Novel association of duodenal gastrinoma and atrophic gastritis: Case report and literature review

Research output: Contribution to journalArticle

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Abstract

Objective: To describe a patient with a duodenal gastrinoma in a setting of atrophic gastritis and hypergastrinemia. Methods: We present historical features and results of laboratory and genetic evaluation in a woman with duodenal gastrinoma and hypergastrinemia due to atrophic gastritis. Results: In a 46-year-old woman with a history of stable pituitary microprolactinoma, multiple gastrointestinal symptoms developed and prompted the performance of an esophagogastroduodenoscopy in conjunction with small bowel biopsies. A 2-mm duodenal gastrin-producing neuroendocrine tumor was discovered. The tumor stained negative for serotonin and somatostatin and involved the mucosa and submucosa. Immunohistochemical staining of the gastrinoma tissue with a monoclonal antibody to the cholecystokinin-B (gastrin) receptor was negative. The patient's random serum gastrin level was elevated at 990 pg/mL. She had been taking pantoprazole for 4 weeks before that test. After pantoprazole therapy was discontinued, the serum gastrin level remained elevated at 403 pg/mL. There was no family history of multiple endocrine neoplasia type 1, and genetic testing for the MEN1 mutation was negative. An upper endoscopy with measurement of gastric pH and performance of gastric biopsies confirmed the presence of chronic atrophic gastritis. This finding was consistent with the patient's persistently elevated serum gastrin levels. Conclusion: Patients with atrophic gastritis and associated hypergastrinemia are known to have a high frequency of hypergastrinemia-induced gastric carcinoid tumors, some of which are actual gastrinomas or are thought to arise from the G cells of the stomach. Gastrin is a well-recognized growth factor for many tissues. We postulate that hypergastrinemia in this patient might have had a trophic effect on the duodenal G cells and led to gastrinoma development. No gastrin receptors were detected on the gastrinoma cells; however, that result might have been attributable to technical (fixation or antibody) or tumor (dedifferentiation) problems.

Original languageEnglish (US)
Pages (from-to)770-775
Number of pages6
JournalEndocrine Practice
Volume13
Issue number7
DOIs
StatePublished - Jan 1 2007

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Gastrinoma
Atrophic Gastritis
Gastrins
Cholecystokinin B Receptor
Stomach
Multiple Endocrine Neoplasia Type 1
Gastrin-Secreting Cells
Serum
Digestive System Endoscopy
Neoplasm Antibodies
Biopsy
Prolactinoma
Neuroendocrine Tumors
Carcinoid Tumor
Genetic Testing
Somatostatin
Endoscopy
Serotonin
Intercellular Signaling Peptides and Proteins
Mucous Membrane

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

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title = "Novel association of duodenal gastrinoma and atrophic gastritis: Case report and literature review",
abstract = "Objective: To describe a patient with a duodenal gastrinoma in a setting of atrophic gastritis and hypergastrinemia. Methods: We present historical features and results of laboratory and genetic evaluation in a woman with duodenal gastrinoma and hypergastrinemia due to atrophic gastritis. Results: In a 46-year-old woman with a history of stable pituitary microprolactinoma, multiple gastrointestinal symptoms developed and prompted the performance of an esophagogastroduodenoscopy in conjunction with small bowel biopsies. A 2-mm duodenal gastrin-producing neuroendocrine tumor was discovered. The tumor stained negative for serotonin and somatostatin and involved the mucosa and submucosa. Immunohistochemical staining of the gastrinoma tissue with a monoclonal antibody to the cholecystokinin-B (gastrin) receptor was negative. The patient's random serum gastrin level was elevated at 990 pg/mL. She had been taking pantoprazole for 4 weeks before that test. After pantoprazole therapy was discontinued, the serum gastrin level remained elevated at 403 pg/mL. There was no family history of multiple endocrine neoplasia type 1, and genetic testing for the MEN1 mutation was negative. An upper endoscopy with measurement of gastric pH and performance of gastric biopsies confirmed the presence of chronic atrophic gastritis. This finding was consistent with the patient's persistently elevated serum gastrin levels. Conclusion: Patients with atrophic gastritis and associated hypergastrinemia are known to have a high frequency of hypergastrinemia-induced gastric carcinoid tumors, some of which are actual gastrinomas or are thought to arise from the G cells of the stomach. Gastrin is a well-recognized growth factor for many tissues. We postulate that hypergastrinemia in this patient might have had a trophic effect on the duodenal G cells and led to gastrinoma development. No gastrin receptors were detected on the gastrinoma cells; however, that result might have been attributable to technical (fixation or antibody) or tumor (dedifferentiation) problems.",
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Novel association of duodenal gastrinoma and atrophic gastritis : Case report and literature review. / Lendel, Irina; Manni, Andrea; Ruggiero, Francesca M.

In: Endocrine Practice, Vol. 13, No. 7, 01.01.2007, p. 770-775.

Research output: Contribution to journalArticle

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