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Atrophic gastritides

Atrophic gastritides. Normal stomach. Body mucosa: Pit:gland 1:3-4. Anral mucosa: pit:gland 1:1. Every mucosa has glands and pits. The antral and body mucosae differ in the type of glands and the thickness of the glands compared to the pits. What is “atrophy” in the stomach?.

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Atrophic gastritides

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  1. Atrophic gastritides

  2. Normal stomach Body mucosa: Pit:gland 1:3-4 Anral mucosa: pit:gland 1:1 Every mucosa has glands and pits. The antral and body mucosae differ in the type of glands and the thickness of the glands compared to the pits

  3. What is “atrophy” in the stomach? In 2008 an international group mainly of pathologists defined atrophy in the stomach as the “loss of appropriate glands” This means, oxyntic glands in the body mucosa and mucus glands in the antral mucosa. Metaplasias may replace glands, but the appropriate glands are lost. Rugge, et al. Digestive and Liver Disease, 40:650-658, 2008

  4. Atrophy Profound loss of glands in any location

  5. Atrophic Gastritis Common Histologic Components • Loss of glands: the atrophy • Metaplasias • Variable inflammation • +/- Pit expansion and distortion

  6. Intestinal metaplasia (goblet cells ± Paneth cells) Atrophy of glands commonly is accompanied by metaplasias Mucus gland (pseudopyloric) metaplasia in the body

  7. Not all atrophic gastritis has metaplasias Profound glandular atrophy Antral type glands No goblet cells (no IM) Antral biopsy

  8. 2 Types of Atrophic Gastritis Type AType B (autoimmune) (multifocal) Locationbody mucosa antral, any mucosa How common? uncommon worldwide Distribution diffuse focal Ulcers no maybe Cause ?autoimmunity H pylori Antibodies intrinsic factor none parietal cell Associated pernicious none disease anemia

  9. H pylori gastritis often has gland atrophy

  10. And intestinal metaplasia

  11. Atrophic gastritis with atrophy and IM Active Hp gastritis When these changes dominate, the result is H pylori induced multifocal atrophic gastritis (MAG)

  12. Autoimmune atrophic gastritis (AAG)affects oxyntic mucosa

  13. AAG probably beginswith lymphocytic attack on the glands (bottom heavy inflammation)

  14. Which destroys all oxyntic glands

  15. Metaplasticmucus glands develop

  16. Add intestinal metaplasia

  17. Autoimmune atrophic gastritis or simply autoimmune gastritis, has some interesting additional features

  18. chromogranin Endocrine cell (ECL-cell) hyperplasia

  19. ECL cell hyperplasia is a response to hypergastrinemia which patients with AAG invariably have Hypergastrinemia is due to the destruction of the acid producing parietal cells This raises the pH in the antrum which prevents decreased gastrin production by the antral G cells.

  20. Normal Autoimmune gastritist

  21. Linear hyperplasia of the enterochromaffin-like (ECL) cells forming an extra layer of cells around the glands at the base of the mucosa

  22. Chromogranin stain : linear hyperplasia

  23. Hyperplasia of the enterochromaffin-like (ECL) cells forming nodules at the base of the mucosa

  24. Chromogranin: nodular hyperplasia

  25. Endocrine cell hyperplasiain autoimmune gastritis Composed of ECL (EnteroChromaffin-Like) cells Patterns: simple,linear and nodular Indicates hypergastrinemia Only occurs with diffuse body glandular atrophy autoimmune: actually a diagnostic feature Precursor of one type of carcinoid tumor

  26. What changes in a biopsy should lead you to suspect autoimmune gastritis?

  27. Basal inflammation

  28. Total or near total oxyntic glandular atrophy

  29. At least mucus gland metaplasia and possibly intestinal metaplasia

  30. Endocrine cell hyperplasia, seen as nodules or as an extra layer of cells around the base of the glands, may be the most important clue.

  31. If there are doubts that there is ECL cell hyperplasia, then use a chromogranin stain to bring out the ECL cells

  32. Since this biopsy only has mucus glands which is characteristic of antral mucosa, we have to determine whether this is antral mucosa or body mucosa with metaplastic mucus glands and no body glands. There are 2 ways of proving this.

  33. First, if we know that the biopsy came from the body, then this is autoimmune gastritis

  34. Second, if we don’t know the site of the biopsy, we can determine if this is antral mucosa by using a gastrin stain. Gastrin producing cells (G cells) only occur in antral mucosa. If the gastrin stain is negative, then that is great evidence that the biopsy did not come from antral mucosa but from body mucosa.

  35. The piece with uniform glands and no inflammation G cells indicating this biopsy is antrum

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