Influence of Smoking on Basal and on Vagally and Maximally Stimulated Gastric Acid and Pepsin Secretion

Abstract

Published data show that smokers have greater basal or peak acid and pepsin outputs, but the mechanisms underlying these effects are unknown. To confirm this and to determine whether these findings extend to, and implicate, any vagal overactivity, gastric secretions collected for 1 h basally, 1 h after 15 min of modified sham feeding (MSF), and 1 h after pentagastrin (6 μg/kg subcutaneously) were analyzed for acid and pepsin content in 204 subjects, 104 with duodenal ulcer (66 smokers) and 101 without (57 smokers). Maximal acid outputs (MAO, μeq/kg/h, x + SEM) were higher in smokers than in non-smokers in both duodenal ulcer (DU) (623 + 35 versus 491 + 35, p < 0.005) and non-DU (502 + 32 versus 376 + 20, p < 0.005). Basal and MSF secretions were generally increased in smokers but, when expressed as a percentage of MAO, were not different in smokers and non-smokers (18% versus 17% and 43% versus 39%, respectively, in DU, and 13% versus 16% and 40% versus 36% in non-DU). Maximal pepsin outputs (units + 10 ²/kg/h) were also higher in smokers than in non-smokers (DU, 129 + 7.9 versus 105 + 9.5, p = 0.05, and non-DU, 101 + 7.5 versus 77 + 10, p = 0.05). Basal and MSF secretions as a percentage of maximal pepsin output were not different in smokers versus non-smokers. Multivariate logistic regression shows that smoking was most strongly associated with MAO and sham feeding outputs, but the duration-intensity (pack-years) of smoking was associated only with elevated MAO. We conclude that smoking is associated with increased maximal acid and pepsin output in both DU and non-DU populations. Smoking does not seem to affect independently vagal stimulation of gastric secretion.

Key Words:

• Acid
• duodenal ulcer
• gastric secretion
• gastrin
• pepsin
• smoking