BACKGROUND: The use of ulcerogenic drugs is the only well documented risk factor for peptic ulcer perforation, but accounts for only a quarter of the events. Smoking is a well known risk factor for uncomplicated ulcer disease, and patients with ulcer bleeding have increased death rates from smoking related disorders. AIM: To assess the role of smoking in ulcer perforation. SUBJECTS: A total of 168 consecutive patients with gastroduodenal ulcer perforation and 4469 control subjects from a population based health survey. METHODS: The association between ulcer perforation and smoking habits was analysed by logistic regression while adjusting for age and sex. RESULTS: Current smoking increased the risk for ulcer perforation 10-fold in the age group 15-74 years (OR 9.7, 95% CI 5.9 to 15.8) and there was a highly significant dose-response relationship (p < 0.001). The results were similar in men (OR 9.3, 95% CI 4.9 to 17) and women (OR 11.6, 95% CI 5.3 to 25), and for gastric (OR 10.5, 95% CI 4.5 to 25) and duodenal (OR 8.6, 95% CI 4.9 to 15.4) ulcer perforation. No increase in risk was found in previous smokers (OR 0.8, 95% CI 0.2 to 2.2). CONCLUSION: Our findings suggest that smoking is a causal factor for ulcer perforation and accounts for a major part of ulcer perforations in the population aged less than 75 years.
BACKGROUND: The use of ulcerogenic drugs is the only well documented risk factor for peptic ulcer perforation, but accounts for only a quarter of the events. Smoking is a well known risk factor for uncomplicated ulcer disease, and patients with ulcer bleeding have increased death rates from smoking related disorders. AIM: To assess the role of smoking in ulcer perforation. SUBJECTS: A total of 168 consecutive patients with gastroduodenal ulcer perforation and 4469 control subjects from a population based health survey. METHODS: The association between ulcer perforation and smoking habits was analysed by logistic regression while adjusting for age and sex. RESULTS: Current smoking increased the risk for ulcer perforation 10-fold in the age group 15-74 years (OR 9.7, 95% CI 5.9 to 15.8) and there was a highly significant dose-response relationship (p < 0.001). The results were similar in men (OR 9.3, 95% CI 4.9 to 17) and women (OR 11.6, 95% CI 5.3 to 25), and for gastric (OR 10.5, 95% CI 4.5 to 25) and duodenal (OR 8.6, 95% CI 4.9 to 15.4) ulcer perforation. No increase in risk was found in previous smokers (OR 0.8, 95% CI 0.2 to 2.2). CONCLUSION: Our findings suggest that smoking is a causal factor for ulcer perforation and accounts for a major part of ulcer perforations in the population aged less than 75 years.
Authors: Kenneth Thorsen; Jon Arne Søreide; Jan Terje Kvaløy; Tom Glomsaker; Kjetil Søreide Journal: World J Gastroenterol Date: 2013-01-21 Impact factor: 5.742
Authors: Kjetil Søreide; Kenneth Thorsen; Ewen M Harrison; Juliane Bingener; Morten H Møller; Michael Ohene-Yeboah; Jon Arne Søreide Journal: Lancet Date: 2015-09-26 Impact factor: 79.321