Salivary and gastric epidermal growth factor in patients with Zollinger-Ellison Syndrome: Its protective potential

OBJECTIVE: Evidence is accumulating that epidermal growth factor (EGF) is a major molecule contributing to the maintenance of the integrity of the upp er alimentary tract mucosa before and after injury by acid and pepsin. Pati ents with Zollinger-Ellison Syndrome (ZES) typically have hypersecretion of acid and pepsin; however, the concentration and rate of secretion of saliv ary and gastric EGF that could counteract these potentially aggressive fact ors are unknown. Accordingly, this study was conducted to determine whether EGF affords mucosal protection in ZES patients. METHODS: The concentration and output of salivary (sEGF) and gastric epider mal growth factor (gEGF) were measured in eight patients with ZES and the r esults compared to those in 17 patients with nonulcer dyspepsia (NUD), serv ing as a control group. All patients had normal esophageal and gastric muco sa as determined by endoscopy. Total saliva was collected during l-h parafi lm- and l-h pentagastrin/parafilm-stimulated conditions, as well as basal a nd pentagastrin-stimulated gastric juice. The concentration and output of E GF were determined by radioimmunoassay. RESULTS: The concentration of EGF in saliva collected from ZES patients aft er parafilm chewing was significantly higher compared to that in NUD patien ts (4.61 +/- 0.59 vs 2.75 +/- 0.50 ng/ml, p < 0.05). The concentration of E GF in saliva collected after pentagastrin stimulation in ZES patients was a lso significantly higher than in NUD patients (4.37 +/- 0.73 vs 2.22 +/- 0. 37 ng/ml, p < 0.05). Salivary EGF output during parafilm chewing in ZES and NUD were similar (68 +/- 6.4 vs 109 +/- 25.2 ng/h). Salivary EGF output af ter administration of pentagastrin in ZES and NUD was also similar (66 +/- 6.1 vs 132 +/- 45.4 ng/h). Basal EGF output in the gastric juice of patient s with ZES was 3-fold higher than in patients with NUD (801 +/- 73 la 271 /- 32 ng/h, p < 0.01). Pentagastrin-stimulated EGF output was similar in bo th groups (705 +/- 92 Is 675 +/- 168 ng/h). CONCLUSIONS: Patients with ZES have a significantly higher EGF concentratio n in saliva and EGF output in basal gastric juice. This elevated content of salivary and gastric EGF in ZES patients may ploy a protective role in pre venting the development of reflux esophagitis and gastric ulcer under the i mpact of gastric acid and pepsin hypersecretion. (C) 2000 by Am. Cell. of G astroenterology.