, such as esophageal cancer, is
controversial. Doctors from Greece explored the
relationship of H. pylori infection, and H. pylori
cagA-positive strain with this malignancy by
performing meta-analysis of all relevant studies
through 2007.

48. • The researchers found that in adenocarcinoma
patients there were inverse significant relationships
with both the H. pylori prevalence, and the
prevalence of H. pylori cagA-positive strain i.e there
is a temporal relationship between a falling
prevalence of H. pylori colonization and a rising
incidence of these conditions Similarly in patients
with Barrett's esophagus, there were inverse
significant relationships, which might suggest a
protective role of the infection in these entities.

49. • The research team noted that in patients with
squamous cell carcinoma there were no significant
relationships with both H. pylori prevalence, and the
prevalence of H. pylori cagA-positive strains.

50. • Several extra-gastrointestinal pathologies have been
linked epidemiologically with H. pylori
colonization. The most notable are ischemic heart
disease and cerebrovascular disease. The
associations have been found more commonly in
small than in large studies, and most authorities
consider them to be noncausal and due to
confounding factors.

52. HOME TAKE MESSAGE

53. # Most H. pylori-colonized persons do not develop
clinical sequelae. That some persons develop overt
disease whereas others do not is probably due to a
combination of bacterial strain differences, host
susceptibility to disease, and environmental factors; of
these, bacterial factors are best studied.
# Clinicians should continue to eradicate H. pylori
when found and not be concerned about aggravating
coexisting reflux disease which should easily respond
to PPI therapy specially in patients who are candidates
for long term PPI.
(Gut 2004;53:310-313)