Xiaobing Sun1, Xiaoquan Huang2, Ruifeng Zhao2, Beibei Chen2, Qin Xie2. 1. Department of Internal Medicine, The Second People's Hospital of Nantong, Nantong, Jiangsu 226002, China. Electronic address: sunxiaob123@126.com. 2. Department of Internal Medicine, The Second People's Hospital of Nantong, Nantong, Jiangsu 226002, China.
Abstract
BACKGROUND AND AIM: Questions remain unclear about the association of smoking status and the development of acute pancreatitis (AP). We performed a meta-analysis of observational studies explore this association. METHODS: A computerized literature search was performed in MEDLINE and EMBASE through November 30, 2014. We also searched the reference lists of pertinent articles. We used a random-effects model to calculate the summary relative risks (SRRs) and their corresponding 95% confidence intervals (CIs). RESULTS: A total of 3690 incident cases of AP included 12 observational studies (6 case-control and 6 prospective cohort/nested case-control studies) were identified. Compared with never smokers, the summary RR estimates were 1.54 (95% CI, 1.31-1.80) for ever smokers, 1.71 (95% CI, 1.37-2.14) for current smokers, and 1.21 (95% CI, 1.02-1.43) for former smokers. Smoking is found to be a potential risk factor for alcohol use, idiopathic factors and drugs related AP, but not for gallstone related AP, in the ever and current smokers. A dose-response effect of tobacco use on the risk was ascertained: current smokers had a 40% (95% CI, 30%-51%) increased risk of AP for every additional 10 cigarettes per day. CONCLUSION: The present analysis suggests that smokers have an elevated risk of AP development. Further studies, however, are warranted before definitive conclusions can be drawn.
BACKGROUND AND AIM: Questions remain unclear about the association of smoking status and the development of acute pancreatitis (AP). We performed a meta-analysis of observational studies explore this association. METHODS: A computerized literature search was performed in MEDLINE and EMBASE through November 30, 2014. We also searched the reference lists of pertinent articles. We used a random-effects model to calculate the summary relative risks (SRRs) and their corresponding 95% confidence intervals (CIs). RESULTS: A total of 3690 incident cases of AP included 12 observational studies (6 case-control and 6 prospective cohort/nested case-control studies) were identified. Compared with never smokers, the summary RR estimates were 1.54 (95% CI, 1.31-1.80) for ever smokers, 1.71 (95% CI, 1.37-2.14) for current smokers, and 1.21 (95% CI, 1.02-1.43) for former smokers. Smoking is found to be a potential risk factor for alcohol use, idiopathic factors and drugs related AP, but not for gallstone related AP, in the ever and current smokers. A dose-response effect of tobacco use on the risk was ascertained: current smokers had a 40% (95% CI, 30%-51%) increased risk of AP for every additional 10 cigarettes per day. CONCLUSION: The present analysis suggests that smokers have an elevated risk of AP development. Further studies, however, are warranted before definitive conclusions can be drawn.