Autoimmune Gastritis
Epidemiology:
- Unknown cause
- H. pylori associated maybe
- Anti-parietal cell antibodies
- Anti-intrinsic factor antibodies
- 1-2% prevalence
Common sites:
- oxyntic-predominant pangastritis
Gross features:
Histologic features:
- atrophy of oxyntic mucosa
- inflammation of oxyntic mucosa
- antrum typically normal unless comorbid H.
pylori infection or bile reflux
- reactive gastropathy
in most patients
- hyperplasia of gastrin cells caused by achlorhydria often
- mucous neck hyperplasia (pseudopyloric
metaplasia)
- microcystic change and hyperplastic polyps in end stage
- endocrine cell hyperplasia (ECL cells - entochromafin-like cells - produce histamine from gastrin
stimulus) (florid and end stages)
- increased risk of neuroendocrine tumours (70-80% of all gastric carcinoid tumours are associated with autoimmune gastritis)
- expansile or infiltrative endocrine growth > 0.5 mm has been suggested
as definition of intramucosal carcinoid
- invasive carcinoid invades the submucosal space
- carcinoids associated with ECL cell hyperplasia
are relatively innocuous compared to sporadic solitary carcinoids in the
stomach
- intestinal metaplasia in more severe
- pancreatic metaplasia maybe
Immunophenotype:
|
Marker:
|
Sensitivity:
|
Specificity:
|
|
IgG4
plasma cells
|
Not highly
sensitive
|
100% in one
study
|
Molecular features:
Other features:
- Low pepsinogen I in serum (<20 ng/mL) is
sensitive and specific indicator for corpus atrophy
- Anti-parietal cell antibodies
- Anti-intrinsic factor antibodies
- Intrinsic factor deficiency with or without
anemia
- Iron deficiency anemia or pernicious anemia
- Hypergastrinemia
- Achlorhydria
in advanced stage of disease typically
- Risk factor for hyperplastic and dysplastic
polyps, carcinoma, and endocrine tumours
- Polyps in 20-40% of patients with pernicious
anemia
- Most hyperplastic
- Up to 10% contain foci of dysplasia
- Mostly intestinal type adenocarcinoma, arising
from intestinal metaplasia
References:
- Odze
& Goldblum Surgical Pathology of the GI Tract, Liver, Biliary Tract,
and Pancreas, 3rd ed (2015)