Abstract Library

#4606 Neuroendocrine mess – Ectopic Cushing syndrome and severe hypokalaemia

Introduction: Cushing Syndrome (CS) is the condition resulting from hypercortisolaemia. Ectopic Cushing Syndrome (ECS) is responsible for up to 20% of all CS cases. Pancreatic neuroendocrine neoplasms (pNEN) are responsible for 10-20% of those cases.

Conference:

Presenting Author:

Authors: Corrêa Figueira C, Alves H, Bento A, Cardoso Gomes C, Oliveira A,

Keywords: Pancreatic neuroendocrine neoplasm, Hepatic neuroendocrine metastasis, Paraneoplastic syndrome, Cushing syndrome, Ectopic Cushing syndrome,

#4223 US real-world study of the burden of medication in patients with gastroenteropancreatic neuroendocrine tumors (GEP-NETs)

Introduction: Patients with NETs experience a range of comorbidities, and often present with carcinoid syndrome (CS).

Conference:

Presenting Author:

Authors: Chan J, Houchard A, Pommie C, Ribeiro-Oliveira Jr A, Starr J,

Keywords: gastroenteropancreatic, neuroendocrine tumor, concomitant medication, burden,

#4190 Burden of medication in patients with lung neuroendocrine tumors (NETs) in a US real-world setting

Introduction: Real-world evidence on patients with lung NETs, specifically on comorbidities and the prevalence of carcinoid syndrome (CS), is lacking.

Conference:

Presenting Author:

Authors: Starr J, Houchard A, Pommie C, Ribeiro-Oliveira Jr A, Chan J,

Keywords: lung, neuroendocrine tumor, concomitant medication, costs,

#2159 Hepatic Steatosis Secondary to Peptide Receptor Radionuclide Therapy with Somatostatin Analogue

Introduction: Peptide Receptor Radionuclide Therapy (PRRT) with 177-Lutetium-DOTA-TATE is a therapeutic modality for neuroendocrine tumors. It has some well known side effects, concerning specially the bone marrow (from cytopenias to myelodysplastic syndrome), in addition to mild renal effects. Hepatotoxicity from PRRT is still being studied.

Conference: 15th Annual ENETSConcerence (2018)

Presenting Author: Matheos de Lima B

Authors: Arruda Matheos de Lima B, Gonçalves R, Romano Gaspar P, Linhares Riello de Mello E, Oliveira Albagli R,

Keywords: peptide receptor radionuclide therapy, lutetium, collateral effects, hepatotoxicity, neuroendocrine tumor, hepatic steatosis,

#18 Long-acting release octreotide induce complete response in type 1 gastric carcinoid tumors

Introduction: Gastric endocrine tumors (GET) are increasingly recognized due to expanding indications of upper gastrointestinal endoscopy. Often silent and benign, GET may also be aggressive when sporadic and may sometimes mimic the course of gastric adenocarcinoma. Current incidence of GETs is estimated at around 8% of digestive endocrine tumors. Yearly age-adjusted incidence is around 0.2 per population of 100,000. Gastric carcinoids (ECLomas) develop from gastric enterochromaffin-like cells (ECL cells) in response to chronically elevated gastrin. Type 1 tumors (ECLomas in the course of atrophic gastritis) may occur in conditions of achlorhydria secondary to auto-immune atrophic fundic gastritis. It occurs mostly in women and they are non-functioning tumors, typically found during upper GI endoscopy performed for dyspepsia. ECLomas present frequently as multiple polyps, usually < 1 cm in diameter in the gastric fundus. Type 1 tumors are almost exclusively benign lesions with little risk of deep invasion of the gastric parietal wall. The neoplastic ECL cells become progressively dedifferentiated with an increasing number of Ki-67 immunoreactive (IR) cell nuclei. In addition, there is a substantial decrease in argynophil and IR NE cells that can be visualized by conventional methods. ECLomas secondary to hypergastrinemia should be closely followed for signs of clinical and histopathological tumor progression. Such ECLomas deserve early, active, radical surgical treatment. Traditionally, gastric carcinoid type 1 (GCA1s) are endoscopically or surgically removed, depending on the number, appearance and size of the tumors. Antrectomy, with surgical excision of the majority of the G cells, is thought to facilitate regression of these tumors by removing the source of excessive gastrin secretion; however, the long-term benefits of antrectomy still remain uncertain. Although proton pump inhibitors are effective in reducing hypergastrinemia-induced gastric acid hypersecretion in GCA2, they do not affect ECL-cell hyperplasia, and therefore their role in GCA1 is limited. Moreover, in selected cases, significant reduction of hypergastrinemia does not prevent development of ECL carcinoid, suggesting that, in addition to hypergastrinemia, other pathogenic or genetic factors may be involved. Treatment with somatostatin analogues (SSA) might impede ECL-cell hyperplasia by suppressing gastrin secretion and/or by a direct anti-proliferative effect on ECL cells. Treatment with SSAs in GCA1 leads to a substantial tumor load reduction, with a concomitant decrease of serum gastrin levels. Published data indicate an important anti-proliferative effect of SSA on ECL cells, providing clinical benefit and obviating, at least temporarily, the need for invasive therapies for GCA1. Morphometric studies demonstrated that, while antrectomy specifically decreased the volume of ECL cells versus the total volume of endocrine cells, octreotide reduces the overall endocrine cell volume. Although the number of treated patients is small, it has been suggested that SSA may exert important anti-proliferative effects either directly, by inhibiting ECL-cells proliferation, or indirectly through suppression of gastrin hypersecretion.

Conference: 7th Annual ENETSConcerence (2010)

Presenting Author: Francis de Oliveira Alves

Authors: Caponero R, Francis de Oliveira Alves , Flávio Issao Sakamoto , Osmar Martins Cruz Jr. ,

Keywords: gastric carcinoid tumors type 1, octreotide LAR, ECLomas, neuroendocrine tumors,