Chronic gastroduodenitis in

children
Head of the Department of
Propedeutics of Childhood
Diseases
Toktabaeva B.Zh.
 DEFINITION

Chronic gastroduodenitis is a chronic

recurrent disease with a tendency to progression, the
morphological manifestation of which is
inflammation, dystrophy of the mucous membrane
of the duodenum, accompanied by a violation of the
secretory, motor-evacuation and endocrine functions
of the stomach and duodenum.
 EPIDEMIOLOGY

In the structure of gastroenterological pathology,

diseases of the stomach and duodenum are 220-280%.
The frequency of chronic H. pylori gastritis varies
depending on the age of the child and is, respectively, at
4-9 years-20%, 10-14 years-40%, and in children over 15
years old - up to 52%.
 CLASSIFICATION
1. By origin • primary; secondary

2. By the presence of H. pylori • (HP-associated, non-associated)

infection
• Gastritis: antral, fundic, pangastritis
3. Topography • Duodenitis: bulbitis, postbulbar, panduodenitis,
gastroduodenitis
• Endoscopic: superficial, hypertrophic, erosive, hemorrhagic,
4. By morphological forms of subatrophic, mixed.
lesions of the stomach and • Histologically: superficial, diffuse (no atrophy, subatrophic,
duodenum atrophic)

5. By the nature of the • With increased function, with retained function, with reduced
function of the acid-forming function.
and secretory stomach
• (yes, no).
6. Duodenogastric reflux

• exacerbation, incomplete clinical remission, completе

7. Phases of the disease clinical remission, clinical-endoscopic-morphological
remission (recovery).
ETIOLOGY

EXOGENOUS

ENDOGENOUS
 EXOGENIC FACTORS

1 ALIMENTARY

2 PSYCHOEMOTIONAL AND VEGETATIVE DYSFUNCTION

3 ECOLOGICAL

4 MEDICIENS

5 FOOD ALLERGY

6 INFECTIOUS, PARASITIC INVASIONS

7 HEREDITARY PREPOSITION
 ENDOGENIC FACTORS

1 PERNICIOUS ANEMIA

2
DIABETES TYPE I

3
AUTOIMMUNE THYROIDITIS

CHRONIC RENAL FAILURE

4

5 CHRONIC ADRENAL CORRECT INSUFFICIENCY

 TYPES OF CHRONIC GASTRITIS

• Infectious • Endogenous, • Exo-endogenous,

(exogenous) autoimmune, associated with
associated with due to the frequent thermal
gastric formation of irritation, drug
helicobacteriosis antibodies to the exposure and / or
(gastritis B- parietal cells of severe GDR (C-
bacterial) the gastric reactive or
glands (gastritis chemical
A- gastritis)
• 85% autoimmune)
• 10-12%
• 1-3%
 More than 30 years have passed since the discovery of H. pylori
infection by Australian researchers Warren and Marshall. In 2005, Barry
Marshall and his colleague Robin Warren received the Nobel Prize in
Physiology or Medicine for their work on the study of the effect of the
bacterium Helicobacter pylori on the occurrence of gastritis and gastric and
duodenal ulcers.
 Frequency of occurrence of Helicobacter pylori by continent

30% USA and

Canada 20%
20%Australia
30% 80% South America
40% Western 80%
40%
Europe

80% Africa
70% Eastern70% 80%
Europe
65%
65% Asia
 Frequency of occurrence of Helicobacter pylori by continent

60% America
54% 54%
51% 52%

50%
43%
Континент бойынша Helicobacter pilori кездесу
40% 36%
жиілігі
30%
30%
Африка

20%

7%
Guatemal

10%
Mexico

Canada
Bolivia

А
и
з
я
Brazil

0% Chile

USA
Peru
70%
69%
70%
60% Europe
a

60%

50%
42% 41%
40% 36%

30%

20%
12% 11% 12%
10%
Czech Re-

Germany
Bulgaria

Switzer-
0%
Albania

Sweden
Nether-
Estonia

Iceland
public

lands

land
 MICROBIOLOGICAL CHARACTERISTICS
Helicobacter pylori is a microaerophilic spiral-shaped gram-
negative bacterium, about 3 microns in length, about 0.5
microns in diameter. It has 4-6 flagella and the ability to move
extremely quickly even in thick mucus or agar. The most
favorable conditions for the existence of helicobacter are a
temperature of 37-420C and a pH of 6-8. At lower pH values (4-
6) bacteria retain their viability, but stop growing and
reproducing.
 TRANSMISSION WAYS
THE SOURCE OF HP-INFECTION IS A HUMAN

CONTACT - FROM THE

PATIENT OR BACTERION
CARRIER ORAL-ORAL OR
FECAL-ORAL WAY

IATROGENIC -
THROUGH MEDICAL
INSTRUMENTS
 BIOCHEMICAL PROPERTIES
flagella urease
colonization of host cells after • neutralization of stomach acid;
mucosal penetration and • damage to the gastric mucosa by ammonia.
chemotaxis
lipopolysaccharide
• attachment to host cells;
• inflammation
surface proteins
• attachment to host cells

exotoxins
• vacuole-forming toxin (VacA)
• mucosal damage
secretion system
flagella-like structure for
introducing effectors
exozymes
(protease, lipase, mucinase)
into host cells effectors (CagA)
damage to the mucous • actin remodeling
membrane • induction of interleukin - 8
• inhibition of host cell growth and apoptosis
B GASTRITIS PATHOGENESIS
gastric juice
mucus layer urea +
water acid
neutralization

epithelial cells

damage to the mucous

membrane by bacterial enzymes
pepsin

Inflammation due to Death of epithelial

acidic environment, cells due to
proteases and ammonia and
effector cytotoxins

Leukocyte chemotaxis
B GASTRITIS PATHOGENESIS

gastric juice

mucus layer

epithelial cells
B GASTRITIS PATHOGENESIS

urea +
water acid
neutralization
B GASTRITIS PATHOGENESIS
B GASTRITIS PATHOGENESIS

damage to the mucous

membrane by bacterial
enzymes
pepsin

Death of epithelial cells due

Inflammation due to to ammonia and cytotoxins
acidic environment,
proteases and effector

Leukocyte chemotaxis
 А GASTRITIS PATHOGENESIS
production of autoantibodies to parietal cells.

Antibodies, binding to the parietal cells, damage

the fundic glands and lead to the death of highly
differentiated cells.

As a result of atrophy of the mucous membrane

of the body of the stomach and the death of the
main glands, a persistent decrease in the
secretory function of the stomach occurs.
The production of gastrin is compensatory
activated, its level in the blood rises, but the
atrophied glands are not able to enhance the
secretory response even to increased gastrin
stimulation.
 С GASTRITIS PATHOGENESIS

The development of gastritis C (reactive, chemical) may be associated with medication or

severe GDR. The most severe adverse effects on the gastric mucosa are NSAIDs,
primarily aspirin. The development of gastritis in this case depends on both the dose and
the duration of the drug intake. NSAIDs can have both local and general effects.

Local depends on the ability

ПАТОГЕНЕЗ
The general is associated with the main pharmacological action
of the drug to attach H + of the drugs - the inhibition of cyclooxygenase, as a result of
in an acidic environment. which the production of prostaglandins in the gastric mucosa
decreases, which means the production of bicarbonates and
mucus.

Under conditions of blocking cyclooxygenase, the metabolism of

arachidonic acid follows the lipoxygenase pathway, resulting in
the formation of leukotrienes, peroxides and hydroperoxides, free
radicals.

In the mucous membrane, the production of leukotriene B4

is significantly increased, which can promote the adhesion
of neutrophils to the vascular endothelium with the
formation of so-called white blood clots, microcirculation
disorders and the formation of erosions.
С GASTRITIS PATHOGENESIS

Bile acids have detergent properties and break

the mucous barrier. Phospholipase A contained
in duodenal juice, when combined with
hydrochloric acid in the stomach, forms
cytotoxic lysolecithin, which has a damaging
effect on the epithelium.
 CLINICAL TYPES:

Ulcerati
ve
DISKINE
TIC
 ULCERATIVE TYPE
aching pains of varying intensity, arising on an empty stomach
or 1.5-2 hours after eating, sometimes night or late evening
pains, characterized by the disappearance or reduction of pain
after eating.

heartburn, sometimes belching with air or

sour.
Occasionally there may be vomiting, usually
single, acidic contents, bringing relief.

common symptoms like fatigue, headaches,

emotional lability, sweating.

On palpation of the abdomen, pain in

the epigastrium or pyloroduodenal zone
is typical.
 DISKINETIC TYPE

early aching pains in the epigastrium and the navel after eating,
especially plentiful, fried and greasy, pains go away on their own after 1-
1, 5 hours.

feeling of heaviness, fullness in the epigastrium, fast satiety,

decreased and selective appetite.

Sometimes there may be a burp of air,

nausea, occasionally vomiting of food eaten, bringing relief.
 DIAGNOSTICS
invasive non-invasive
methods methods

Bacteriological Serological (ELISA) (material

(biopsy material of the gastric - blood plasma)
mucosa)

rapid urease test

(biopsy material of the gastric 13 C / 14C-urease breath test (material
mucosa) - exhaled air of the patient, after taking
urea labeled with carbon isotopes 13 C
or 14 C)
histological
(biopsy material of the gastric
mucosa)
Stool antigen testing for H. pylori
Molecular (PCR)
(biopsy material of the gastric
mucosa))
 METHODS RECOMMENDED FOR THE PRIMARY DIAGNOSIS
OF H.PYLORI.

Invasive Non-invasive
FGDS with biopsy  Antibodies to H.pylori IgG
 Morphological examination *  13C – urease breath test *
 Cytological examination *  14С – urease breath test *
 Rapid urease test *  Antigen monoclonal in stool *
 Bacteriological examination *

Note: * The test is reliable if the patient has taken antibiotics,

bismuth preparations for any reason for more than a month, PPIs,
H2 blockers for more than 2 weeks.
UREASE BREATHING TEST
 PURPOSE OF TREATMENT

normalization of
reparative
suppression of
properties and
acid-peptic normalization of
morphological
factor, secretory-motor
state of the
eradication of activity of the
mucous
Helicobacter stomach
membrane of the
Pylori,
stomach and
duodenum
 NON-MEDICINAL TREATMENT
diet number 1A for 5-7
days: milk (if tolerated),
with high acidity, Food is fractional, 5-6
fresh cottage cheese,
products with a high times a day.
jelly, jelly, slimy and
pureed soups from buffering capacity are
used
cereals and milk, fish
soufflé, with limited salt (milk, oatmeal dishes,
boiled beef, veal).
A good effect is the
inclusion of dietary fiber
diet number 1B for 14 in the diet (wheat bran in
days: with the expansion of a daily dose (age + 5g) for
the diet - crackers, meat, diet number 2 - with one month).
fish, mashed cereals, soups CGD with secretory
from cereals in milk, salt in insufficiency
moderation

diet number 4 (dairy-free Medical and

diet number 1: in diet) - if the child receives protective regime.
compliance with the colloidal bismuth,
principle of mechanical and tripotassium dicitrate
chemical sparing.
 MEDICAL TREATMENT
Proton pump inhibitors omeprazole,
lansoprazole, esomeprazole)

Cytoprotectors (sucralfate, bismuth

tripotassium dicitrate, bismuth subgallate)

Prokinetics (domperidone)

H2 blockers of histamine receptors

(ranitidine, famotidine)

Vegetotropic drugs
 Maastricht Consensus

• in 1996, in the Dutch city of Maastricht, a consensus

19 was adopted on the problem of Helicobacter pylori,
which was named the "Maastricht Consensus"
96
• Maastricht Consensus-2. test-and-treat
20
00

20 • Maastricht Consensus-3
05

20 • Maastricht 4 / Florence.
10

20 • Maastricht 5 / Florence.
16
 SCHEMES FOR ERADICATION THERAPY
Quadrotherap Квадротеап
Triple standard Sequential ия на основе Тройная
y without
therapy therapy препаратов терапия на
bismuth
висмута основе
• PPI + preparations • PPI + •левофлоксац
• PPIs • PPI+amoxi PPI
(omeprazole amoxicillin bismuth +levofloxa
ина
cillin
or (5 days), tripotassiu cin
+clarithrom
lansoprazole ycin + m dicitrate +amoxicill
or metronidaz + in (10
esomeprazol • then PPI + ole(10 tetracyclin days)
e)+ clarithromy days) e+
amoxicillin cin + metronida
+clarithromy metronidazo zole (10
cin; le (5 days) days)

• PPI +
amoxicillin +
imidazole
(metronidazo
le,
tinidazole)
 LITERATURE
Мельникова И.Ю. Детская
гастроэнтерология.
Практическое руководство
Москва, 2018

• Клинический протокол
МЗ РК от «30» ноября 2015 года
Протокол №18

Рекомендации Маастрихт V Malfertheiner

P et al. Management of Helicobacter
pylori infection — the Maastricht V/Florence
Consensus Report.Gut 2016 Oct 5

Степанов Ю.М. , Будзак И.Я.

Маастрихтский консенсус-5:
аналитический обзор положений
Гастроэнтерология, 2017.
Стр.36-45.