Chronic Pancreatitis: A Risk Factor for Cancer?

The Pancreas ◽  
2009 ◽  
pp. 437-443
Author(s):  
Albert B. Lowenfels ◽  
Patrick Maisonneuve
Pancreatology ◽  
2013 ◽  
Vol 13 (1) ◽  
pp. 29-32 ◽  
Author(s):  
Anja Ragvin ◽  
Karianne Fjeld ◽  
F. Ulrich Weiss ◽  
Janniche Torsvik ◽  
Ali Aghdassi ◽  
...  

Pancreas ◽  
2000 ◽  
Vol 21 (2) ◽  
pp. 109-114 ◽  
Author(s):  
Yingsong Lin ◽  
Akiko Tamakoshi ◽  
Tetsuo Hayakawa ◽  
Michio Ogawa ◽  
Yoshiyuki Ohno

Pancreatology ◽  
2011 ◽  
Vol 10 (6) ◽  
pp. 713-719 ◽  
Author(s):  
Dhiraj Yadav ◽  
Adam Slivka ◽  
Stuart Sherman ◽  
Robert H. Hawes ◽  
Michelle A. Anderson ◽  
...  

2020 ◽  
Vol 48 (3) ◽  
pp. 23-31
Author(s):  
T. Muniraj ◽  
D. Yadav ◽  
J. N. Abberbock ◽  
S. Alkaade ◽  
S. T. Amann ◽  
...  

Background: We have previously reported that physicians under-recognize smoking as a chronic pancreatitis (CP) risk factor. We hypothesized that availability of empiric data will influence physician recognition of this relationship. Methods: We analyzed data from 508 CP patients prospectively enrolled in the North American Pancreatitis Study-2 Continuation and Validation (NAPS2-CV) or NAPS2-Ancillary (AS) studies (2008–2014) from 26 US centers who self-reported ever-smoking. Information on smoking status, physician-defined etiology and identification of smoking as a CP risk factor was obtained from structured patient and physician questionnaires. We compared how often physician identified smoking as a CP risk factor in NAPS2-CV/NAPS2-AS studies with NAPS2-original study (2000–2006). Results: Enrolling physician identified smoking as a risk factor in significantly (all p< 0.001) greater proportion of patients in NAPS2-CV/AS studies when compared with NAPS2-original study among ever (80.7 vs. 45.3%), current (91.3 vs. 53%), past (60.3 vs. 30.2%) smokers, in those who smoked ≤1 pack/day (79.3 vs. 39.5%) or ≥1 packs/day (83 vs. 49.8%). In multivariable analyses, the enrolling physician was 3.32–8.49 times more likely to cite smoking as a CP risk factor in the NAPS2-CV/NAPS2-AS studies based on smoking status and amount after controlling for age, sex, race and alcohol etiology. The effect was independent of enrolling site in a sub-analysis limited to sites participating in both phases of enrollment. Conclusions: Availability of empiric data likely enhanced physician recognition of the association between smoking and CP. Wide-spread dissemination of this information could potentially curtail smoking rates in subjects with and those at risk of CP.


2015 ◽  
Vol 110 ◽  
pp. S4-S5
Author(s):  
Mitesh Patel ◽  
Ben P. Bradenham ◽  
Elie Chahla ◽  
Antonio R. Cheesman ◽  
Ravi Nayak ◽  
...  

Pancreas ◽  
2016 ◽  
Vol 45 (10) ◽  
pp. 1478-1484 ◽  
Author(s):  
Shallu Midha ◽  
Vishnubhatla Sreenivas ◽  
Madhulika Kabra ◽  
Tushar Kanti Chattopadhyay ◽  
Yogendra Kumar Joshi ◽  
...  

2012 ◽  
Vol 30 (3) ◽  
pp. 277-283 ◽  
Author(s):  
Petr Díte ◽  
Markéta Hermanová ◽  
Jan Trna ◽  
Ivo Novotný ◽  
Miloš Ružicka ◽  
...  

2018 ◽  
pp. 103-108
Author(s):  
O. S. Khukhlina ◽  
O. O. Ursul ◽  
I.V. Dudka ◽  
K. V. Viligorska ◽  
L. V. Kaniovska ◽  
...  

In the result of the study examined 79 patients, among them 30 patients with isolated course of COPD, stage ІІВ, 22 patients with COPD, stage ІІВ with comorbid CP in exacerbation phase, 27 patients with isolated course of CP. Smoking impacts deprivation of CFTR function, which regulates chlorine ions transport through chorine channel, localized in the epithelial cells of exocrine glands. The inhibition of the functioning of the chloride channel leads to thickening of the exocrine glands secret that results in its poor evacuation and then obstruction with fibrosis in the organs, such as lungs, liver, gallbladder, pancreas. That why tobacco smoking may be a risk factor for development not only COPD, but also CP.


Pancreatology ◽  
2018 ◽  
Vol 18 (4) ◽  
pp. S22
Author(s):  
Lu Hao ◽  
Yu Liu ◽  
Teng Wang ◽  
Ya-Wei Bi ◽  
Zhuan Liao ◽  
...  

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