Endocrine Abstracts (2012) 29 P1124

Autoimmune thyroid disease and neuroendocrine gastric tumors: early detection and efficacy of somatostatin analogue treatment

G. Accardo1, A. Renzullo1, A. De Bellis1, A. Bizzarro1, M. Romano1, A. Federico1, A. Gravina1, A. Faggiano2, V. Marotta2, D. Esposito1, A. Bellastella1 & D. Pasquali1

1Second University of Naples, Naples, Italy; 2University Federico II, Naples, Italy.

Autoimmune chronic thyroid disease (AITD) is associated with atrophic gastritis (CAG) in 29–42% of the cases. CAG and the consequent hypergastrinemia, listed as precancerous lesion, can predispose to neuroendocrine cells hyperplasia and the development of neuroendocrine gastric tumors (NET). Aim of this study was to evaluate the association of AITD with risk of gastric NET and the efficacy of somatostatin analogues treatment.

Patients: From 2009 to 2011, we selected 92 AITD patients referred to the author’s endocrinology practice (83 female, 9 male, aged 16–70 years). All cases underwent hormonal profile, including serum gastrin, CgA, parietal cell antibodies (PCA). Patients with gastrin and CgA significantly higher than normal level (cut off were > 250 pg/ml and >80 ng/ml respectively) underwent to gastro esophageal endoscopy (EGDS). The patients positive for neuroendocrine cells hyperplasia at EGD, underwent somatostatin receptor scintigraphy and treatment with Sandostatina LAR 30 mg 1 fl i.m. each 28 days. Gastrin and CgA assays were repeated every three months and after one year they performed EGDF.

Results: Out of 92, only 58 patients exhibited gastrin and CgA. In 11 patients (18%) gastrin and CG were higher than normal (552,6±250 pg/ml; 288±152.3 ng/ml respectively), and only eight were PCA positive. Eleven patients with hypergastrinemia underwent EGDS, that showed in 2 patients diffused hyperplasia of the neuroendocrine cells of the body and in one a carcinoid. These patients, all negative to Octreoscan, were treated with Sandostatina LAR 30 mg fl every 28 days. After 3 months of treatment gastrin and CG levels were significantly reduced (P<0.001) and patients referred a decrease of clinical symptoms. After one year they showed normal gastrin and CgA values and EGDS detected absence of neuroendocrine hyperplasia.

Conclusions: We show that in 18% of AITD with hypergastrinemia was found neuroendocrine hyperplasia, a precancerous condition predisposing to NET risk. The remission, shown by EGDS, after one year of treatment, gives us evidence of the efficacy of somatostatin analogue in the prevention of gastric NET risk.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.