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 . 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 α-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 onendothelin-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 .
|Number of pages||2|
|Journal||Austin Pancreatic Disorders|
|Publication status||Published - 2017|
- Acute Pancreatitis