Gastritis

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Gastritis refers to an inflammatory process that affects the stomach.

Gastritis
Diagnosis in short

LM acute: PMNs in the lamina propria or intraepithelial; (usual) chronic: cluster of plasma cells (mild), several clusters (moderate), +/-mucosal erosions (severe); lymphocytic: intraepithelial lymphocytes
Subtypes acute gastritis, chronic gastritis, focal acute gastritis (pill gastritis), lymphocytic gastritis
LM DDx Helicobacter gastritis, collagenous gastritis, Crohn's disease, intestinal metaplasia of the stomach, gastric columnar dysplasia, gastric carcinoma
Stains Diff-Quik -ve, cresyl violet -ve
IHC Helicobacter -ve
Site stomach

Associated Dx intestinal metaplasia of the stomach - esp. in chronic gastritis
Prevalence very common
Blood work H. pylori -ve or previously +ve
Endoscopy erythema
Prognosis good
Other neg. Helicobacter breath test
Clin. DDx reactive gastropathy

There are several types of gastritis:

This article deals with acute gastritis and chronic gastritis without an apparent histologic cause.

General

  • Very common.
  • A specific cause is uncommonly identified histologically.

Etiology

Gastritis causes:[1]

Endoscopic appearance

  • Erythematous.

Microscopic

  • Inflammatory cells - see below.

Acute gastritis

  • AKA active gastritis.

Features:

  • Neutrophils - especially when intraepithelial.
Focal active gastritis

DDx:

  1. Drugs,[2] esp. NSAIDs.
  2. Infectious.
  3. Inflammatory bowel disease.

Chronic gastritis

Features:

  • Plasma cells (in lamina propria).
    • Various criteria:
      1. Two plasma cells kissing, i.e. two plasma cells touching/overlapping.
      2. Three is a crowd, i.e. three plasma cells in close proximity.

Note:

Lymphocytic gastritis
General

The DDx is limited:

  1. Helicobacter gastritis.
  2. Celiac disease.
  3. NSAIDs.[citation needed]
  4. Idiopathic.
  5. HIV/AIDS.
Microscopic

Features:[4]

  • 25 lymphocytes / 100 epithelial cells.

Sydney criteria for gastritis

A bunch of pathologists in Sydney came-up with criteria... and these were revised in Houston.[5]

Classification

Updated Sydney classification:[5]

Feature Non-atrophic Helicobacter Atrophic Helicobacter Autoimmune
Inflammation pattern antral or diffuse antrum & corpus, mild inflammation corpus only
Atrophy & metaplasia nil atrophy present, metaplasia at incisura corpus only

Notes:

  • Corpus = gastric body.
  • Incisura = angular incisure, incisura angularis (Latin) - notched transition point on lesser curvature of the stomach between pylorus and body.[6]
Severity

The Sydney group suggests grading severity with the following language:[5]

  • Mild.
  • Moderate.
  • Marked.

These terms are applied to the parameters described in a biopsy. The Sydney criteria lists H. pylori, neutrophils, mononuclear cells, antrum (atrophy), corpus (atrophy) and intestinal metaplasia. The paper that discusses this also give a visual analogue scale.

Parameters & Severity (adapted from Dixon et al.[5]):

Feature Mild Moderate Marked
H. pylori few touching many touching piles
Neutrophils few bunches crowded
Mononuclear cells not touching kissing partying

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Minimal chronic inactive

STOMACH, BIOPSY: 
- BODY AND ANTRAL-TYPE GASTRIC MUCOSA WITH MINIMAL CHRONIC INACTIVE INFLAMMATION. 
- NEGATIVE FOR HELICOBACTOR-LIKE ORGANISMS. 
- NEGATIVE FOR INTESTINAL METAPLASIA. 
- NEGATIVE FOR DYSPLASIA AND NEGATIVE FOR MALIGNANCY.

Mild chronic inactive

STOMACH, BIOPSY: 
- BODY AND ANTRAL-TYPE GASTRIC MUCOSA WITH MILD CHRONIC INACTIVE INFLAMMATION. 
- NEGATIVE FOR HELICOBACTOR-LIKE ORGANISMS. 
- NEGATIVE FOR INTESTINAL METAPLASIA. 
- NEGATIVE FOR DYSPLASIA AND NEGATIVE FOR MALIGNANCY.

Moderate chronic active

STOMACH, BIOPSY: 
- BODY AND ANTRAL-TYPE GASTRIC MUCOSA WITH MODERATE CHRONIC ACTIVE INFLAMMATION. 
- NEGATIVE FOR HELICOBACTOR-LIKE ORGANISMS. 
- NEGATIVE FOR INTESTINAL METAPLASIA. 
- NEGATIVE FOR DYSPLASIA AND NEGATIVE FOR MALIGNANCY.

Micro - inactive

The sections show gastric body type mucosa with small clusters of plasma cells. There are no intraepithelial neutrophils. Goblet cells are not identified. The epithelium matures normally to the surface. No Helicobacter organisms are seen.

See also

References

  1. Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 812-3. ISBN 0-7216-0187-1.
  2. Parfitt, JR.; Driman, DK. (Apr 2007). "Pathological effects of drugs on the gastrointestinal tract: a review.". Hum Pathol 38 (4): 527-36. doi:10.1016/j.humpath.2007.01.014. PMID 17367604.
  3. Voutilainen, M.; Färkkilä, M.; Mecklin, JP.; Juhola, M.; Sipponen, P. (Nov 1999). "Chronic inflammation at the gastroesophageal junction (carditis) appears to be a specific finding related to Helicobacter pylori infection and gastroesophageal reflux disease. The Central Finland Endoscopy Study Group.". Am J Gastroenterol 94 (11): 3175-80. doi:10.1111/j.1572-0241.1999.01513.x. PMID 10566710.
  4. El-Zimaity. 18 October 2010.
  5. 5.0 5.1 5.2 5.3 Dixon MF, Genta RM, Yardley JH, Correa P (October 1996). "Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994". Am. J. Surg. Pathol. 20 (10): 1161-81. PMID 8827022. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0147-5185&volume=20&issue=10&spage=1161.
  6. http://en.wikipedia.org/wiki/Angular_incisure