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

c N

apro

xen

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