Classification Des Gastrites

8/11/2019 Classification Des Gastrites

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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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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



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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



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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



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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



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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



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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



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Staging



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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



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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



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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

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Classification Des Gastrites