Chronic gastritis, chronic gastroduodenitis

Definition. Chronic gastritis (CG), chronic gastroduodenitis (CGD) represent a chronic

recurrent inflammation of stomach and/or duodenum mucosa and submucosa.

CG and CGD occupy 58-65% from all gastroenterologic pathologies in children. The isolated
affection of stomach and duodenum is met in 10-15% of children, in 85-90% - associated
affection, fact that indicates the resemblance of pathogenic mechanisms of CG and CGD
development.

Etiopathogenesis

There are 3 groups of causes, conformable to which CG and CGD are classifying in 3 groups:

1. Exogenous infectious provoked by Helicobacter pylori (HP). They constitute 85% from
CGD and are characterizing through affection of mucosa in the distal portions of stomach
(antral), gastric hypersecretion and vegetation in pyloroantral level of HP.
2. Endogenous autoimmune. Prevailing in matures (in children – only 1-3% in the structure
of CGD), they are characterizing through the appearance of specific autoantibodies
against the parietal glandulocytes and deployment of primary atrophic progressive
process, without clear inflammatory phenomena. The process is localizing preferentially
in cardiofundal region and evolves with hypoacidity, hypergastrinemia and presence of
antibodies against Castle factor.
3. Exo-endogenous – chemical, reflux; constitute 10-12% from CGD.

International classification of gastritis

The type of gastritis
 Acute gastritis
 Induced by H. pylory
 Hemorrhagic or/and erosive
 Phlegmonous
 Chronic gastritis
 Induced by H. pylori
 Atrophic, autoimmune gastritis
 Special forms of chronic gastritis
 Lymphocytary
 Eosinophilic
 Granulomatous
 Endoscopic forms of gastritis
 Exudative-erythematous
 Maculo-erosive
 Papulo-erosive
 Atrophic
 Hemorrhagic
 Gastritis with hypertrophic folds
 Localization
 Antral gastritis
  Gastritis of gastric body
 Pangastritis
 Histological activity
 Active
 Inactive
 Etiology
 In function of etiologic agent

Clinical picture

The symptoms of chronic gastrites are very varied, because they differ from etiopathogenetic and
morphologic point of view. There are distinguishing two clinical types of CG: algic and
dyspeptic syndrome.

Algic syndrome. The clinical picture resembles to that in ulcer disease. The patient presents
complaints to pains by different intensity, that appear in interval of 2 hours before meal or 2
hours after meal; they can be also nocturnal. The pains are suppressed through alimentation,
heartburn, eructations, vomits after meal, that provoke relief. The appetite is preserved. Also
there can be general symptoms, such as physical and psycho-emotional asthenia, nervousness,
irritability, headache. The abdomen palpation is painful in epigastric region and pyloroduodenal
area.

At endoscopic examination we can see the affection of central zone of duodenal bulb
(antroduodenitis). The character of endoscopic changes can be different: superficial,
hyperplastic, erosive, with pronounced edema and hyperemia.

The secretory function of stomach is normal or increased. Etiologically this type of gastritis is
associated with HP.

Dyspeptic syndrome is characterizing through dull pains in epigastric region or around

umbilicus. The pains often appear immediately after meal, especially after intake of greasy,
roasted aliments. The patients present sensation of plenitude in epigastric region. Eructations
with air, nausea and vomiting appear. The appetite is decreased. At abdomen palpation we
determine the pain in the umbilicus region.

At endoscopic examination we determine the affection of stomach fundus or some diffuse

process. The signs of inflammation are minimal, and hystologically we can determine the
atrophy of mucosa, intestinal metaplasia. The secretory function of stomach can be normal or
decreased. After genesis, this type of gastritis can be autoimmune or associated with HP.

Also there can be clinically atypical and asymptomatic forms. As a rule, they manifest a
clinical picture characteristic for associated pathology. Around 40% from CG occur latent
asymptomatic, fact that can be explained through the absence of nerve endings in stomach
mucosa and the appearance of symptoms from the account of motor disorders (spasms, refluxes).

Table

Differential diagnosis of chronic gastritis

Differential-diagnostic Chronic autoimmune Chronic H. Pylori gastritis
criteria gastritis
Localization Fundus, body Antral region
Inflammation Moderated Pronounced
Atrophy Appears initially in the body Appears gradually in antral
region region
HP - +
Antibodies against parietal + -
cells
Stomach secretion Decreased Normal or increased
Gasrinemia Increased Normal or a little increased

Elements of diagnosis

1. Anamnesis
2. Clinical examination
3. Endoscopic examination
4. Ultrasonography of internal organs
5. Functional methods of stomach examination
6. Radiologic examination

At endoscopic examination we can determine focal or diffuse hyperemia of stomach mucosa,

edema, hypertrophy of folds. These changes are associated with HP. The stomach mucosa is
pale, pink-whitish, sometimes – bluish, the surface is thinned, resembling with atrophic tongue,
the folds are weakly pronounced, typical for atrophic process, the degree of which can be
ascertained only at histological examination.

The secretor function of stomach is determining using intragastral pH-metry and

reogastrography.

Intragastral pH-metry. The normal values of pH: basal secret in corpus – 1,5-2; in antrum – 6,0-
8,0, in stimulated secret in corpus – 5,0-8,0.

Reogastrography allows to determine with special sound the resistance of tissues in more points
of stomach and esophagus.

Incretor function of stomach is appreciating in dependence from the level of pepsinogen in

blood and urine. The pepsinogen of plasma in norm – 70-100 pmol/l, the excretion of
uropepsinogen in 24 hours in norm – 0,3-0,8 mg; the proteolytic activity of pepsinogen
constitutes 0,2-0,07 units.

The motor function is appreciating at FEGDS performing (refluxes).

Radiologic examination with barium, in the last years, is not performing, but is useful for to
appreciate the evacuator function and for differential diagnosis with such diseases as pyloric
stenosis, tumors.

Models of HP infection diagnostic

1. Invasive (need biopsy)

  histological;
 bacterioscopic;
 bacteriologic
 biochemical (urease test)

2. Noninvasive

 serologic (ELISA technique);

 respiratory test;
 reaction of chain polymerization

Differential diagnosis

Chronic gastritis and gastroduodenitis are differentiating from ulcer disease and functional
disorders of stomach (FDS). The latter are motor and secretor disorders of stomach, that occur
with gastric dyspeptic manifestations in the absence of morphologic changes in the stomach
mucosa. The diagnosis is established at endoscopic examination.

The ulcer disease represents an chronic recurrent affection characterized by the appearance of
ulcerative defect at the gastroduodenal level, followed by secretor functional, motor disorders
and disorders of stomach or/and duodenal absorption. The diagnosis is establishing at endoscopic
examination.

The treatment of gastroduodenitis

The treatment is complex and adapted to the:

 etiology;
 morphologic changes;
 secretor function;
 motor function

The diet. Normocaloric alimentary regime sparing from mechanical, thermic and chemical point
of view, functionally equilibrated, rich in vitamins and fragmented (5-6 times per day, meal N1
after Pevzner). In the case of decreased stomach secretion, we prescribe the meal N2 after
Pevzner (soups on the base of meat bullion, salads, juices, kefir).

The drug treatment

Correction of secretion disorders:

a) antacid preparations (almagel, Maalox, gastal);

b) H2-histaminolytics (ranitidine, famotidine, mizatidine);

c) blockers of H*K*ATP-ase (omeprazol, lansoprazol).

HP eradication (absence of bacteria one month after treatment stopping):

a) triple scheme: omeprazol + antibiotic (amoxicylline, claritromycine) + metronidazol, duration

of cure – 7 days; it is recommended in gastroduodenites with normal secretion;
b) cuadruple scheme: omeprazol + de-nol + antibiotic + metronidazol; duration of cure – 7 days.

Correction of motor disorders – the spasmolytics are indicated (no-spa, papaverin). In the case
of reflux (duodeno-gastral or gastro-esophageal reflux) the prokinetics are recommended
(metoclopramid, domperidon, cizaprid).

Amelioration of metabolic processes in stomach mucosa: the follows are indicated: vitamins B1,
B2, B3, B5, B6, B12, folic acid, vitamins A and E, membranostabilizers (essential forte, lipostabil),
biostimulators (carnitin chloride, apilac) The cure of treatment – 1 month.

Substitutive treatment in hyposecretory forms: stimulant phytotherapy – decoction of wild rose,

milfoil (Achillea millefolium), roadweed (Plantago), also calcium preparations, diluted
chlorhydric acid.

In reactive gastritis there are indicated the cytoprotectors – prostaglandins (mizoprostol,

enprostol, saitotec) and indirect cytoprotectors – biogastron, carbenoxolon.

The normalizing of neuro-vegetative state includes sedative therapy (tincture of valerian, beloid,
belataminal), adaptogens (eleuterococcus, ginseng).

Physiotherapeutic procedures

In the period of exacerbation there is indicated the electrophoresis with platiphyllin or Novocain
on epigastric region, electrophoresis with calcium or brome on cervical region. In the period of
remission there are indicated applications with paraffin, ozokerit, mud in epigastric region.

In the period of incomplete and complete remission the phytotherapy with plants is applying:
plants with anti-inflammatory action (wild chamomile, St. John’s wort (Hypericum perforatum),
calendula), plants with astringent action (shell of oak); with stimulant action (wild rose, milfoil
(Achillea millefolium), roadweed (Plantago)). The cure of treatment – 3-4 weeks.

Dispensary control

The children with CG are maintained at evidence during 5 years. In the first year they are
examined 3 times, in the second year – 2 times. The basic methods of follow-up in dynamics
remain FEGDS and HP determining. As antirecidivant treatment there are applying the
antihelicobacter therapy, biostimulators, polyvitamins, phytotherapy, sanatorium treatment.

Prognosis

The healing is possible in the case of HP eradication. The persistence of HP leads to the disease
progressing and the possibility of ulcer disease development.

Prophylaxis

The prophylaxis of HP infection consists in the respecting of elementary rules of hygiene,

especially in hospital, because the transmission is performing on oral pathway.

DUODENITES

Etiology
The duodenites can appear in three general below-named situations:

1. Primary inflammation of duodenal mucosa, apparently without any cause, that is known
as non-specific duodenitis, gastroduodenitis, peptic duodenitis, chronic duodenitis. In
present, the primary duodenitis is attributed to HP which is developing on the isles of
gastric metaplasia on duodenal bulb and provokes the inflammation of mucosa.
2. Inflammation of accompaniment in gastritis and duodenal ulcer.
3. Duodenites secondary to some infections: TBC, parasitic infestations (giardia lamblia,
ankilostoma), viruses (rotaviruses, cytomegaloviruses, hepatic viruses) or some entities
known as celiac disease, Crohn disease, acute pancreatitis, angiocolites etc.

Clinical picture

The completely asymptomatic duodenites are rare. Most often they are presented with algic
syndrome. The pain has all characters of that from ulcer, with regularity, localization, conditions
of appearance, periodicity, amelioration at aliments intake.

The diagnosis is performing at endoscopy and biopsy. At endoscopy we can see congestion,
erosions, petechiae, at biopsy we can find the inflammation of duodenal mucosa and its type. As
a rule, in primary duodenites there is present also the antral inflammation, and HP is positive.

The treatment of primary duodenites is identical with that of chronic gastritis. The pains
diminish at antacids administration or administration of acid secretion inhibitors. The treatment
of Helicobacter Pylori leads to disappearance of symptoms and histological improvement.

The prognosis is favorable.