Gallstones are a common cause of pancreatitis. Gallstones, produced in the gallbladder, can slip out of the gallbladder and block the bile duct, stopping pancreatic enzymes from traveling to the small intestine and forcing them back into the pancreas.
The enzymes then begin to irritate the cells of the pancreas, causing the inflammation associated with pancreatitis. Pancreatitis is inflammation of the pancreas. The pancreas is a long, flat gland that sits tucked behind the stomach in the upper abdomen. The pancreas produces enzymes that help digestion and hormones that help regulate the way your body processes sugar glucose.
Pancreatitis can occur as acute pancreatitis — meaning it appears suddenly and lasts for days. Some people develop chronic pancreatitis, which is pancreatitis that occurs over many years. Mild cases of pancreatitis improve with treatment, but severe cases can cause life-threatening complications. Make an appointment with your doctor if you have acute onset or persistent abdominal pain. Seek immediate medical help if your abdominal pain is so severe that you can't sit still or find a position that makes you more comfortable.
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Also called somatic mutations, this means the genetic changes that led to cancer developed by chance after a person was born. They occur when gene mutations or changes are passed within a family from 1 generation to the next see below , raising the risk of pancreatic cancer.
These are also called germline mutations. See below for specific inherited conditions that increase a person's risk of pancreatic cancer. The risk of developing pancreatic cancer increases with age. Most people who develop pancreatic cancer are older than However, adults of any age can be diagnosed with pancreatic cancer. More men are diagnosed with pancreatic cancer than women see Statistics. Black people are more likely than Asian, Hispanic, or white people to develop pancreatic cancer.
People of Ashkenazi Jewish heritage are also more likely to develop pancreatic cancer see Family history, below. Learn more about quitting smoking. Obesity, diet, and alcohol. Regularly eating foods high in fat is a risk factor for pancreatic cancer. Research has shown that obese and even overweight people have a higher risk of being diagnosed with and dying from pancreatic cancer.
Chronic, heavy alcohol use can also increase the risk of pancreatic cancer, most likely by causing recurrent pancreatitis, which is repeated inflammation of the pancreas.
Learn more about how cancer risk relates to obesity , food choices , and drinking alcohol. Many studies have indicated that diabetes increases the risk of developing pancreatic cancer, especially when a person has had diabetes for many years. In addition, suddenly developing diabetes later in adulthood can be an early symptom of pancreatic cancer. However, it is important to remember that not all people who have diabetes or who are diagnosed with diabetes as adults develop pancreatic cancer.
Family history. This is called familial pancreatic cancer. You and your family may be at risk if 2 or more first-degree relatives or at least 3 members of the family have been diagnosed with pancreatic cancer. First-degree relatives include parents, children, and siblings.
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. This complication may present as gastrointestinal bleeding.
Other risk factors for the development of this complication include young age, female sex, repeated attempts of papilla cannulation and poor emptying of pancreatic duct after contrast injection. This complication can occur after abdominal or thoracic surgery.
It has been described in about 0. Significant risks for postoperative pancreatitis include renal insufficiency, hypotension, and infections. Intraoperative or postoperative medications may also cause pancreatitis [ 34 , 35 ].
Pancreatitis after transarterial embolization for the treatment of hepatocellular carcinoma results from a retrograde injection of the chemotherapeutic or embolic agents into pancreatic arteries, giving rise to ischemic pancreatitis [ 36 ].
Many infectious agents are associated with AP Table 1 , but no microorganism has ever been identified within the pancreas. Mumps and Coxsackie B virus are the most common causes of infectious pancreatitis. Clonorchis sinensis and Ascaris cause pancreatitis by invading and blocking the pancreatic duct [ 2 , 37 ].
AP may be caused by HIV infection or secondary to anti-retroviral treatment. In acquired immunodeficiency syndrome AIDS , other infectious agents may cause pancreatitis including Cytomegalovirus, Candida , Cryptosporidium neoformans , Toxoplasma gondii, Pneumocystis carinii and Mycobacterium avium complex [ 38 ]. Pancreatic ischemia has been reported in the following circumstances: hypotension, hemorrhagic shock, vasculitis systemic lupus erythematosus and polyarteritis nodosa , atheroembolism, hypothermia, haemolysis and emboli to pancreatic vessels.
It has been described episodes of AP in long-distance runners, on an ischemic basis [ 2 ]. AIP has distinct clinical and histological features. Two subtypes are known, the type 1 lymphoplasmacytic sclerosing pancreatitis is a multi-organ disease associated with IgG4, and type 2 idiopathic duct centric pancreatitis appears to be a pancreas-specific disorder with characteristic granulocyte-epithelial lesions [ 39 ].
Immunologic abnormalities including hypergammaglobulinemia, elevated serum IgG4 levels and the presence of autoantibodies against lactoferrin and carbonic anhydrase are important serological markers of the type 1 AIP.
Because the diagnosis can be elusive, several criteria have proposed to diagnose AIP. The most widely used in the United States are the HISORT criteria histology, imaging, serology, other organ involvement and response to therapy [ 40 ].
Abnormal imaging can be observed in computed tomography, magnetic resonance imaging or endoscopic ultrasound as multifocal or diffuse pancreatic-ductal narrowing, and abnormal enhancement or enlargement of the pancreas. Histologic confirmation is desirable and can be obtained by endoscopic ultrasound-guided biopsy of the pancreas.
AIP clearly responds to steroid therapy although spontaneous resolution without treatment has also been described; however relapses are relatively common.
In some cases, other immunosuppressive agents are necessary. It has been described that celiac disease is associated with a 3-fold increased risk of development any form of pancreatitis and even higher for CP HR: This increased risk was only found among celiac individuals diagnosed in adulthood, and was generally noted in the first year of diagnosis especially for CP and enzyme supplementation, but remained even 5 years after [ 7 ].
Several factors might contribute to the association between celiac disease and pancreatitis [ 13 ]. The earliest proposed mechanism was malnutrition, which impairs the secretion of pancreatic enzymes and influences the composition of the bile inducing microlithiasis, thus predisposing to development of pancreatitis.
Malnutrition has also been described to be associated with increased levels of pro-inflammatory cytokines as well as pancreatic acinar cell damage, ductal disruption and other structural changes, such as acinar atrophy.
Other proposed mechanisms include altered levels of autoregulatory enteric hormones cholecystokinin and papillary stenosis resulting from localized duodenal inflammation. Villous atrophy is associated with pancreatic insufficiency, and restored pancreatic enzyme levels are observed after introduction of a gluten-free diet. By contrast, the relationship between autoimmune pancreatitis and celiac disease has not been demonstrated, since there is only so far a case report of this association [ 42 ].
This condition is defined as pancreatitis with unknown etiology established after initial laboratory and imaging studies. In some patients the cause may be found after further investigations, but in others no definitive etiology is detected.
These patients should be evaluated at centers of excellence focusing on pancreatic diseases. Additionally, the role of genetic testing in idiopathic pancreatitis has yet to be determined, but the study of genetic abnormalities is being increasingly recognized [ 16 , 44 ]. Pancreatitis is a common digestive disorder with a broad spectrum of etiologies.
One of the primary goals in the diagnostic process of the pancreatitis should be to reduce the rate of idiopathic pancreatitis, because the identification of the cause of the disease may help to prevent subsequent relapses when the etiological factor is eliminated. Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution 3. Help us write another book on this subject and reach those readers.
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Our readership spans scientists, professors, researchers, librarians, and students, as well as business professionals. Downloaded: Introduction 1. Age and sex Although the incidence of AP do not differ according to sex, CP is more common among men.
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