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Are patients with autoimmune thyroid disease and autoimmune gastritis at risk of gastric neuroendocrine neoplasms type 1?
Author(s) -
Alexandraki Krystallenia I.,
Nikolaou Argiro,
Thomas Dimitrios,
Syriou Vassiliki,
Korkolopoulou Penelope,
Sougioultzis Stavros,
Kaltsas Gregory
Publication year - 2014
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/cen.12346
Subject(s) - autoimmune gastritis , medicine , autoimmune disease , gastritis , chromogranin a , gastrin , hyperplasia , atrophic gastritis , thyroiditis , gastroenterology , autoimmune thyroiditis , thyroid , hashimoto disease , helicobacter pylori , thyroid disease , pathology , disease , immunohistochemistry , secretion
Summary Objective The aim of this study was to investigate the prevalence of autoimmune gastritis, enterochromaffin‐like cell ( ECL ‐cell) hyperplasia and gastric neuroendocrine neoplasms type 1 ( GNEN 1) in patients with autoimmune thyroid disease. Design Prospective observational study in a single institutional study. Patients and Measurements One hundred and twenty patients with autoimmune thyroid disease were consecutively recruited from the E ndocrine U nit. 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 37·5 ± 14·4 months. Autoimmune gastritis was defined by the presence of antiparietal cell antibodies ( APCA ) and histological confirmation after UGE . Serum gastrin and chromogranin Α were also measured. Results One hundred and eleven patients had Hashimoto's thyroiditis and nine G raves' disease. Autoimmune gastritis was identified in 40 (38 with H ashimoto's thyroiditis and two with G raves' disease) patients all of whom had increased levels of gastrin and chromogranin Α ; H elicobacter pylori infection was histologically identified in 15 of 40 (37·5%) patients. Six patients had isolated nodular ECL ‐cell hyperplasia and one mixed nodular and linear ECL ‐cell hyperplasia [7 of 40 (17·5%)]. Only increased gastrin ( P = 0·03) levels predicted the presence ECL ‐cell hyperplasia. A GNEN 1 developed in one patient with nodular ECL ‐cell hyperplasia after 39 months of follow‐up. Conclusions Concomitant autoimmune gastritis was found in 33·3% of patients with autoimmune thyroid disease, 17·5% of whom had ECL ‐cell hyperplasia that evolved to GNEN 1 in one (2·5%). Larger studies with longer follow‐up are needed to define the incidence of GNEN 1 in patients with autoimmune thyroid disease and ECL ‐cell hyperplasia and potential implications.