Classification and Clinical Implications of Atrophic Gastritis

Distribution Patterns and Classification Systems

• The American Gastroenterological Association recommends classifying atrophic gastritis into two main distribution patterns: H. pylori-associated atrophic gastritis (HpAG) and autoimmune gastritis (AIG), with HpAG beginning in the antrum and progressing proximally, and AIG being corpus-predominant with antral sparing 1, 2
• The European Society of Gastrointestinal Endoscopy suggests that HpAG is characterized by antrum-predominant pattern with atrophic changes arising initially in the incisura and the antrocorporal transitional mucosa, and progressive proximal spread over time 1
• The American College of Gastroenterology states that AIG is characterized by corpus-predominant pattern with destruction of individual oxyntic glands by lymphocytes, and antral sparing 2

Risk Stratification and Clinical Implications

• The International Agency for Research on Cancer recommends using the OLGA (Operative Link for Gastritis Assessment) system, which incorporates severity and topographic distribution of atrophic lesions as determinants of gastric cancer risk 1
• The American Gastroenterological Association advises that extensive atrophy and metaplasia are associated with increased cancer risk regardless of distribution pattern, and proper biopsy technique is essential to accurately determine distribution 1, 2
• The European Society of Gastrointestinal Endoscopy suggests that corpus-predominant atrophy leads to loss of gastric acidity and hypergastrinemia, with risk of type 1 gastric neuroendocrine tumors 2

Diagnostic Considerations

• The American College of Gastroenterology recommends obtaining separate antral and corpus biopsies to accurately classify distribution pattern, and using special stains to discriminate between pseudopyloric metaplasia and antral mucosa when anatomic location is uncertain 1
• The American Gastroenterological Association states that intestinal metaplasia presence almost invariably implies underlying atrophic gastritis, even when not explicitly noted on pathology reports 3, 4