Chronic gastritis

The chronic inflammation of gastric mucosa.
Definition

Chronic gastritis

pylori
Helicobacter
infection
Etiology

Helicobacter pylori

auto-immunologic fator
high positive rate (90%) of serum anti- parietal cell antibody (APCA)
animal model: gastritis induced by injecting APCA repeatedly
high positive rate (75%) of serum anti-intrinsic factor antibody
Etiology

reflux of duodenal juice incompetence of pyloric sphincter post operate stomach
alcohol
heavy salty foods aging
portal hypertension
…...
Other factors

Classification of chronic gastritis
Chronic antral gastritis (Type B gastritis)
H. Pylori infection (90%)
NSAIDs
alcohol
…...

Classification of chronic gastritis
Chronic corpus gastritis (Type A gastritis)
auto-immunologic factors
Chronic pangastritis

Histology
Chronic superficial gastritis Chronic inflammation without
glandular atrophy

Chronic superficial gastritis

Chronic atrophic gastritis
Chronic inflammation with glandular atrophy

Chronic atrophic gastritis

Chronic gastritis
Active stage:
with polymorhpy nuclear neutrophils infiltration
Quiescent stage:
without polymorhpy nuclear neutrophils
infiltration

Chronic gastritis
With
Metaplasia: intestinal
Psueodopyloric

Intestinal metaplasia

chronic gastritis with
Dysplasia
mild, moderate, severe

Chronic gastritis with dysplasia

Clinical Manifestations
Most of patients are asymptomatic
Dyspepsia: upper abdominal pain or discomfort (bloating, belching, nausea vomiting)
The symptoms are not specific
No typical physical sign found

Laboratory and other examinations
Endoscopy examination with mucosal biopsy
the most reliable method for diagnosis

Endoscopy examination
superficial gastritis
edema, erythema, exudate, erosion

Edema erythema

Atrophic gastritis
grey, reduced mucosa folds, submucosal visible vessels

Visible vessels

Note
imperfect co-relations between endoscopic appearances and histological classification, the final diagnosis should be made by histological examination.

Detection of H. pylori
Urease test
Histology
Microbiological culture
Breath test:
13C-urea 14C-urea
Serology: IgG

Gastric acid secretion and serology tests
Type A gastritis
serum anti-parietal cell antibody: (+)
serum anti-intrinsic factor antibody: (+)
serum gastrin:
basic and maximal (pengastrin stimulated) gastric acid secretion :

Type B gastritis
usually in normal range of above tests
gastrin and gastric acid secretion decreased when severe atrophy occurred

Etiology
Type A
auto immunity
Type B H.p.
Environment factors antrum
-- or ↓ ↑
--
--
pernicious anemia
peptic ulcer
Topography corpus BAO & MAO ↓
gastrin ↑
APCA +
Associated disease

Treatment
Exclusion of causative factors smoking, alcohol, NSAIDs, salty food
Medication
relief of pain: antacid, H2-RA, PPI
prokinetic agents: to enhance gastric motility, promote gastric empty

Anti-microbiotic therapy
There are still some arguments
No a effective, low side-effect and low price medicine available
Eradication of Hp is not means improvement of symptoms

How should we do?
Eradication of H.p.
When the patient’s symptom is intractable
When the patient from the high risk area of gastric cancer
When the patient wishes to be treated

Surgery
Only in chronic gastrits with severe dysplasia , because of dysplasia is regarded as precancerous lesion and it is hard to distinguish severe dysplasia and early gastric cancer

Prognosis
Normal mucosa→ CSG → CAG?→ GC
There is a risk from atrophic gastritis (especially with moderate to severe dysplasia) developing to gastric cancer.