gastritis is defined as the presence of chronic mucosal inflammatory
changes leading eventually to mucosal atrophy and intestinal
The epithelial changes
may become dysplastic and constitute a backround for the development of
30% of endoscopically
normal biopsies may show chronic gastritis.
Type A :
gastritis- Associated with pernicious anaemia. Body of the stomach is
Type B :
Environmental gastritis- Result from dietary or intraluminal factors,
specially Helicobacter pylori. Usually localized in the antrum. In
severe cases, the inflammation spreads to the proximal part of the
Type C : Chemical gastritis- Associated with ingestion of non-steroidal
anti-inflammatory drugs or bile influx
is Helicobacter Pylori?
Small curved gram negative bacillus that colonizes the mucus layer of
The organisms adheres to the foveolar epithelium and in the crevices
between foveolar cells.
Corkscrew-like movement and production of enzymes play an important
role in the pathogenesis.
Bacterial adhesins identify cell surface proteins, glycoconjugates and
helps in colonization.
H. pylori move along the lateral border of the foveolar cells and
weaken the mucosal barrier.
The intracellular space is widened and there is invasion by neutrophil
Proteases produced by the H. pylori digest gastric mucin and further
damage the epithelium.
Helicobacter associated patterns of
(principal cause of peptic ulcer)
Multifocal atrophic gastritis
involving corpus, fundus and antrum (may develop gastric ulcer and
gastric carcinoma). Helicobacter pylori are also associated with the development of gastric lymphoma.
Cag A+ strains of Helicobacter pylori (more ulcerogenic) are protective against
development of gastroesophageal reflux disease.
|What is Helicobacter
Images Link (Dr Yutaka Tsutsumi MD
This bacteria has an elongated spiral appearance and are present only in
small number of patients.
Helicobacter helmannii is a possible cause of gastric ulcer.
-In the initial active phase there are features of acute gastritis
characterised by neutrophil polymorphs in mucous neck region. In severe
infection there is pit abscess formation.
-Cellular swelling and vacuolization, mucin loss and desquamation of
-Erosion and frank ulceration.
-Degenerative and regenerative changes present.
-Regenerative changes - There are hyperplastic neck cells and elongated,
distorted and tubular structures. The cells display cytoplasmic
basophilia, increased mitoses and hyperchromatic nuclei, however the
enlarged nuclei show smooth regular nuclear membrane.
-As the disease progresses there is superimposed chronic inflammation
(Active chronic gastritis).
Neutrophils, eosinophils, basophils, macrophages, monocytes, plasma cells
infiltrate the mucosa.
-Mucosa appears normal in thickness or slightly expanded by mononuclear
-In early stage, lymphocytes and plasma cells are present in the
superficial mucosa mostly along lesser curvature. (Chronic superficial
-The inflammation extends into the glandular compartment.
-Focal epithelial cell dropout is noted.
-There is lymphoid follicle formation with or without germinal centres. This is a marker for H. pylori infection.
-Gradually develops pangastritis.
-There is glandular atrophy (Chronic atrophic gastritis)
-Intestinal metaplasia replaces the gastric glands. H. pylori is markedly
decreased in the late stage as intestinal metaplasia creates an
unfavourable environment for H. pylori.
- Gastric atrophy is the end stage of chronic gastritis and is
characterized by thinning of gastric mucosa in the absence of
Parietal and chief cells are decreased in number in the body (autoimmune
gastritis). Antrum shows loss of pyloric glands (type B gastritis).
[ 2 main causes of Atrophic gastritis -
i) Helicobacter pylori associated
multifocal atrophic gastritis involving corpus and antrum.
ii) Autoimmune gastritis restricted to the corpus ]
Following treatment of H. pylori infection the features of chronic
gastritis with lymphoid follicles may persist .
These features are gradually resolve after few years.
Following long term therapy with proton pump inhibitors there may be
pseudo hypertrophy of parietal cells. Tiny fundic glands cysts lined by
parietal and chief cells may be noted.
Histological responses to Helicobacter pylori
infection: gastritis, atrophy and preneoplasia.
Pyloric metaplasia: Replacement of fundic type glands by mucus
Intestinal metaplasia: Begins at the antral corpus junction then spreads
to the antrum and fundus.
(i) Small intestinal type (ii) Large intestinal type.
I - Complete : Mainly sialomucin or
II - Incomplete : Neutral mucin (IIA) or
1- Initially there is epithelial type change.
2- Followed by villiform architecture of the mucosa.
3- Enterocytes disappear and there is colonic metaplasia.
Colonic mucosa is more likely to be associated with dysplasia and
Pancreatic metaplasia: Associated with autoimmune gastritis.