Abstract
Clearly, hypersecretion of gastric acid exists in the clinical setting and at times is the reason why many acid-peptic disorders do not respond to standard antisecretory medication (Collen et al. 1987a,b, 1988a,b, 1989a,b, 1991; Collen and Gallagher 1990; Collen and Johnson 1991; Collen and Loebenberg 1989; Collen 1989, 1990; Jensen et al. 1983). It is recommended that patients with refractory acid-peptic symptoms and/or mucosal disease (i.e., duodenal ulcer) be evaluated for gastric acid hypersecretion, namely, Zollinger-Ellison syndrome (Jensen et al. 1983; Collen et al. 1989d, 1991; Spindel et al. 1986; Baron 1981). Patients with Zollinger-Ellison syndrome can be identified by noting gastric acid hypersecretion and an elevated serum gastrin concentration and by demonstrating a positive provocative secrelin test (Jensen et al. 1983). However, it is estimated that less than 1% of patients with gastric acid hypersecretion actually have Zollinger-Ellison syndrome, and almost all other patients except for less than 1% with other specific causes for gastric acid hypersecretion have no apparent etiology for their gastric acid hypersecretory states (Jensen et al. 1983; Collen 1989; MCCarthy 1982) (Table 1). The patients with no apparent etiology for their gastric acid hypersecretory states are classified as having idiopathic gastric acid hypersecretion.
Published Version
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