Smoking and peptic ulcer in the Helicobacter pylori era

Before the recent understanding of the central importance of Helicobacter pylori in the pathogenesis of peptic ulcer disease, smoking had been regarded as an important contributor to the cause and perpetuation of the disease. In this review, we find that (1) clinical observations indicate that smokers are more likely to develop ulcers, ulcers in smokers are more difficult to heal, and relapse of ulcer disease is more likely in smokers, (2) smoking adversely affects the gastroduodenal mucosal protective mechanisms, thus predisposing to ulcer disease, (3) smoking adversely affects gastroduodenal motility, allowing reflux of harmful duodenal contents into the stomach, (4) smokers appear to be at higher risk of becoming infected with H. pylori and this increased risk may be due to the adverse effects of smoking on antioxidants or the immune system that may interfere with the normal protection against H. pylori, and (5) once H,pylori is eradicated in smokers, they appear to be at no greater risk of peptic ulcer disease. We conclude that smoking in itself appears not to be an independent ulcerogen, but may act by augmenting the harmful effects of H. pylori, both by adversely affecting upper gastrointestinal mucosal protection and physiology and by increasing the risk of H. pylori infection. Thus, we recommend that appropriate advice to ulcer patients who smoke continues to be: stop smoking, (C) 2000 Lippincott Williams & Wilkins.