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Difficulty: HardPathology and Biopsy Interpretation

A 62-year-old woman is evaluated in the gastroenterology clinic for progressive fatigue, lower extremity paresthesias, and a burning sensation in her tongue. Laboratory testing reveals a hemoglobin level of 9.2 g/dL and a mean corpuscular volume of 114 fL. An upper gastrointestinal endoscopy is performed, revealing a thinned, featureless mucosa in the gastric body and fundus, with preservation of the normal rugal architecture in the gastric antrum. Random biopsies are obtained. The synoptic pathology report indicates the following:

Gastric body and fundus: Marked loss of specialized oxyntic glands with extensive replacement by intestinal-type epithelium containing goblet cells. The lamina propria contains a dense lymphoplasmacytic inflammatory infiltrate. Immunohistochemical staining for chromogranin A demonstrates nodular hyperplasia of neuroendocrine cells.

Gastric antrum: Unremarkable foveolar epithelium and mucinous glands. No acute inflammation is present, and immunostains for *Helicobacter* species are negative.

Which of the following is the most likely diagnosis based on these clinicopathologic findings?

  1. Autoimmune metaplastic atrophic gastritisAnswer
  2. B
    Helicobacter pylori-associated multifocal atrophic gastritis
  3. C
    Zollinger-Ellison syndrome
  4. D
    Menetrier disease
  5. E
    Reactive (chemical) gastropathy

Answer

Autoimmune metaplastic atrophic gastritis
The correct diagnosis is autoimmune metaplastic atrophic gastritis (AMAG). AMAG is mediated by CD4+ T-cell destruction of parietal cells, leading to profound loss of oxyntic glands in the body and fundus. The resulting achlorhydria stimulates antral G-cells to overproduce gastrin. This prolonged hypergastrinemia trophic effect on enterochromaffin-like (ECL) cells leads to their linear or nodular hyperplasia, as highlighted by chromogranin A staining. The antrum remains pathologically spared, differentiating it from other causes of chronic gastritis. The clinical presentation of macrocytic anemia and paresthesias correlates perfectly with the resulting vitamin B12 deficiency (pernicious anemia) due to intrinsic factor loss.

Step-by-Step Solution

1
Analyze the clinical presentation.
The patient has macrocytic anemia and neurologic symptoms (paresthesias), consistent with vitamin B12 deficiency (pernicious anemia).
Identifying the underlying clinical syndrome helps guide the interpretation of the histopathologic findings.
2
Evaluate the topographic distribution of the endoscopic and biopsy findings.
Pathology is restricted to the gastric body and fundus (thinned mucosa, glandular atrophy), while the antrum is entirely spared.
Topographic distribution is a key differentiator between etiologies of gastritis; autoimmune gastritis strictly involves the oxyntic mucosa (body/fundus) and spares the antrum.
3
Interpret the specific histopathologic and immunohistochemical features.
There is a dense lymphoplasmacytic infiltrate, oxyntic gland atrophy, intestinal metaplasia, and nodular ECL cell hyperplasia (chromogranin A positive).
These findings represent the complete histologic picture of end-stage autoimmune metaplastic atrophic gastritis. The destruction of parietal cells causes achlorhydria, triggering reflex hypergastrinemia which drives the ECL cell hyperplasia.

Key Concept

Autoimmune metaplastic atrophic gastritis presents with body- and fundus-restricted oxyntic gland atrophy, intestinal metaplasia, and neuroendocrine (ECL) cell hyperplasia secondary to achlorhydria-induced hypergastrinemia, while strictly sparing the gastric antrum.
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Topics

Pathology and Biopsy Interpretation

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