Classification of gastritis. Pieter Demetter Department of Pathology Erasme University Hospital, Brussels

Transcription

1 Classification of gastritis Pieter Demetter Department of Pathology Erasme University Hospital, Brussels

2 The broad spectrum of gastritis General agreement on morphological aspects Great variety of names resulting in confusion Many controversies caused by semantics

3 Walery Jaworski

4 Robin Warren and Barry Marshall

5 Helicobacter pylori Major cause of nonautoimmune chronic gastritis discovery has led to recognition of other forms of gastritis (lymphocytic, reflux )

6 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

7 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

8 Dixon MF, Am J Surg Pathol 1996

9 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

10 Biopsies needed for correct gastritis evaluation

11 Helicobacter pylori

12 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

13 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

14 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

15 Neutrophils in a post-treatment biopsy: search carefully for H. pylori!

16 HP

17 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

18 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

19 This is atrophy

20 but this also, since there is metaplasia!

21 Development of intestinal metaplasia Correa P, Cancer Res 1988

22 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

23 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

24 Grading Rugge M, Hum Pathol 2005

25 Staging Rugge M, Hum Pathol 2005

26 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

27 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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29 CMV

30 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

31 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

32 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

33 Iatrogenic gastritis: iron-pill gastritis Mucosal erosion Regenerative epithelial changes Golden-brown pigments Abraham SC, Am J Surg Pathol 1999 Srivastava A, Histopathology 2007

34 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

35 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

36 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 % of cases of chronic active gastritis > women Haot J, Gut 1988 Wu TT, Am J Surg Pathol 1999

37 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

38 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

39 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

40 Diagnosis of non-helicobacter pylori gastritis: schematic approach Srivastava A, Histopathology 2007