4.4 Article

Are patients with autoimmune thyroid disease and autoimmune gastritis at risk of gastric neuroendocrine neoplasms type 1?

Journal

CLINICAL ENDOCRINOLOGY
Volume 80, Issue 5, Pages 685-690

Publisher

WILEY
DOI: 10.1111/cen.12346

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ObjectiveThe aim of this study was to investigate the prevalence of autoimmune gastritis, enterochromaffin-like cell (ECL-cell) hyperplasia and gastric neuroendocrine neoplasms type 1 (GNEN1) in patients with autoimmune thyroid disease. DesignProspective observational study in a single institutional study. Patients and MeasurementsOne hundred and twenty patients with autoimmune thyroid disease were consecutively recruited from the Endocrine Unit. Upper gastrointestinal tract endoscopy (UGE) and biochemical parameters for autoimmune thyroid disease and autoimmune gastritis were assessed at recruitment and annually thereafter in patients with a mean follow-up of 375144months. Autoimmune gastritis was defined by the presence of antiparietal cell antibodies (APCA) and histological confirmation after UGE. Serum gastrin and chromogranin were also measured. ResultsOne hundred and eleven patients had Hashimoto's thyroiditis and nine Graves' disease. Autoimmune gastritis was identified in 40 (38 with Hashimoto's thyroiditis and two with Graves' disease) patients all of whom had increased levels of gastrin and chromogranin ; Helicobacter pylori infection was histologically identified in 15 of 40 (375%) patients. Six patients had isolated nodular ECL-cell hyperplasia and one mixed nodular and linear ECL-cell hyperplasia [7 of 40 (175%)]. Only increased gastrin (P=003) levels predicted the presence ECL-cell hyperplasia. A GNEN1 developed in one patient with nodular ECL-cell hyperplasia after 39months of follow-up. ConclusionsConcomitant autoimmune gastritis was found in 333% of patients with autoimmune thyroid disease, 175% of whom had ECL-cell hyperplasia that evolved to GNEN1 in one (25%). Larger studies with longer follow-up are needed to define the incidence of GNEN1 in patients with autoimmune thyroid disease and ECL-cell hyperplasia and potential implications.

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