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Classification of gastritis
Pieter Demetter
Department of Pathology
Erasme University Hospital, Brussels
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The broad spectrum of gastritis
General agreement on morphological aspects
Great variety of names resulting in confusion
Many controversies caused by semantics
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Walery Jaworski
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Robin Warren and Barry Marshall
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Helicobacter pylori
Major cause of nonautoimmune
chronic gastritis
discovery has led to recognition of
other forms of gastritis (lymphocytic,
reflux)
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Original Sydney System (1990)
Endoscopic and histological divisions
Histological arm: combining topographical,
morphological and etiological informationto generate reproducible and clinically
useful diagnoses
Misiewicz JJ,J Gastroenterol Hepatol1991
Price AB,J Gastroenterol Hepatol1991
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Updated Sydney System (1994)
General principles and grading retained
Terminology improved to emphasize the
distinction between atrophic and
nonatrophic stomach
Provision of a visual analogue scale
Dixon MF,Am J Surg Pathol1996
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Dixon MF,Am J Surg Pathol1996
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What do we need for correct gastritis evaluation?
Two antral biopsies (highest number of H. pyloriorganisms)
Two corpus biopsies (particularly valuable for
finding H. pylori after treatment)
One biopsie from the incisura angularis (maximaldegrees of atrophy and intestinal metaplasia)
Haematoxylin-eosin
Special stain for H. pylori (modified Giemsa,Whartin-Starry, Genta)
Genta RM, Gastrointest Endosc1994
Sugimura T,Mol Carcinog1994
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Biopsies needed for correct gastritis evaluation
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Helicobacter pylori
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H. pylori density
Presence/absence of H. pylori is most
important information for clinical
management Intestinal metaplasia usually not colonized
Grade the bacterial density on the gastric
epithelium alone
Dixon MF,Am J Surg Pathol1996
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Mononuclear cells (chronic inflammation)
Normal: maximum of 5 lymphocytes, plasma cells andmacrophages per high-power (x40 objective) field
Plasma cells especially important indicator of chronic
inflammatory response
Intra-epithelial lymphocytes: maximum 5 per 100 epithelialcells is normal
Mononuclear cells slowly disappear after H. pylori
eradication
Grade away from lymphoid follicles
Witteman EM,J Clin Pathol1995
Dixon MF,Am J Surg Pathol1996
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Polymorphonuclear neutrophil activity
Linked to tissue damage (reactive oxygen
species, proteases)
Almost universal phenomenon in H. pylorigastritis
Disappears within days of cure of infection
Davies GR, Scand J Gastroenterol1994
Dixon MF,Am J Surg Pathol1996
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Neutrophils in a post-treatment biopsy:
search carefully for H. pylori!
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HP
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Atrophy
Defined as loss of appropriateglands
Common denominator in all processes causing
severe mucosal damage
Relationship between atrophic gastritis and gastric
cancer
Recognition of minor degree of antral atrophy is
difficult because of the greater amount of
connective tissue compared to fundus/corpus
Cassaro M,Am J Gastroenterol2000
Rugge M,Aliment Pharmacol Ther2002
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Intestinal metaplasia
Common in chronic gastritis of all causes
Increases in prevalence with disease
duration
Presence of goblet cells, absorptive cells
and cells resembling colonocytes
Generally regarded as condition
predisposing to malignancy
Dixon MF,Am J Surg Pathol1996
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This is atrophy
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but this also, since there is metaplasia!
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Development of intestinal metaplasia
Correa P, Cancer Res1988
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Recommendations
The presence or absence of H. pylori,
chronic inflammation, polymorphonuclear
neutrophil activity, atrophy and intestinal
metaplasia should be recorded in all casesof gastritis
When present, each of these variables can
be graded as mild, moderate or severe
Dixon MF,Am J Surg Pathol1996
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Generating a clinically helpful
histology report
Grading:measure of the severity of the
inflammatory lesions; should represent the
semiquantitative assessment of combined
severity of mononuclear and granulocyticinflammation in both antral and oxyntic
biopsy samples
Staging:extent of atrophy with or without
intestinal metaplasia
Rugge M,Hum Pathol2005
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Grading
Rugge M,Hum Pathol2005
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Staging
Rugge M,Hum Pathol2005
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Non-Helicobacter infectious gastritis
Bacterial: Mycobacterium tuberculosis,
Mycobacterium avium-intracellulare,
Treponema pallidum
Viral: cytomegalovirus
Fungal: Candida, Histoplasma capsulatum,
Mucormycosis
Parasitic: Cryptosporidium, giardiasis,Strongyloides stercoralis, Anisakis
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CMV
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Non-infectious gastritis Acute gastritis
-caustic gastritis
-ulcero-haemorrhagic gastritis
Reactive gastropathy Iatrogenic gastritis
-drug related gastritis (iron, mucosal calcinosis, colchicine, )
-radiation gastritis
Autoimmune and other immunologically mediated gastritides
-type A autoimmune gastritis
-graft-versus-host disease-other forms of autoimmune and immunogical gastritis
Gastric manifestations of inflammatory bowel disease
-Crohns disease
-focally enhancing gastritis
Miscellaneous forms of gastritis with a distinctive histology
-granulomatous gastritis
-lymphocytic gastritis
-collagenous gastritis
-eosinophilic gastritis
Vascular gastropathiesSrivastava A,Histopathology2007
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Acute gastritis
Caustic: mainly antral
Ulcero-haemorrhagic:
mainly corpus/fundus
Oedema,haemorrhage,
erosions, typically
little inflammatory
cells
Poley JW, Gastrointest Endosc2004
Srivastava A,Histopathology2007
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Reactive gastropathy
Foveolar hyperplasia
Oedema
Smooth muscle
hyperplasia Normal numbers or only
minor increase in chronic
inflammatory cells
No neutrophils, unlessthere is erosionAppelman HD,Hum Pathol1994
Carpenter HA, Gastroenterology1995
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Autoimmune gastritis
Classic autoimmune gastritis:hypochlorhydria orachlorhydria resulting fromparietal cell destructionsecondary to circulatingantibodies directed againstH+/K+ ATPase
Intrinsic factor autoantibodies(60%)
Intense mononuclear infiltratein fundus and corpus, deeplycentred
Antrum: no significant
inflammation (G cellhyperplasia)
Atrophy with metaplasticchanges
Torbenson M,Mod Pathol2002
Srivastava A,Histopathology2007
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Granulomatous gastritis
Commonest cause: Crohns
disease (50%)
Sarcoidosis: 10%
H. pylori ???
Bacterial, fungal, parasitic
infections
Foreign body granulomas
If no obvious etiology (25%):
granulomatous gastritis ofuncertain aetiology
Shapiro JL,Am J SurgPathol 1996
Srivastava A,Histopathology2007
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Lymphocytic gastritis
Increased number of
intraepithelial T
lymphocytes along the
surface epithelium (> 25
IEL/100 epithelial cells)
and in gastric pits Lymphoplasmocytic
infiltrate in the lamina
propria
1.7 4.5% of cases ofchronic active gastritis
> women
Haot J, Gut1988
Wu TT,Am J Surg Pathol1999
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Lymphocytic gastritis: aetiologies
Coeliac sprue: 38%
H. pylori: 20%
Crohns disease, HIVinfection, lymphoma
20%: no aetiology or
associated diseaseCD3
Wolber R, Gastroenterology1990
Wu TT,Am J Surg Pathol1999
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Collagenous gastritis
Chronic superficial gastritis
(lymphoplasmacytic cells,
eosinophils, neutrophils)
Subepithelial deposition of
collagen bands
Intestinal metaplasia almost
never present
Adult women: association
with coeliac disease and
collagenous colitis Children: usually restricted to
stomach Winslow JL,Am J Clin Pathol2001Srivastava A,Histopathology2007
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Eosinophilic gastritis
Eosinophilic infiltrateinvolving the gastric wallor the gastric epithelium
Allergic or idiopathic
Most often in the setting ofan eosinophilicgastroenteritis
Food or drug allergies,
connective tissue diseases,parasitic infections
Johnstone JM,Histopathology1978
Rothenberg ME,J Allergy Clin Immunol2004
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Diagnosis of non- elicobacter pylorigastritis:schematic approach
Srivastava A, Histopathology2007