Successful Endoscopic and Medical Management of a PYLORIC Channel Stenosis in a Patient with Metastatic Gastrinoma and Multiple Gastric Carcinoid Tumors

Abstract

Purpose: To describe a case of gastric outlet obstruction and multiple carcinoid tumors in a patient with metastatic gastrinoma. Methods: A 58 year old man with past medical history significant for multiple endocrine neoplasia type 1 who had a pancreatic tail resection 25 years ago for a gastrinoma presented to our hospital with intractable nausea and vomiting. Two months prior to his current admission, a EGD done for workup of anemia showed diffuse nodularity (Image 1) involving the body and fundus of the stomach with antral sparing as well as smaller nodules in the duodenal bulb and 2nd portion of the duodenum. Gastric pH was 6 on proton pump inhibitor therapy. Multiple biopsies of the gastric nodules exhibited well differentiated neuroendocrine tumors in the setting of foveolar gland hyperplasia; duodenal and antral biopsies revealed metastatic gastrinoma. Results: Two month later, he returned with intractable nausea and vomiting. A repeat EGD showed nodules that were partially obstructing the pylorus as well as a high grade non-transversable stenosis of the pylorus. Gastric pH was 7. Incremental balloon dilation to 20 mm was then performed resulting in decreased resistance to scope passage. Antral biopsies from the procedure were positive for H. Pylori for which he received treatment. Two months following the procedure, the patient has had no recurrence of nausea and vomiting is tolerating a full diet. Conclusion: Carcinoid tumors arise from enterochromaffin-like cells in oxyntic glands of the stomach, of which gastrin is a potent stimulant. The antrum is relatively void of these glands, which explains the antral sparring of carcinoid tumors on endoscopy in our patient. The dramatic nodular appearance on endoscopy likely represents carcinoid tumors and foveolar hypertrophy accompanied by areas of glandular atrophy due to chronic H. pylori infection. We have two potential explanations why our patient would have developed a gastric outlet obstruction after several years on proton pump inhibitor therapy. First, active H. pylori infection may have caused significant acute edema in the setting of chronic fibrosis. In addition, partially obstructing metastatic gastrinoma nodules deforming the prepyloric area may have contributed to the obstruction.Figure