Spurious Elevations of Chromogranin A in the Setting of Autoimmune Metaplastic Atrophic Gastritis

TL;DR

A patient with autoimmune gastritis had elevated tumor markers, but no tumor was found, highlighting the need for better diagnostic guidelines.

Contribution

This case highlights spurious CgA and gastrin elevations in AMAG without GNETs, urging improved diagnostic guidelines.

Findings

Elevated chromogranin A and gastrin levels were observed in a patient with AMAG.

No gastric neuroendocrine tumor was identified despite extensive testing.

Enterochromaffin cell hyperplasia was attributed to hypergastrinemia from AMAG.

Abstract

Autoimmune metaplastic gastritis (AMAG) is a form of autoimmune gastritis that is characterized by the immune system’s attack on gastric parietal cells, leading to chronic inflammation. Gastric neuroendocrine tumors (GNETs) are rare neoplasms that can develop in the gastrointestinal tract in the presence of AMAG. This case presents a 69-year-old female who presented with dyspepsia, and on subsequent endoscopic evaluation, she was found to have AMAG in the context of elevated levels of serum chromogranin A (CgA) and gastrin, suggestive of a GNET. Despite an extensive diagnostic workup, including imaging, colonoscopy, small bowel follow-through, capsule study, and oncology workup, no GNET was identified. She was also found to have antibodies to parietal cells, suggestive of pernicious anemia. The elevated markers were attributed to enterochromaffin cell hyperplasia, secondary to hypergastrinemia from AMAG. This case invites a discussion about the need for more evidence-based guidelines in the workup and monitoring of spurious elevations of CgA and gastrin in the presence of AMAG. It also highlights the importance of careful and intentional clinical evaluation to avoid unnecessary tests and costs to the patient.

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