Atrophic Atrophic gastritidesgastritides

Normal Normal stomachstomach

Body mucosa: Pit:gland 1:3-4Body mucosa: Pit:gland 1:3-4 Anral mucosa: pit:gland 1:1Anral mucosa: pit:gland 1:1

Every mucosa has Every mucosa has glands and pits. The glands and pits. The antral and body antral and body mucosae differ in the mucosae differ in the type of glands and the type of glands and the thickness of the glands thickness of the glands compared to the pitscompared to the pits

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

What is “atrophy” in the stomach?What is “atrophy” in the stomach?

Profound loss of glands in any location Profound loss of glands in any location

Atrophy

Atrophic GastritisAtrophic Gastritis

Common Histologic ComponentsCommon Histologic Components

• Loss of glands: the atrophyLoss of glands: the atrophy

• MetaplasiasMetaplasias

• Variable inflammationVariable inflammation

• +/- Pit expansion and distortion+/- Pit expansion and distortion

Atrophy of Atrophy of glands glands commonly is commonly is accompanied accompanied by by metaplasiasmetaplasias

Intestinal metaplasia Intestinal metaplasia (goblet cells (goblet cells ± ± Paneth cells)Paneth cells)

Mucus glandMucus gland(pseudopyloric(pseudopyloric) )

metaplasia metaplasia in the bodyin the body

Antral type glandsAntral type glandsNo goblet cells (no IM)No goblet cells (no IM)

AntralAntral biopsy biopsy

Not all atrophic gastritis has metaplasiasNot all atrophic gastritis has metaplasias

Profound glandular atrophyProfound glandular atrophy

2 Types of Atrophic Gastritis2 Types of Atrophic Gastritis Type AType A Type BType B(autoimmune)(autoimmune) ((multifocal)multifocal)

LocationLocation body mucosabody mucosa antral, any mucosaantral, any mucosa

How common?How common? uncommonuncommon worldwide worldwide

DistributionDistribution diffusediffuse focalfocal

UlcersUlcers nono maybemaybe

CauseCause ?autoimmunity?autoimmunity H pyloriH pylori

AntibodiesAntibodies intrinsic factorintrinsic factor nonenoneparietal cellparietal cell

Associated Associated perniciouspernicious nonenone diseasedisease anemia anemia

H pyloriH pylori gastritis often has gland atrophy gastritis often has gland atrophy

And intestinal metaplasiaAnd intestinal metaplasia

When these changes When these changes dominate, the result dominate, the result is is H pyloriH pylori induced induced multifocal atrophic multifocal atrophic gastritis (MAG)gastritis (MAG)

Active Hp gastritisActive Hp gastritisAtrophic gastritis with Atrophic gastritis with atrophy and IMatrophy and IM

Autoimmune atrophic gastritis Autoimmune atrophic gastritis (AAG)(AAG) affects oxyntic mucosa affects oxyntic mucosa

AAG probably beginsAAG probably begins with lymphocytic attack with lymphocytic attack on the glands (bottom heavy inflammation)on the glands (bottom heavy inflammation)

Which destroys all oxyntic glandsWhich destroys all oxyntic glands

Metaplastic mucus glands developMetaplastic mucus glands develop

Add intestinal metaplasiaAdd intestinal metaplasia

Autoimmune atrophic Autoimmune atrophic gastritis or simply gastritis or simply autoimmune gastritis, autoimmune gastritis, has some interesting has some interesting additional featuresadditional features

Endocrine cell Endocrine cell (ECL-cell) (ECL-cell) hyperplasiahyperplasia

chromograninchromogranin

ECL cell hyperplasia ECL cell hyperplasia is a response is a response to to hypergastrinemiahypergastrinemia which patients which patients with AAG invariably havewith AAG invariably haveHypergastrinemiaHypergastrinemia is due to the is due to the destruction of the acid producing destruction of the acid producing parietal cellsparietal cellsThis raises the pH in the antrum This raises the pH in the antrum which prevents decreased gastrin which prevents decreased gastrin production by the antral G cells.production by the antral G cells.

Autoimmune gastritisAutoimmune gastritist t NormalNormal

Linear hyperplasia of the enterochromaffin-like (ECL) cells forming Linear hyperplasia of the enterochromaffin-like (ECL) cells forming an extra layer of cells around the glands at the base of the mucosaan extra layer of cells around the glands at the base of the mucosa

Chromogranin stain : linear hyperplasiaChromogranin stain : linear hyperplasia

Hyperplasia of the enterochromaffin-like (ECL) cells Hyperplasia of the enterochromaffin-like (ECL) cells forming nodules at the base of the mucosaforming nodules at the base of the mucosa

Chromogranin: nodular hyperplasiChromogranin: nodular hyperplasiaa

Endocrine cell hyperplasiaEndocrine cell hyperplasiain autoimmune gastritisin autoimmune gastritis

Composed of Composed of ECLECL ( (EEnteronteroCChromaffin-hromaffin-LLike) cellsike) cells

Patterns: Patterns: simple,simple, linearlinear and and nodularnodular

Indicates Indicates hypergastrinemiahypergastrinemia

Only occurs with diffuse body glandular atrophy Only occurs with diffuse body glandular atrophy autoimmune: actually a diagnostic featureautoimmune: actually a diagnostic featurePrecursor of one type of carcinoidPrecursor of one type of carcinoid tumor tumor

What changes in a What changes in a biopsy should lead biopsy should lead you to suspect you to suspect autoimmune gastritis?autoimmune gastritis?

Basal inflammationBasal inflammation

Total or near total oxyntic glandular atrophyTotal or near total oxyntic glandular atrophy

At least mucus gland metaplasia At least mucus gland metaplasia and possibly intestinal metaplasiaand possibly intestinal metaplasia

Endocrine cell hyperplasia, seen as Endocrine cell hyperplasia, seen as nodules or as an extra layer of cells nodules or as an extra layer of cells around the base of the glands, may around the base of the glands, may

be the most important clue.be the most important clue.

If there are doubts that there is ECL cell If there are doubts that there is ECL cell hyperplasia, then use a chromogranin stain hyperplasia, then use a chromogranin stain to bring out the ECL cellsto bring out the ECL cells

Since this biopsy only has Since this biopsy only has mucus glands which is mucus glands which is characteristic of antral mucosa, characteristic of antral mucosa, we have to determine whether we have to determine whether this is antral mucosa or body this is antral mucosa or body mucosa with metaplastic mucus mucosa with metaplastic mucus glands and no body glands. glands and no body glands. There are 2 ways of proving thisThere are 2 ways of proving this..

First, if we know that First, if we know that the biopsy came from the biopsy came from the body, then this is the body, then this is autoimmune gastritisautoimmune gastritis

Second, if we don’t know the site of Second, if we don’t know the site of the biopsy, we can determine if this the biopsy, we can determine if this is antral mucosa by using a gastrin is antral mucosa by using a gastrin stain. stain. Gastrin producing cells (G cells) Gastrin producing cells (G cells) only occur in antral mucosa. only occur in antral mucosa. If the gastrin stain is negative, then If the gastrin stain is negative, then that is great evidence that the biopsy that is great evidence that the biopsy did not come from antral mucosa did not come from antral mucosa but from body mucosa.but from body mucosa.

G cells G cells indicating indicating this biopsy is this biopsy is antrumantrum

The piece with The piece with uniform glands uniform glands and no and no inflammationinflammation