Smoking and Acute Pancreatitis - It is about Time we Extinguish the Cigarette

Barreto SG*

Hepatobiliary and Oesophagogastric Unit, Division of Surgery and Perioperative Medicine, Australia

*Corresponding author: Savio George Barreto, Hepatobiliary and Oesophagogastric Unit, Division of Surgery and Perioperative Medicine, Australia

Received: January 27, 2017; Accepted: February 03, 2017; Published: February 06, 2017

Keywords

Disease; Pancreas; Inflammation; Public health

Short Communication

Alcohol and gallstones are the better known causes of acute pancreatitis (AP) the world over [1-3]. However, recent studies have unearthed a likely association between smoking and AP [4-7].

In an attempt to tease out the exact relationship between the two, I reviewed the evidence linking smoking, more specifically, the constituents of cigarette smoke, and their potential to trigger an attack of AP [8]. This led to the appreciation that the two main metabolites of cigarette smoke, nicotine and 4-(methylnitrosamino)- 1-(3-pyridyl)-1-butanone (NNK), are capable of inducing functional and histological changes within the pancreas consistent with AP. The pathways involved in the pathogenesis of smoking-induced AP include the sympathetic (via the a-7 nicotinic acetylcholine receptor and β-adrenergic receptors) and parasympathetic systems (through nicotinic preganglionic receptors), as well as, cholecystokinin (CCK) through their actions on acinar cells and zymogen secretion. Besides, nicotine with its inherent vasoconstrictive potential (inhibitory effect on endothelial nitric oxide synthase or stimulatory effect on endothelin-1) can act on the pancreatic microvasculature worsening AP that has been triggered off by another cause (alcohol or gallstones). Nicotine and acrolein have the potential (yet to be conclusively proven) to influence ductal secretion by contributing to cystic fibrosis trans membrane regulator (CFTR) dysfunction [8].

Edwin Thrower eloquently dissected out the cellular mechanisms by which the chemical constituents of cigarette smoke can alter calcium signalling, zymogen activation as well as affect thiamin levels in the acinar cell contributing to the development of AP [9].

Both these manuscripts provided a strong base to stimulate further research on the association between smoking and acute pancreatitis. More importantly, though, they lent credibility to the clinical concerns [4-7] raised about smoking being involved in the causation of AP. This has led to AP being added to the already long list of diseases (cardiovascular, metabolic and respiratory) caused by tobacco use. In the pancreas, itself, smoking has been acknowledged to be not only an important cause for chronic pancreatitis [10], but a leading risk factor for pancreatic cancer, including early onset disease [11].

We are well aware that smoking is a major contributor to the global burden of disease [12]. Recent reports have provided sufficient evidence that tobacco use and exposure begins at an early age [13]. As pancreatologist, we can no longer ignore the risks of smoking. We cannot afford to turn a blind eye and opt to sit out this ‘war against tobacco’ [14]. It is everyone’s problem!

The question remains, ‘how can we contribute?’. Adopting negative strategies such as Tobacco Industry Denormalization (TID) is less likely to yield success, owing to the lack of interest in such approaches by heavy smokers [15]. More so, these are strategies best left to policy makers. Instead, as clinicians we can adopt a more positive approach not only with patients, but our acquaintances as well, focusing on the ‘good’ effects of the cessation of smoking [15,16]. The use of such simple, but significant, strategies in our clinics, hospitals and everyday lives, needs to be more readily embraced if we are to do our bit in reducing the ever growing burden of tobaccorelated diseases.

Smoking and Acute Pancreatitis - It is about Time we Extinguish the Cigarette

Keywords

Short Communication

References