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Impact of Smoking on Patients With Idiopathic Chronic Pancreatitis

Maisonneuve, Patrick ING*; Frulloni, Luca MD†; Müllhaupt, Beat MD‡; Faitini, Katia MD†; Cavallini, Giorgio MD†; Lowenfels, Albert B. MD§; Ammann, Rudolf W. MD‡

doi: 10.1097/01.mpa.0000227916.94073.fc
Original Articles

Objectives: Chronic pancreatitis is usually caused by heavy alcohol intake and, in many studies, also smoking. Because heavy drinkers usually smoke, making it difficult to separate the effects of these 2 factors, we thought to study the impact of smoking on the progression of nonalcoholic idiopathic chronic pancreatitis (ICP)

Methods: We used data from 83 patients with ICP in Switzerland and from 83 patients in Italy. We studied the impact of smoking on progression of disease as measured by the appearance of calcification and diabetes using Cox regression models.

Results: In both centers, the prevalence of smoking was significantly higher in patients with ICP than in the background population. In Italian patients, smoking increased the risk of pancreatic calcifications (hazard ratio = 2.09; 95% confidence interval, 1.07-4.10). Smoking also shortened the time to appearance of calcification. Heavy smoking (>20 cigarettes per day) was associated with the appearance of diabetes (hazard ratio = 3.94; 95% confidence interval, 1.14-13.6). For those patients who never reported consuming alcohol, smoking remains a significant risk factor.

Conclusions: In nonalcoholic ICP, smoking is associated with disease progression as measured by the appearance of pancreatic calcification and, to a lower extent, of diabetes. These findings were chiefly observed in patients who were older than 35 years at the time of onset of disease.

From the *Epidemiology Unit, European Institute of Oncology, Milan, Italy; †Department of Surgical and Gastroenterological Sciences, University of Verona, Verona, Italy; ‡Gastroenterology Service, Department of Medicine, University Hospital, Zurich Switzerland; and §Department of Surgery, New York Medical College, Valhalla, NY.

Received for publication February 3, 2006; accepted April 18, 2006.

Supported in part by grants from the C.D. Smithers Foundations; Solvay Pharmaceuticals Corporation; A. Waring Foundation, Zurich; and the Italian Association for Cancer Research.

Reprints: Patrick Maisonneuve, ING, Epidemiology Unit, European Institute of Oncology, Via Ripamonti 435 20141, Milan, Italy (e-mail: Patrick.maisonneuve@ieo.it).

© 2006 Lippincott Williams & Wilkins, Inc.