Cigarette Smoking Is Independently Associated with Chronic Pancreatitis

Early diagnosis of chronic pancreatitis: understanding the factors associated with the development of chronic pancreatitis

“…There are studies reporting that in patients who developed idiopathic CP at 35 years of age or older, calcification of pancreatic calculi occurred earlier and more frequently, accelerating the progression of CP in smokers compared to nonsmokers 24,25) . Law et al 26) also analyzed the relationship between CP and smoking and demonstrated a significant positive correlation between higher total smoking amounts and higher rates of being diagnosed with CP. They concluded that smoking is a distinct independent risk factor from drinking.…”

Evaluation of Patients’ Knowledge Regarding Smoking and Chronic Pancreatitis: A Pilot Study

“…Recently, smoking has been identified as a major independent risk factor for chronic pancreatitis [2][3][4][5][6][7]. Along with alcohol, smoking is a strong lifestyle factor used to predict a patient's risk of developing pancreatitis [1].…”

“…Smoking has an additive effect when combined with alcohol [4] making it imperative that physicians stress both smoking and alcohol cessation. Law et al [5] found that smoking and its association with chronic pancreatitis can be considered independent of alcohol, is dosedependent and increases with alcohol consumption.…”

Smoking induced pancreatitis and pancreatic cancer

“…In light of the medical evidence linking tobacco smoking and pancreatitis, closer attention has been paid to smoking-induced changes in pancreatic tissue from patients enrolled in such studies (53,56,60,98,99,102,112). Some of those changes are highlighted below.…”

“…Rare mutations in CRTC prevent it from degrading trypsinogen and are associated with RAP and CP (128). The occurrence of such mutations in patients was evaluated from the North American Pancreatitis Study cohort II and it was found that a genetic variant, CTRC Variant G60G (c.180T), acted as a disease modifier, promoting progression of RAP to CP, particularly in the smoking population (60). The mechanism of how tobacco smoke or toxins interact with variants of CRTC to produce this disease phenotype is not yet clear.…”