OBJECTIVES: To assess the evidence for tobacco smoking as a risk factor for the causation of chronic pancreatitis. METHODS: We performed a meta-analysis with random-effects models to estimate pooled relative risks (RRs) of chronic pancreatitis for current, former, and ever smokers, in comparison to never smokers. We also performed dose-response, heterogeneity, publication bias, and sensitivity analyses. RESULTS: Ten case-control studies and 2 cohort studies that evaluated, overall, 1705 patients with chronic pancreatitis satisfied the inclusion criteria. When contrasted to never smokers, the pooled risk estimates for current smokers was 2.8 (95% confidence interval [CI], 1.8-4.2) overall and 2.5 (95% CI, 1.3-4.6) when data were adjusted for alcohol consumption. A dose-response effect of tobacco use on the risk was ascertained: the RR for subjects smoking less than 1 pack per day was 2.4 (95% CI, 0.9-6.6) and increased to 3.3 (95% CI, 1.4-7.9) in those smoking 1 or more packs per day. The risk diminished significantly after smoking cessation, as the RR estimate for former smokers dropped to a value of 1.4 (95% CI, 1.1-1.9). CONCLUSIONS: Tobacco smoking may enhance the risk of developing chronic pancreatitis. Recommendation for smoking cessation, besides alcohol abstinence, should be incorporated in the management of patients with chronic pancreatitis.

Andriulli, A., Botteri, E., Vantini, I., Uomo, G., Maisonneuve, P., Almasio PL (2010). Smoking as a cofactor for causation of chronic pancreatitis: a meta-analysis. PANCREAS, 39 [10.1097/MPA.0b013e3181df27c0.].

Smoking as a cofactor for causation of chronic pancreatitis: a meta-analysis.

ALMASIO, Pier Luigi
2010-01-01

Abstract

OBJECTIVES: To assess the evidence for tobacco smoking as a risk factor for the causation of chronic pancreatitis. METHODS: We performed a meta-analysis with random-effects models to estimate pooled relative risks (RRs) of chronic pancreatitis for current, former, and ever smokers, in comparison to never smokers. We also performed dose-response, heterogeneity, publication bias, and sensitivity analyses. RESULTS: Ten case-control studies and 2 cohort studies that evaluated, overall, 1705 patients with chronic pancreatitis satisfied the inclusion criteria. When contrasted to never smokers, the pooled risk estimates for current smokers was 2.8 (95% confidence interval [CI], 1.8-4.2) overall and 2.5 (95% CI, 1.3-4.6) when data were adjusted for alcohol consumption. A dose-response effect of tobacco use on the risk was ascertained: the RR for subjects smoking less than 1 pack per day was 2.4 (95% CI, 0.9-6.6) and increased to 3.3 (95% CI, 1.4-7.9) in those smoking 1 or more packs per day. The risk diminished significantly after smoking cessation, as the RR estimate for former smokers dropped to a value of 1.4 (95% CI, 1.1-1.9). CONCLUSIONS: Tobacco smoking may enhance the risk of developing chronic pancreatitis. Recommendation for smoking cessation, besides alcohol abstinence, should be incorporated in the management of patients with chronic pancreatitis.
2010
Andriulli, A., Botteri, E., Vantini, I., Uomo, G., Maisonneuve, P., Almasio PL (2010). Smoking as a cofactor for causation of chronic pancreatitis: a meta-analysis. PANCREAS, 39 [10.1097/MPA.0b013e3181df27c0.].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10447/81124
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