Classification of gastritis

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
Case distribution (%) by gastritis staging in 439 patients
*
*
*Prevalence of
neoplastic and
indefinite for
neoplasia cases
among the patients
clustered in stages III
and IV
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
-Crohn’s 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: Crohn’s
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%
• Crohn’s 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