Classification of gastritis

Pieter Demetter
Department of Pathology
Erasme University Hospital, Brussels
The broad spectrum of gastritis
General agreement on morphological aspects
Great variety of names resulting in confusion
Many controversies caused by semantics
Walery Jaworski
Robin Warren and Barry Marshall
Helicobacter pylori
Major cause of nonautoimmune
chronic gastritis
discovery has led to recognition of
other forms of gastritis (lymphocytic,
reflux)
Original Sydney System (1990)
Endoscopic and histological divisions
Histological arm: combining topographical,
morphological and etiological information
to generate reproducible and clinically
useful diagnoses
Misiewicz JJ, J Gastroenterol Hepatol 1991
Price AB, J Gastroenterol Hepatol 1991
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 Pathol 1996
Dixon MF, Am J Surg Pathol 1996
What do we need for correct gastritis evaluation?
Two antral biopsies (highest number of H. pylori
organisms)
Two corpus biopsies (particularly valuable for
finding H. pylori after treatment)
One biopsie from the incisura angularis (maximal
degrees of atrophy and intestinal metaplasia)
Haematoxylin-eosin
Special stain for H. pylori (modified Giemsa,
Whartin-Starry, Genta)
Genta RM, Gastrointest Endosc 1994
Sugimura T, Mol Carcinog 1994
Biopsies needed for correct gastritis evaluation
Helicobacter pylori
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 Pathol 1996
Mononuclear cells (chronic inflammation)
Normal: maximum of 5 lymphocytes, plasma cells and
macrophages per high-power (x40 objective) field
Plasma cells especially important indicator of chronic
inflammatory response
Intra-epithelial lymphocytes: maximum 5 per 100 epithelial
cells is normal
Mononuclear cells slowly disappear after H. pylori
eradication
Grade away from lymphoid follicles
Witteman EM, J Clin Pathol 1995
Dixon MF, Am J Surg Pathol 1996
Polymorphonuclear neutrophil activity
Linked to tissue damage (reactive oxygen
species, proteases)
Almost universal phenomenon in H. pylori
gastritis
Disappears within days of cure of infection
Davies GR, Scand J Gastroenterol 1994
Dixon MF, Am J Surg Pathol 1996
Neutrophils in a post-treatment biopsy:
search carefully for H. pylori!
HP
Atrophy
Defined as loss of appropriate glands
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 Gastroenterol 2000
Rugge M, Aliment Pharmacol Ther 2002
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 Pathol 1996
This is atrophy
but this also, since there is metaplasia!
Development of intestinal metaplasia
Correa P, Cancer Res 1988
Recommendations
The presence or absence of H. pylori,
chronic inflammation, polymorphonuclear
neutrophil activity, atrophy and intestinal
metaplasia should be recorded in all cases
of gastritis
When present, each of these variables can
be graded as mild, moderate or severe
Dixon MF, Am J Surg Pathol 1996
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 granulocytic
inflammation in both antral and oxyntic
biopsy samples
Staging: extent of atrophy with or without
intestinal metaplasia
Rugge M, Hum Pathol 2005
Grading
Rugge M, Hum Pathol 2005
Staging
Rugge M, Hum Pathol 2005
*Prevalence of
neoplastic and
indefinite for
neoplasia cases
among the patients
clustered in stages III
and IV
*
*
Case distribution (%) by gastritis staging in 439 patients
Rugge M, Gut 2007
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
CMV
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 gastropathies
Srivastava A, Histopathology 2007
Acute gastritis
Caustic: mainly antral
Ulcero-haemorrhagic:
mainly corpus/fundus
Oedema,
haemorrhage,
erosions, typically
little inflammatory
cells
Poley JW, Gastrointest Endosc 2004
Srivastava A, Histopathology 2007
Reactive gastropathy
Foveolar hyperplasia
Oedema
Smooth muscle
hyperplasia
Normal numbers or only
minor increase in chronic
inflammatory cells
No neutrophils, unless
there is erosion
Appelman HD, Hum Pathol 1994
Carpenter HA, Gastroenterology 1995
Iatrogenic gastritis: iron-pill gastritis
Mucosal erosion
Regenerative epithelial
changes
Golden-brown
pigments
Abraham SC, Am J Surg Pathol 1999
Srivastava A, Histopathology 2007
Autoimmune gastritis
Classic autoimmune gastritis:
hypochlorhydria or
achlorhydria resulting from
parietal cell destruction
secondary to circulating
antibodies directed against
H+/K+ ATPase
Intrinsic factor autoantibodies
(60%)
Intense mononuclear infiltrate
in fundus and corpus, deeply
centred
Antrum: no significant
inflammation (G cell
hyperplasia)
Atrophy with metaplastic
changes
Torbenson M, Mod Pathol 2002
Srivastava A, Histopathology 2007
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 of
uncertain aetiology
Shapiro JL, Am J Surg Pathol 1996
Srivastava A, Histopathology 2007
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 of
chronic active gastritis
> women
Haot J, Gut 1988
Wu TT, Am J Surg Pathol 1999
Lymphocytic gastritis: aetiologies
Coeliac sprue: 38%
H. pylori: 20%
Crohns disease, HIV
infection, lymphoma
20%: no aetiology or
associated disease
CD3
Wolber R, Gastroenterology 1990
Wu TT, Am J Surg Pathol 1999
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 Pathol 2001
Srivastava A, Histopathology 2007
Eosinophilic gastritis
Eosinophilic infiltrate
involving the gastric wall
or the gastric epithelium
Allergic or idiopathic
Most often in the setting of
an eosinophilic
gastroenteritis
Food or drug allergies,
connective tissue diseases,
parasitic infections
Johnstone JM, Histopathology 1978
Rothenberg ME, J Allergy Clin Immunol 2004
Diagnosis of non-Helicobacter pylori gastritis:
schematic approach
Srivastava A, Histopathology 2007