Cigar smoking and the use of smokeless tobacco products also increase the risk. However, the risk of pancreatic cancer starts to drop once a person stops smoking. Being very overweight obese is a risk factor for pancreatic cancer. Gaining weight as an adult can also increase risk.
Carrying extra weight around the waistline may be a risk factor even in people who are not very overweight. Pancreatic cancer is more common in people with diabetes. The reason for this is not known.
Most of the risk is found in people with type 2 diabetes. This type of diabetes is increasing in children and adolescents as obesity in these age groups also rises. Type 2 diabetes in adults is also often related to being overweight or obese. Chronic pancreatitis, a long-term inflammation of the pancreas, is linked with an increased risk of pancreatic cancer.
Chronic pancreatitis is often seen with heavy alcohol use and smoking. Pathogenesis and the natural course of chronic pancreatitis. Eur J Gastroenterol Hepatol.
Drug-induced acute pancreatitis: an evidence-based review. Clin Gastroenterol Hepatol. Drug-induced pancreatitis: incidence, management and prevention. Drug Saf. Drug-induced pancreatitis: a practical review. Drugs Today Barc. Drug induced pancreatitis. Best Pract Res Clin Gastroenterol. Acute pancreatitis in inflammatory bowel disease, with special reference to azathioprine-induced pancreatitis. Aliment Pharmacol Ther.
A case of simva-statin-associated pancreatitis and review of statin-associated pancreatitis. Emergent management of pancreatitis. Updated June 9, Accessed November 14, Featured Issue Featured Supplements. It makes fluids that help to break down food in the small intestine. This problem is more common in men and people who are Black. Other things that may raise the risk are:. The main problem is mild to severe pain in the upper belly.
It may also spread to the back. Pain may be all the time or it may come and go. A pancreatic function test may be done. This test measures how well the pancreas is making a hormone needed to digest food. People who are not helped by these methods may need surgery. The type of surgery done depends on the reason for the pancreatitis.
Some choices are:. Chronic pancreatitis. Updated February 20, Accessed December 21, Tulane University School of Medicine website. Nutrition in chronic pancreatitis. World J Gastroenterol. The importance of this condition as cause of recurrent AP is not clearly established, although it has been considered to cause up to one third of all cases of idiopathic pancreatitis [ 16 ].
Sphincter of Oddi dysfunction. Revised Classification Milwaukee. The prevalence of AP is approximately 4-fold higher among subjects who are alcohol consumers compared to nondrinkers. Chronic alcoholic patients eventually develop CP after 10 to 20 years of continuous alcohol abuse. The contribution of the beverage type to this risk requires further studies [ 19 , 20 ].
Two pathogenic theories have been described. In one, alcohol-related injury is the result of perturbations in exocrine function leading to an increase of the lithogenicity of pancreatic juice and the formation of protein plugs and stones. Atrophy and fibrosis develop as a result of the obstructive process.
The other theory proposed a stepwise progression to fibrosis after recurrent attacks of AP. Inflammation and necrosis from the initial episodes of AP lead to areas of scarring, ductal obstruction, stasis and subsequent stone formation.
However, given the low rate of pancreatitis among heavy drinkers, it has been suggested that other genetic and environmental cofactors would be required for the development of alcoholic pancreatitis [ 19 , 21 ].
Tobacco and alcohol are cofactors that increase the risk of pancreatitis. Furthermore, both habits often coexist and are enhanced in a dose-dependent manner. However, large studies have suggested that smoking alone is an independent risk factor for both AP and CP [ 22 , 23 ].
It has been reported that smoking increases by approximately 2-fold the risk of non-gallstone-related AP, but not for gallstone-related pancreatitis. This risk was higher in patients who consumed alcohol, current smokers and those with more than 20 packs-years of smoking, particularly if they met the three characteristics relative risk, 4.
At this time, there is very little information about the pathogenesis of smoking-induced pancreatitis compared with those of other causes. Data from animal models suggest several potential mechanisms such as altered gene expression in the exocrine pancreas and activation of pancreatic enzymes with acinar cell damage.
Nicotine has also been shown to modulate the oxidative stress and lipid peroxidation and these processes might be involved in the pathophysiology of acute and chronic pancreatitis. Over one hundred of different medications have been related in the development of the disease by several mechanims. These include immunologic reactions azathioprine, 6-mercaptopurine, aminosalicylates, sulfonamides , a direct toxic effect diuretics, sulfonamides , accumulation of toxic metabolites valproic acid, didanosine, pentamidine, tetracycline , ischemia diuretics, azathioprine , intravascular thrombosis estrogen , and increased viscosity of pancreatic juice diuretics and steroids.
No medications are known to cause CP. The time interval between beginning of the drug and the development of the disease is highly variable, depending on the substance involved and its pathogenic mechanism. Therefore, a high index of suspicion and a detailed drug history are essential for making the diagnosis [ 27 , 28 ]. Organophosphate pesticides, arachnids and reptiles venoms have been described to cause AP by cholinergic stimulation [ 2 ].
Cocaine consumption may cause pancreatitis by vasoconstrictor and ischemic effects [ 29 ]. Data modified from Badalov N et al [ 28 ]. Mild-to-moderate hyperlipidemia is often secondary to alcoholic AP, and should not be confused with marked hypertriglyceridemia causing AP [ 2 ]. The mechanism of hypertriglyceridemia induced pancreatitis is unclear though some authors suggest stimulation of amylase release, cell damage from free fatty acids and chylomicrons in acinar cells, and sluggish flow in the capillaries resulting in ischemic injury [ 13 ].
This is a rare cause of AP and almost always happens as result of concomitant hyperparathyroidism. Pancreatitis has been reported to be related to endogenous hypercalcemia by disseminated carcinoma and after iatrogenic effect, for example with total parenteral nutrition or vitamin D poisoning.
Proposed mechanisms include deposition of calcium in pancreatic duct and calcium activation of trypsinogen within the pancreatic parenchyma. Because the incidence of pancreatitis is low in patients with chronic hypercalcemia, additional factors are probable necessary to induce acute episodes [ 13 , 30 ]. In pancreatitis, alterations in several genes have so far been described [ 31 ].
This disorder is associated with mutations in the trypsinogen gen PRSS1 that promotes the premature conversion of trypsinogen to active trypsin, resulting in pancreatic autodigestion. This genetic syndrome is characterized by a strong family history of pancreatic disease, and most patients develop recurrent pancreatitis from childhood, with progressive evolution to CP and a significant increase in risk of pancreatic cancer. Severe homozygote mutations in CFTR gene cause cystic fibrosis. Patients who are compound heterozygotes for mild mutations have 40 to fold increased risk of developing CP compared with the general population, without presenting other manifestations of cystic fibrosis and with a normal sweat chloride test.
Patients who have severe mutations typically develop CP in childhood. Other mutations predispose to the development, but do not necessarily cause pancreatitis. Both types of injuries may cause pancreatitis in about 0. These conditions can lead to acute duct rupture and pancreatic ascites.
The low rates of AP after trauma result from the retroperitoneal location of the gland. The injury healing may result in a narrowing of the main pancreatic duct, causing obstructive pancreatitis in the gland downstream from the stricture. Rarely a posterior duodenal ulcer can penetrate into the pancreas and thereby induce AP.
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