The link between smoking and an increased risk of gastric and duodenal ulcer disease has been examined by investigating the effect of cigarette smoke on individual gastrointestinal physiological mechanisms. We conclude that the mechanism is likely to be multifactorial but habitual smokers appear to have (a) greater rates of maximal gastric acid outflow, (b) lower rates of pancreatic bicarbonate secretion, (c) reduced gastric mucosal blood flow and (d) reduced concentrations of gastroduodenal mucosal prostaglandins. All these could account for the increased incidence of ulcer disease. However, such a conclusion should be tempered with the awareness that most research on smoking and gastrointestinal pathophysiology took place before the important aetiological role of Helicobacter pylori had been identified. Further work will have to take this factor into consideration.
|Original language||English (US)|
|Number of pages||18|
|Journal||Journal of Smoking-Related Disorders|
|State||Published - Jan 1 1994|
- Helicobacter pylori
- Peptic ulcer disease
ASJC Scopus subject areas