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Diseases of the stomach and the duodenum
Gastritis and ulcer disease. Helicobacter pylori
Papp János MD
February 25 th 2013
Peptic ulcer diseases Dispepsia Helicobacter pylori
infection NSAID gastropathy
The peptic ulcer disease
The proven etiologic factors of the peptic ulcer disease
Helicobacter pylori infection Non steroidal anti-inflammatori drugs
(NSAID) Smoking
Hypotethic but not proven factors Diet Coffee Alkohol consumption
The rare causes of ulcer disease
Stress ulcer Different pills (steroid, potassium
iron, 5-FU) Crohn’s d. Dieulafoy ulcer
The diagnosis of the peptic ulcer disease
History Physical examination Helicobacter pylori Endoscopy Radiology
History
The pain
The majoritiy of the peptic ulcer patients complaints pain
The majority of the abdominal pain is not due to peptic ulcer disease
The characteristics of the abdominal pain caused by peptic ulcer
Epigastrial or right upper abdominal localized, not irradiating, can be shown
by pointing the finger at the site Deminishing after meal Lasting for a several days of weeks
period Accompanied by nausea
The diagnosis of the peptic ulcer is based on the history, on the characteristic
pattern of pain
In case of a long lasting peptic ulcer the complaints are not tipical
Using an anacid or antisecretory therapy the complaints are not typical
In case of complications the complaints are not typical
In a quarter of the peptic ulcer cases there is no pain.
but
The „characteristic” complaints
Lord Moynihan stated in the begening of the 1900 years, the 90 % of the cases can be diagnosed solely by the characteristic complaints.
It was recommended to call the peptic ulcer disease having the characteristic complaints Moynihan’s disease.
The frequency of the different complaints in the“ulcer-like” and in the „not ulcer like” dyspepsia and their
predictiv value for peptic ulcer disease
Ulcer like (%)
Not ulcer like (%)
PV SD
The pain diminishes after meal
43 18 0,8 0,2
Pain with empty stomach 21 14 0,4 0,3 The duration of the pain is 1/2-2 hours
33 22 0,4 0,1
Epigastriac localization 95 68 0,3 0,1 “Finger pointing” sign 49 36 0,3 0,1 Heartburn, diminishing after taking antacid, H2 bl, PPI
36 29 0,2 0,2
Pain, diminishing after taking antacid, H2 bl, PPI
43 34 0,2 0,2
Regular use of antacids 31 26 0,2 0,2
Koch 1994
The „silent” ulcer Among 857 peptic ulcer 86 % had pain
before treatment (i. e. 14 %had no pain – „silent” ulcer )
The frequency of the different complaints:
% pain bleeding bloating vomiting ulcus duodeni 79,3 33 30,6 14,5 ulcus ventriculi 43,2 45 12,8 7,1
Porro et al. 1994
Mungan et al. 1994
There is not a single complaint which has a real predictive value
The predictive value of the complaints in peptic ulcer disease
The pain as a marker of the peptic ulcer disease
Sensitivity (complaint positive − ulcer
is present) 60 % Specificity (complaint negative – ulcer is
absent) 70 % Petersen et al. 1988
The „silent” ulcer
10 % of the peptic ulcer cases treated because of complications had no pain earlier.
In 2 % of the duodenal ulcer patients the perforation is the first symptome
The the majority of the complication of the NSAID treatment are without any earlier symptomes.
The physical examination
Epigastric tenderness Differentiation other diseases Complication (perforation
stenosis?)
The role of endoscopy and radiology in the diagnosis of peptic ulcer disease
The biopsy (histology) is always necessary in gastric ulcer to differenciate the malignant lesions
The treatment of peptic ulcer disease I.
Helicobacter pylori eradication Diet Antacid treatment Antisecretory drugs
H2 receptor blockers Proton pump inhibitors
Only in case of complication - surgery
Helicobacter pylori
Epidemiology
High prevalence and incidence in the developing countries
The H. pylori prevalence is increasing with the age
The socio-economic condition has a great influence on prevalance of the H. pylori infection: The condition is better – the infection is less frequent
Epidemiology II.
The infection is more frequent in communities living in close, dense connection.
Genetic factors perhaps play a role (the infection is less frequent among whites than in other races in the USA. More frequent anong mozygotic twins ).
Epidemiology III.
The route of transmission
The exact route of transmission is not known – possibly it is oro-oral
Berry Marshall (who discovered the H. pylori) in a self experiment proved the possibility of oral infection.
The oro-oral route plays a more important role in the developed countries.
The route of transmission
The infection can be transferred by endoscopy
The frequency is estimated 4/1000 upper endoscopy.
The proper desinfection of the endoscope prevents the transmission.
Tytgat: Aliment. Pharmacol. Ther. 9:Suppl2:105 (1995)
The route of transmission
The frequency of H. pylori infection is 30 % in the developed countries
The frequency of H. pylori infection can reach as high as 80 % in the developing
countries
The prevalence of H. pylori infection in the youth
The prevalence of H. pylori infection in Africa and India is as high as 80 % among 20 year old population.
The same number in Italy is 29 %,
In Belgium 4 %.
Peeters M et al. Gut 37: A11 (1995)
Afrika,India Olaszország
Belgium 0
20 40 60 80
100
The sustained healing of peptic ulcer disease in Helicobacter pylori positive and negative cases
1 8 16 24 32 40 48 56
20
40
60
80
100
Helicobacter pylori negative
Helicobacter pylori positive
months
%
Helicobacter pylori The effect of infection on the rebleeding rate
Graham ‘93 RAN+BIS+TET +MET Rokkas ‘93 OME + AMO Labenz ‘94 OME + AMO Jaspersen ’94 OME + AMO
29 0 40 0 38 0 40 3
Rebleeding rate (%) HP + Hp-
Do not test, if you do not treat !
When to treat ?
Perform diagnostic tests only if you intend to treat !
Exceptions: Epidemiological screening done partly
from blood bank repositories Monitoring the success rate of
eradication
Do not test, if you don’t treat !
• Many well-known researchers consider Helicobacter pylori infection as one of the highest morbidity diseases of the world therefore they regard its eradication absolutely necessary in as many patients as possible.
When to treat?
Comparison of the various H. pylori diagnostic methods
Thijs, van Zwet és mtsai 1995
Method
Sensitivity
(%)
Specificity
(%)
Pos. pr.v.
(%)
Neg. prev.v.
(%) Culture 98 100 100 98
PCR 97 100 100 96
Urease detn. 90 100 100 88
Histology 97 98 98 96 13C urea breath test
100 100 100 100
Serology (IgG) 98 88 92 97
Tartam
N beteg eradikáció (%)
hetek szám BIS MET TET 1 hét 13 834 85,8 BIS MET TET 2 hét 24 2520 86,5 BIS MET AMO 1 hét 10 672 73,4 BIS MET AMO 2 hét 12 570 84,9 OME 1 × AMO 2 hét 34 1225 54,5 OME 2 × AMO 2 hét 33 979 71,8 OME 1 × CLA 2 hét 16 567 66,4 OME 2 × CLA 2 hét 11 431 73,5 OME CLA MET 1 hét 17 745 87,5 OME CLA AMO 1 hét 3 75 95,0 OME BIS MET TET 1 hét 8 471 97,8
Helicobacter pylori eradication in 1996
Duration
No of Pts Success of
erad. Weeks
The Helicobacter pylori eradication (ulcus duodeni)’98
0
20
40
60
80
100
Vaira D. és mtsai. Curr. Opinion in Gastroenterology 1998;114 (Suppl.1.):71-8
Helicobacter pylori eradication in 2013 Sequential eradication therapy
2 × standard dose of PPI for 10 days
+ 2 × 1000 mg amoxicillin for the first 5 days
+ 2 × 500 mg clarithyromycin for the second 5 days
2 × 500 mg metronidazol for the second 5 days
The treatment of peptic ulcer disease I.
Helicobacter pylori eradication Diet Antacid treatment Anti secretory drugs
H2 receptor blockers Proton pumpa inhibitors
Only in case of complication - surgery
Burget DW et al. Gastroenterology. 1990;99:345-351.
The role of pH and its daily duration on the acute healing of duodenal ulcer
Daily duration (hours)
pH
468
1012141618202224
1 2 3 4 5
90
80 70
60 50
40
100
Dyspepsia, functional dyspepsia
dyspepsia Long lasting (or recurrent) upper abdominal pain, discomfort, bloating,
flatulence
functional dyspepsia * : dyspepsia which has not an evident, known organic
backgroung
Definition
* or: Non-Ulcer dyspepsia (NUD)
NSAID gastropathy
According of endoscopic observations and using isotope Cr lebelled erythrocytes could be proven, that the NSAIDs but especially the aspirin causes gastrointestinal bleeding.
51
Grossman és mtsai.: Gastroenterology 40:383 (1961)
NSAID gastropathy
There are differences between the effect of the aspirin and the other NSAID - the aspirin causes bleeding only in the stomach all the others causes bleeding in the small bowel as well.
In pathologic studies the prevalence of gastric ulcer among chronic NSAID users is 21,7 % compared with the control group (12,3 %)
0
10
20
25
NSA
ID
Kont
rol
%
Allison MC és mtsai: N.Engl.J.Med. 327:749 (1992)
NSAID gastropathy
Pathology – NSAID gastropathy –
superficial erosions and bleeding
– Deep ulcers
NSAID gastropathy
There are differences among the different NSAID causing gastropathy or ulcer
0
2
4
6
8
10
Ibup
rofe
n
Indo
met
haci
n
Sul
inda
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Feno
prof
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Piro
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Tolm
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Pincus és mtsa.: Am.J.Med. 91:209 (1991.
relatív rizikó
NSAID gastropathy
The mucosa injury caused by NSAID is pH dependent
Elliott és mtsai. 1996
pH 2.0 pH 4.0 pH 5.5 pH 7.0 0
0.5
1
1.5
2
2.5
3
3.5
4
intraduodenal indomethacin
intraduodenalis Salt solution
The comparison of omeprazole and misoprostole for prevention the gastropathy caused by aspirin
0 10 20 30 40 50 60 70
OMNIUM -Yeomans és mtsai. 1996
Pts. in remission (%) after 6 months treatment
daily 20 mg omeprazole
Daily 200 µg misoprostol
Placebo
The healing of gastric NSAID ulcer during omeprazole and misoprostole
treatment
OMNIUM - Hawkey és mtsai 1997
0
20
40
60
80
100 Pts. healed (%)
Omeprazole 20 mg/day
4 weeks 8 weeks
Misoprostole 200 µg/day