Gastric Neuroendocrine Tumor Type 1 Associated with Autoimmune Polyglandular Syndrome Type 3B: A Case Report Abstract #533
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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.
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#37 Gastric GIST with synchronous neuroendocrine tumor of the pancreas, Case Report and Literature Review
The occurrence of neuroendocrine tumors of the pancreas is rare, representing 1-5% of pancreatic cancers, and it is estimated that its incidence does not exceed 5 to one million. The tumors considered nonfunctioning (15-32% of pancreatic neuroendocrine tumors) are not associated with any syndrome, and are usually incidental. They have a slight predominance in males, and are more frequent in the 6th decade of life. Nonfunctioning tumors of islet cells are virtually all malignant tumors, and the treatment consists of surgical resection.