chemical gastritis

Definition: Nonspecific reactive epithelial changes in response to variety of gastric mucosal irritants.

Synopsis

 Nonspecific reactive epithelial changes
 Etiology

• Reflux of alkaline duodenal contents
• Chronic usage of NSAIDs and corticosteroids
• Periphery of mucosal ulceration

 Microscopic Pathology

• Foveolar hyperplasia with mucin depletion and serrated gastric pits
• Mucosal edema with dilated capillaries and little inflammation

 Top Differential Diagnoses

• Low-grade dysplasia

Etiology

 Bile Reflux (bile reflux gastritis)
 Post partial gastrectomy
 Post-cholecystectomy
 Post ampullary sphincterotomy
 Drugs

• Corticosteroids
• Chronic use of NSAIDs (30-40% of chronic NSAID users present with mucosal changes)

 Toxic

• Chemoradiation therapy
• Alcohol (large consumption)

 Periphery of mucosal ulceration
 Underlying mass

Clinical synopsis

 May be asymptomatic
 Dyspepsia
 Nausea
 Bloating

Endoscopy - Macroscopy

 Erythema, edema, and friability

 Enlarged folds

 Stromal polyps

Treatment

 Withdrawal of causative factor(s), if possible

Prognosis

 Excellent if causative factors can be withdrawn

Endoscopic Appearance

 Mucosa can be normal

 If present, lesions are generally confined to antrum and include
Patchy erythema
Polypoid mucosal changes
Superficial erosions

 Bile can also be seen in cases of reflux

Microscopy

 Foveolar hyperplasia
 Serrated gastric pits
 Mucin depletion

• Cuboidal cells
• Hyperchromatic nuclei
• Subnuclear cytoplasmic vacuolization reported in operated stomach

 Mucosal edema with dilated capillaries and little inflammation
 Splaying of muscularis mucosa
 Eosinophilic infiltrate (mild)

Differential diagnosis

 Low-Grade Dysplasia

• Absence of atrophy and intestinal metaplasia
• Cuboidal epithelial cells with round nuclei (Dysplasia has tall columnar epithelium with penicillate hyperchromatic nuclei)
• Seamless transition with surrounding epithelium (Dysplasia has sharp transition)
• Mitoses limited to transition zone (Dysplasia has mitoses on surface)

 Helicobacter pylori Gastritis

• Foveolar hyperplasia can be seen in subset of patients
• H. pylori should have much more inflammation
  • Plasma cells in lamina propria
  • Foci of neutrophils in epithelium (neck region)

Diagnostic Checklist

 Cuboidal, mucin-poor, reactive foveolar cells with hyperchromasia should not be mistaken for low-grade dysplasia
 Neutrophilic infiltrate is not feature of diagnosis

 Mucosal atrophy and intestinal metaplasia are not features of chemical gastropathy

• However, can develop over time in
  • Operated stomachs with bile reflux
  • Elderly patients

References

 Genta RM: Differential diagnosis of reactive gastropathy. Semin Diagn Pathol. 22(4):273-83, 2005

 Haber MM et al: Gastric histologic findings in patients with nonsteroidal anti-inflammatory drug-associated gastric ulcer. Mod Pathol. 12(6):592-8, 1999

 Wolfe MM et al: Gastrointestinal toxicity of nonsteroidal antiinflammatory drugs. N Engl J Med. 340(24):1888-99, 1999

 Wallace JL: Nonsteroidal anti-inflammatory drugs and gastroenteropathy: the second hundred years. Gastroenterology. 112(3):1000-16, 1997

 El-Zimaity HM et al: Histological features do not define NSAID-induced gastritis. Hum Pathol. 27(12):1348-54, 1996

 Quinn CM et al: Gastritis in patients on non-steroidal anti-inflammatory drugs. Histopathology. 23(4):341-8, 1993

 Sobala GM et al: Reflux gastritis in the intact stomach. J Clin Pathol. 43(4):303-6, 1990

 Dixon MF et al: Reflux gastritis: distinct histopathological entity? J Clin Pathol. 39(5):524-30, 1986