Abstract
Comment Our data show that smoking is associated with reduced salivary secretion of epidermal growth factor and an increased prevalence of peptic ulc?ration in patients attending for endoscopy. Cigarette smoking could thus predispose to peptic ulcer by depressing salivary secretion of epidermal growth factor. Depression of submandibular epidermal growth factor concentration in a small group of patients with gastric and duodenal ulcers has been reported.4 Our data suggest that reductions in epidermal growth factor secretion in patients with ulcers are likely to be attributable to the higher proportion of patients with ulcers who are smokers. Smoking is associated with depressed prostaglandin synthesis, while nicotine can enhance platelet aggre? gation, vasoconstriction, and increased concentrations of circulating catecholamines.5 Carbon monoxide may depress oxygen transport.5 However, neither the mediator nor the mechanism by which smoking depresses production of salivary epidermal growth factor is clear. Epidermal growth factor is produced by Brunner's glands in the duodenum, as well as by a cell lineage which develops at the site of gastrointestinal ulc?ration. If smoking also depresses local mucosal synthesis or secretion of epidermal growth factor this might represent an additional factor predisposing to duodenal ulc?ration as well as a plausible explana? tion for the link between smoking and Crohn's disease.
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