Upper endoscopy findings: Micronodular mucosa in gastric fundus with multiple 1-mm lesions. 3 lessions > 1mm were resected.
Anatomopathology results: Diffuse chronic atrophic gastritis. Focal intestinal metaplasia with no dysplasia.Neuro endocrine micronodular hyperplasia. Type-1 neuroendocrine tumor suspected.
The patient refused surgical antrectomy.
A somatostatin receptor scintigraphy was ordered to identify a gastrinoma and to rule out a gastric carcinoid.
Teaching points:
In type 1 gastric carcinoids, diminution of parietal cell function (eg. autoimmune destruction in pernicious anaemia or atrophic gastritis) reduce luminal acidity, which stimulates gastrin secretion and prolonged hypergastrinemia, culminatinf in ECL cell proliferation through phases of hyperplasia, dysplasia and neoplasia.
Gastric carcinoids are of increasingf clinical conCern because they may develop hypergastrinemic state. However, they are difficult to diagnose.
Somatostatin receptor scintigraphy is a reasonably sensitive and highly specific imaging modality to localize gastric carcinoids in patients with hypergastrinemic states.
No abnormal uptake was seen in the gastric fundus, therefore we can confidently rule out a gastric carcinoid.
We can only speculate that the focal uptake in the gastric antrum was a false poisitve result induced by G cell hyperplasia.
Antrectomy is no longer considered a useful treatment because the antrum only produces 60% of the body gastrin, whereas the duodenum can produce the remaining 40%.
