Sixty patients with surgically correctable hypergastrinemia were treated between 1960 and 1988. Provocative testing was used when available to select appropriate operations. Sources of hypergastrinemia included
antral G cell
hyperplasia (AGCH) (17), pancreatic
gastrinomas (14), duodenal
gastrinomas (11), multiple
gastrinomas in patients with type I
multiple endocrine neoplasia (MEN I) (five), lymph node
gastrinomas (four), and the source not found in nine patients. Eugastrinemia was achieved by resection in 17 of 17 patients with AGCH, nine of 11 patients with duodenal
gastrinomas, three of four patients with lymph node
gastrinomas, zero of 14 patients with pancreatic
gastrinomas, zero of five patients with MEN I, and zero of nine patients in whom the source was not found. Hepatic
metastases developed in 11 patients with pancreatic
gastrinomas, two patients with MEN I, one patient with duodenal
gastrinomas, and one patient with lymph node
gastrinomas. One patient in whom the source of the hypergastrinemia was not found developed hepatic
metastases, and seven required total
gastrectomy. This experience suggests the following: (1) that patients with AGCH, duodenal
gastrinomas, or lymph node
gastrinomas can usually be rendered eugastrinemic by resection; (2) that patients with pancreatic
gastrinomas, whether sporadic or familial (MEN I), are rarely cured by resection and frequently develop hepatic
metastases; and (3) that patients in whom the source of the hypergastrinemia is not identified and removed frequently require total
gastrectomy, but antroduodenectomy should be considered because it may uncover an occult duodenal microneurogastrinoma or may correct AGCH.