Atrophic Gastritis

 

 

  1. Environmental Metaplastic Atrophic Gastritis (EMAG)
  2. Autoimmune Metaplastic Atrophic Gastritis (AMAG)

 

                                              Environmental Metaplastic Atrophic Gastritis (EMAG)

  • – It involves
  •               • Gastric antrum + Corpus with
  •               • Atrophy + Intestinal metaplasia
  • – Also called multifocal atrophic gastritis
  • Biopsy: 5 biopsy from antrum, incisura and body
  • – Corpus involvement may be associated with pseudopyloric metaplasia in which the mucosa resembles antral mucosa but stains pepsinogenI, a proenzyme expressed in the corpus mucosa
  • Endoscopic findings:
  • – Pale mucosa
  • – Shiny surface
  • – Prominent submucosal vessels
  • – Auto-fluorescence endoscopy is more sensitive and specific
  • Pathogenesis:
  • – Hp infection plays the most important role
  • – Genetic factor, diet also important
  • – Intestinal metaplasia is a risk factor for intestinal type gastric cancer
  • – During chronic inflammation of the stomach, the rate of cell loss may exceed the ability of the stomach to replace lost cell by stem cell

             

 

                                  Autoimmune Metaplastic Atrophic Gastritis (AMAG)

 

  • – Also called diffuse corporal atrophic gastritis
  • – An autoimmune destruction of glands in corpus of the stomach
  • – Antrum is spared
  • – So, gastrin production is increased
  • – Achlorhydria/hypochlorhydria
  • – Low PGI/PGII
  • – Circulating antibody to parietal cell/intrinsic factor
  • – These antibodies can cross placenta and can cause factor B12 deficiency
  • – Incomplete metaplasia (TypeIII) may occur in AMAG and is a risk factor for gastric carcinoma
  • – Early in the course, the atrophy is focal, rarely diffuse
  • – Enterochromafin-like cells hyperplasia occur due to hypergastrinemia that ultimately causes carcinoid syndrome
  • – Many patients with AMAG have antibody to Hp and Hp may play a role in the early pathogenesis of AMAG

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