Article Text
Abstract
Background Several studies have shown that smoking increases the risk of chronic pancreatitis. However, the impact of smoking on the development of acute pancreatitis has not been fully studied.
Objective To clarify the association between cigarette smoking, smoking cessation and the risk of acute pancreatitis.
Design A follow-up study was conducted of 84 667 Swedish women and men, aged 46–84, during 12 years to study the association between smoking status, smoking intensity and duration, duration of smoking cessation and the risk of acute pancreatitis. Only those with the first event of the disease and no previous history of acute pancreatitis were included. Cox proportional hazards models were used to estimate rate ratios (RRs) with 95% CI for different smoking-related variables, adjusted for age, gender, body mass index, diabetes, educational level and alcohol consumption.
Results In total, 307 cases with non-gallstone-related and 234 cases with gallstone-related acute pancreatitis were identified. The risk of non-gallstone-related acute pancreatitis was more than double (RR=2.29; 95% CI 1.63 to 3.22, p<0.01) among current smokers with ≥20 pack-years of smoking as compared with never-smokers. The corresponding risk among individuals with ≥400 g monthly consumption of alcohol was increased more than fourfold (RR=4.12; 95% CI 1.98 to 8.60, p<0.01). The duration of smoking rather than smoking intensity increased the risk of non-gallstone-related acute pancreatitis. After two decades of smoking cessation the risk of non-gallstone-related acute pancreatitis was reduced to a level comparable to that of non-smokers. There was no association between smoking and gallstone-related acute pancreatitis.
Conclusion Smoking is an important risk factor for non-gallstone-related acute pancreatitis. Early smoking cessation should be recommended as a part of the clinical management of patients with acute pancreatitis.
- Acute pancreatitis
- smoking
- smoking cessation
- epidemiology
- abdominal surgery
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Footnotes
Funding This work was supported by research grants from the Swedish Cancer Foundation and the Swedish Research Council Committee for Infrastructure. The first author was supported as a postdoctoral researcher by a grant from Olle Engkvist Byggmästare Foundation and the Swedish Society of Medicine. The funding sources had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; or preparation, review, or approval of the manuscript.
Competing interests None.
Ethics approval Institutional ethical committee at Karolinska Institutet.
Provenance and peer review Not commissioned; externally peer reviewed.