Atrophic
gastritides
Normal
stomach
Body mucosa: Pit:gland 1:3-4
Every mucosa has
glands and pits. The
antral and body
mucosae differ in the
type of glands and the
thickness of the glands
compared to the pits
Anral mucosa: pit:gland 1:1
What is “atrophy” in the stomach?
In 2008 an international group mainly of
pathologists defined atrophy in the stomach as
the “loss of appropriate glands”
This means, oxyntic glands in the body
mucosa and mucus glands in the antral
mucosa. Metaplasias may replace glands,
but the appropriate glands are lost.
Rugge, et al. Digestive and Liver Disease, 40:650-658, 2008
Atrophy
Profound loss of glands in any location
Atrophic Gastritis
Common Histologic Components
• Loss of glands: the atrophy
• Metaplasias
• Variable inflammation
• +/- Pit expansion and distortion
Intestinal metaplasia
(goblet cells ± Paneth cells)
Atrophy of
glands
commonly is
accompanied
by metaplasias
Mucus gland
(pseudopyloric)
metaplasia
in the body
Not all atrophic gastritis has metaplasias
Profound glandular atrophy
Antral biopsy
Antral type glands
No goblet cells (no IM)
2 Types of Atrophic Gastritis
Location
Type A
(autoimmune)
Type B
(multifocal)
body mucosa
antral, any mucosa
How common? uncommon
worldwide
Distribution
diffuse
focal
Ulcers
no
maybe
Cause
?autoimmunity H pylori
Antibodies
intrinsic factor none
parietal cell
Associated
disease
pernicious
anemia
none
H pylori gastritis often has gland atrophy
And intestinal metaplasia
Atrophic gastritis with
atrophy and IM
Active Hp gastritis
When these changes
dominate, the result
is H pylori induced
multifocal atrophic
gastritis (MAG)
Autoimmune atrophic gastritis
(AAG) affects oxyntic mucosa
AAG probably begins with lymphocytic attack
on the glands (bottom heavy inflammation)
Which destroys all oxyntic glands
Metaplastic mucus glands develop
Add intestinal metaplasia
Autoimmune atrophic
gastritis or simply
autoimmune gastritis,
has some interesting
additional features
chromogranin
Endocrine
cell (ECL-cell)
hyperplasia
ECL cell hyperplasia is a response
to hypergastrinemia which patients
with AAG invariably have
Hypergastrinemia is due to the
destruction of the acid producing
parietal cells
This raises the pH in the antrum
which prevents decreased gastrin
production by the antral G cells.
Normal
Autoimmune gastritist
Linear hyperplasia of the enterochromaffin-like (ECL) cells forming
an extra layer of cells around the glands at the base of the mucosa
Chromogranin stain : linear hyperplasia
Hyperplasia of the enterochromaffin-like (ECL) cells
forming nodules at the base of the mucosa
Chromogranin: nodular hyperplasia
Endocrine cell hyperplasia
in autoimmune gastritis
Composed of ECL (EnteroChromaffin-Like) cells
Patterns: simple, linear and nodular
Indicates hypergastrinemia
Only occurs with diffuse body glandular atrophy
autoimmune: actually a diagnostic feature
Precursor of one type of carcinoid tumor
What changes in a
biopsy should lead
you to suspect
autoimmune gastritis?
Basal inflammation
Total or near total oxyntic glandular atrophy
At least mucus gland metaplasia
and possibly intestinal metaplasia
Endocrine cell hyperplasia, seen as
nodules or as an extra layer of cells
around the base of the glands, may
be the most important clue.
If there are doubts that there is ECL cell
hyperplasia, then use a chromogranin stain
to bring out the ECL cells
Since this biopsy only has
mucus glands which is
characteristic of antral mucosa,
we have to determine whether
this is antral mucosa or body
mucosa with metaplastic mucus
glands and no body glands.
There are 2 ways of proving this.
First, if we know that
the biopsy came from
the body, then this is
autoimmune gastritis
Second, if we don’t know the site of
the biopsy, we can determine if this
is antral mucosa by using a gastrin
stain.
Gastrin producing cells (G cells)
only occur in antral mucosa.
If the gastrin stain is negative, then
that is great evidence that the biopsy
did not come from antral mucosa
but from body mucosa.
The piece with
uniform glands
and no
inflammation
G cells
indicating
this biopsy is
antrum