Zollinger–Ellison syndrome (ZES) is caused by a non–beta islet cell (islet of Langerhans), gastrin-secreting tumor of the pancreas that stimulates the acid-secreting cells of the stomach (parietal cells) to maximal activity, with consequent gastrointestinal mucosal ulceration. ZES may occur sporadically or as part of an autosomal dominant familial syndrome calledmultiple endocrine neoplasia type 1 (MEN 1). The primary tumor is usually located in the pancreas, duodenum or abdominallymph nodes, but ectopic locations have also been described (e.g., heart, ovary, gallbladder, liver, kidney)
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https://www.hindawi.com/journals/crim/2011/156937/ seyed saeid sarkeshikian and mohammad reza ghadir, “a 41-year-old man with two types of metachronous peptic ulcer complication due to zollinger-ellison syndrome—regression of pancreatic primary after chemoembolization of hepatic metastases: a case report,” case reports in medicine, vol. 2011, article id 156937, 5 pages, 2011. doi:10.1155/2011/156937
https://www.hindawi.com/journals/cjgh/2001/462456/ barbara désir and pierre poitras, “oral pantoprazole for acid suppression in the treatment of patients with zollinger-ellison syndrome,” canadian journal of gastroenterology, vol. 15, no. 12, pp. 795-798, 2001. doi:10.1155/2001/462456
https://www.hindawi.com/journals/dte/2009/298381/ emil kohan, david oh, hank wang, salar hazany, gordon ohning, and joseph r. pisegna, “duodenal bulb mucosa with hypertrophic gastric oxyntic heterotopia in patients with zollinger ellison syndrome,”diagnostic and therapeutic endoscopy, vol. 2009, article id 298381, 6 pages, 2009. doi:10.1155/2009/298381