Gastritis Classification and Causes

Acute Gastritis

NSAID related
Ethanol and smoking related
ICU – burns (curling ulcer) and trauma, such as head trauma and hypovolemic states    Toxins and elements  – alkali ingestion, chemotherapy and radiation treatments, hypothermia                                                                                                                                          Ischemia

Acute Gastritis Histology

NSAIDS usually  affect the antrum. Stress ulcers affect fundus and body.  Findings depend on the biopsy interval. Changes are limited to the mucosa. Superficial lamina propria hemorrhage, mucosal sloughing, PMN infiltration and mucosal necrosis. The healing phase is associated with regenerative epithelium  with dark enlarged nuclei and prominent nucleoli and syncitial glandular architecture, which can be mistaken for malignancy.

Chronic Gastritis

Autoimmune  Gastritis – ie. pernicious anemia -  predominant  in the fundus, normal antrum                                                                                                                                              – autoimmune gastritis patients are at an increased risk of carcinoids and adenocarcinomas

H Pylori

-antrum – increased acid production, increased risk of duodenal ulcers

-pangastritis – multifocal atrophic gastritis – decreased acid production, increased risk of adenocarcinoma and MALT lymphoma

Chemical gastritis, chemical gastropathy – post antrectomy or idiopathic, chronic aspirin or NSAID use

Granulomatous – uncommon – Crohn s disease -50%, isolated granulomatous gastritis  – 25%,   foreign body reaction (food, suture material, barium, mucin) -10%,  sarcoidosis 1%, vasculitis associated granulomata ( ie. Churg Strauss),  infections ( TB, schistosomiasis, histoplasmosis, Whipple’s disease, leprosy, syphilis, H pylori)

Lymphocytic (rare) – associated with celiac disease and H. Pylori gastritis

Other infections  – CMV, HSV, Syphillis, Whipple, TB, leprosy, candida, asperigillus, anisakiasis, strongyloides,

Eosinophilic ( rare) – association with allergy, asthma, eczema, drug hypersensitivity, peripheral blood eosinophilia and

Radiation

Graft versus Host Disease (GVHD)

Chronic Gastritis Histology

Autoimmune Gastritis appears as prominent lamina propria lymphocytic and plasma cell infiltration with loss of parietal and chief cells.

Metaplasias – pyloric, intestinal and pancreatic. Linear and nodular enterochromaffin cells (ECL) hyperplasia in the body mucosa.  The linear and nodular hyperplasia of ECL cells ( in the body) is shown by chromogranin. Gastrin stains shows the G cells ( which may be hypertrophied also) in the antrum.

Chemical gastritis and gastropathy – foveolar hyperplasia with corkscrewing of gastric pits, mucin depletion on the surface epithelium and paucity of inflammatory cells

H pylori  gastritis histology L

Lymphoplasmacytic inflammation (positive for neutrophils if acute on chronic – gastric pititis and crypt abscesses), helicobacter organisms in the mucosal blanket ( usually present if there is an acute component and absent if there is intestinal metaplasia or atrophy) , prominent lymphoid aggregates – do not mistake for MALT lymphoma. Intestinal metaplasia is uncommon in the antral H pylori gastritis ( H pylori gastritis is typically not associated with adenocarcinoma )

Lymphocytic  Gastritis – >1 lymphocyte  per 4-5 epithelial cells, when you count 100 epithelial cells. Differential diagnosis is a MALT lymphoma – distinguished easily by noticing that the intraepithelial lymphocytess are T cells.

Granulomatous Gastritis – granulomata involving any layer. Other findings

Infectious Gastritis – CMV, HSV, Syphillis, Whipple, TB, leprosy, histoplasma, candida, asperigillus, anisakiasis, strongyloides, schisto. – need to work these cases up through histology, stains, cultures, detection assays.

Eosinophilic Gastritis -intense eosinophilic infiltration with prominent lamina propria eosinophils, eosinophilic crypt abscesses and epithelial damage. Antral involvement.