Autoimmune pancreatitis

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Autoimmune Pancreatitis
Other namesAIP
Specialty Gastroenterology
Symptoms Painless jaundice, pancreatic mass
TypesType 1 and Type 2
Causes IgG4-related disease
Diagnostic method Biopsy, imaging, serology
Differential diagnosis Pancreatic cancer
Treatment Corticosteroids (first line), azathioprine, rituximab

Autoimmune Pancreatitis (AIP) is an increasingly recognized type of chronic pancreatitis that can be difficult to distinguish from pancreatic carcinoma but which responds to treatment with corticosteroids, particularly prednisone. [1] Although autoimmune pancreatitis is quite rare, it constitutes an important clinical problem for both patients and their clinicians: the disease commonly presents itself as a tumorous mass which is diagnostically indistinguishable from pancreatic cancer, a disease that is much more common in addition to being very dangerous. Hence, some patients undergo pancreatic surgery, which is associated to substantial mortality and morbidity, out of the fear by patients and clinicians to undertreat a malignancy. However, surgery is not a good treatment for this condition as AIP responds well to immunosuppressive treatment. There are two categories of AIP: Type 1 and Type 2, each with distinct clinical profiles.

Contents

Type 1 AIP is now regarded as a manifestation of IgG4-related disease, [2] and those affected have tended to be older and to have a high relapse rate. Type 1 pancreatitis, is as such as manifestation of IgG4 disease, which may also affect bile ducts in the liver, salivary glands, kidneys and lymph nodes. Type 2 AIP seems to affect only the pancreas, although about one-third of people with type 2 AIP have associated inflammatory bowel disease. AIP occurring in association with an autoimmune disorder has been referred to as "secondary" or "syndromic" AIP. AIP does not affect long-term survival. [3]

Signs and symptoms

Autoimmune pancreatitis may cause a variety of symptoms and signs, which include pancreatic and biliary (bile duct) manifestations, as well as systemic effects of the disease. Two-thirds of patients present with either painless jaundice due to bile duct obstruction or a "mass" in the head of the pancreas, mimicking carcinoma. As such, a thorough evaluation to rule out cancer is important in cases of suspected AIP. [4]

Type 1 AIP typically presents in a 60–70-year-old male with painless jaundice. In some cases, imaging reveals a mass in the pancreas or diffuse pancreatic enlargement. [4] Narrowing in the pancreatic duct called strictures may occur. [4] Rarely, Type 1 AIP presents with acute pancreatitis. [4] Type 1 AIP presents with manifestations of autoimmune disease (IgG4 related) in at least half of cases. The most common form of systemic involvement is cholangitis, which occurs in up to 80 percent of cases of Type 1 AIP. Additional manifestations include inflammation in the salivary glands (chronic sclerosing sialadenitis), in the lungs resulting in scarring (pulmonary fibrosis) and nodules, scarring within the chest cavity (mediastinal fibrosis) or in the anatomic space behind the abdomen (retroperitoneal fibrosis) and inflammation in the kidneys (tubulointerstitial nephritis). [4]

AIP is characterized by the following features:

  1. Scleral Icterus (yellow eyes), jaundice (yellow skin) which is usually painless, usually without acute attacks of pancreatitis.
  2. Relatively mild symptoms, such as minimal weight loss or nausea.
  3. Increased serum levels of gamma globulins, immunoglobulin G (IgG) or IgG4.
  4. The presence of serum autoantibodies such as anti-nuclear antibody (ANA), anti-lactoferrin antibody, anti-carbonic anhydrase II antibody, and rheumatoid factor (RF).
  5. Contrast-enhanced CT demonstrates a diffusely enlarged (sausage-shaped) pancreas.
  6. Diffuse irregular narrowing of the main pancreatic duct, and stenosis of the intrapancreatic bile duct on endoscopic retrograde cholangiopancreatography (ERCP).
  7. Rare pancreatic calcification or cyst formation.
  8. Marked responsiveness to treatment with corticosteroids.

Histopathology

Histopathologic examination of the pancreas reveals a characteristic lymphoplasmacytic infiltrate of CD4- or CD8-positive lymphocytes and IgG4-positive plasma cells, and exhibits interstitial fibrosis and acinar cell atrophy in later stages. At the initial stages, typically, there is a cuff of lymphoplasma cells surrounding the ducts but also more diffuse infiltration in the lobular parenchyma. However, localization and the degree of duct wall infiltration are variable. Whereas histopathologic examination remains the primary method for differentiation of AIP from acute and chronic pancreatitis, lymphoma, and cancer. By Fine Needle Aspiration (FNA) the diagnosis can be made if adequate tissue is obtained. In such cases, lymphoplasmacytic infiltration of the lobules are the key finding. Rarely, granulomatous reaction could be observed. It has been proposed that a cytologic smear primarily composed of acini rich in chronic inflammatory cells (lymphocytes, plasma cells), with rare ductal epithelial cells lacking atypia, favors the diagnosis of AIP. The sensitivity and the specificity of these criteria for differentiating AIP from neoplasia are unknown. In cases of systemic manifestation of AIP, the pathologic features are similar in other organs. [5]

Although the exact mechanism explaining the clinical manifestations of autoimmune pancreatitis remain for an important part obscure, most professionals would agree that the development of IgG4 antibodies, recognizing an epitiope on the membrane of pancreatic ancinar cells is an important factor in the pathophysiology of the disease. These antibodies are postulated to provoke an immune response against these ancinar cells resulting in pancreatic inflammation and destruction. [5] Knowing the auto-antigens involved would allow early diagnosis of the disease, its differentiation from a diagnosis of pancreatic cancer, and potentially even prevention, but unfortunately these remain obscure. An earlier publication suggested that the human ubiquitin-protein ligase E3 component n-recognin 2 (UBR2) was an important antigen [6] but follow up studies suggested this finding is likely to be an artifact. [7] Hence improved diagnosis, understanding and treatment of autoimmune pancreatitis awaits the identification of the auto-antigens involved.

Diagnosis

Criteria

Most recently the fourteenth Congress of the International Association of Pancreatology developed the International Consensus Diagnostic Criteria (ICDC) for AIP. The ICDC emphasizes five cardinal features of AIP which includes the imaging appearance of pancreatic parenchyma and the pancreatic duct, serum IgG4 level, other organ involvement with IgG4-related disease, pancreatic histology and response to steroid therapy. [8]

In 2002, the Japanese Pancreas Society proposed the following diagnostic criteria for autoimmune pancreatitis: [9]

I. Pancreatic imaging studies show diffuse narrowing of the main pancreatic duct with irregular wall (more than 1/3 of length of the entire pancreas).
II. Laboratory data demonstrate abnormally elevated levels of serum gamma globulin and/or IgG, or the presence of autoantibodies.
III. Histopathologic examination of the pancreas shows fibrotic changes with lymphocyte and plasma cell infiltrate.

For diagnosis, criterion I (pancreatic imaging) must be present with criterion II (laboratory data) and/or III (histopathologic findings). [10]

Mayo Clinic has come up with five diagnostic criteria called HISORt criteria which stands for histology, imaging, serology, other organ involvement, and response to steroid therapy. [11]

Radiologic features

Computed tomography (CT) findings in AIP include a diffusely enlarged hypodense pancreas or a focal mass that may be mistaken for a pancreatic malignancy. [8] A low-density, capsule-like rim on CT (possibly corresponding to an inflammatory process involving peripancreatic tissues) is thought to be an additional characteristic feature (thus the mnemonic: sausage-shaped). Magnetic resonance imaging (MRI) reveals a diffusely decreased signal intensity and delayed enhancement on dynamic scanning. The characteristic ERCP finding is segmental or diffuse irregular narrowing of the main pancreatic duct, usually accompanied by an extrinsic-appearing stricture of the distal bile duct. Changes in the extrapancreatic bile duct similar to those of primary sclerosing cholangitis (PSC) have been reported.[ citation needed ]

The role of endoscopic ultrasound (EUS) and EUS-guided fine-needle aspiration (EUS-FNA) in the diagnosis of AIP is not well described, and EUS findings have been described in only a small number of patients. In one study, EUS revealed a diffusely swollen and hypoechoic pancreas in 8 of the 14 (57%) patients, and a solitary, focal, irregular mass was observed in 6 (46%) patients. Whereas EUS-FNA is sensitive and specific for the diagnosis of pancreatic malignancy, its role in the diagnosis of AIP remains unclear.[ citation needed ]

Treatment

AIP often completely resolves with steroid treatment. The failure to differentiate AIP from malignancy may lead to unnecessary pancreatic resection, and the characteristic lymphoplasmacytic infiltrate of AIP has been found in up to 23% of patients undergoing pancreatic resection for suspected malignancy who are ultimately found to have benign disease. In this subset of patients, a trial of steroid therapy may have prevented a Whipple procedure or complete pancreatectomy for a benign disease which responds well to medical therapy. [12] "This benign disease resembles pancreatic carcinoma both clinically and radiographically. The diagnosis of autoimmune pancreatitis is challenging to make. However, accurate and timely diagnosis may preempt the misdiagnosis of cancer and decrease the number of unnecessary pancreatic resections." [13] Autoimmune pancreatitis responds dramatically to corticosteroid treatment. [13]

If relapse occurs after corticosteroid treatment or corticosteroid treatment is not tolerated, immunomodulators may be used. Immunomodulators such as azathioprine, and 6-mercaptopurine have been shown to extend remission of autoimmune pancreatitis after corticosteroid treatment. If corticosteroid and immunomodulator treatments are not sufficient, rituximab may also be used. Rituximab has been shown to induce and maintain remission. [14]

Prognosis

AIP does not affect long-term survival. [3]

Epidemiology

AIP is relatively uncommon, [15] with an overall global prevalence less than 1 per 100,000. Type 1 AIP is more common in East Asia, whereas type 2 is relatively more common in the US and Europe. The prevalence of AIP may be increasing in Japan. [16] Type 1 AIP occurs three times more often in men than women. [4]

Controversies in nomenclature

As the number of published cases of AIP has increased, efforts have been focused on defining AIP as a distinct clinical and pathologic entity and toward developing some generally agreed upon diagnostic criteria and nomenclature. Terms frequently encountered are autoimmune or autoimmune-related pancreatitis, lymphoplasmacytic sclerosing pancreatitis, idiopathic tumefactive chronic pancreatitis, idiopathic pancreatitis with focal irregular narrowing of the main pancreatic duct, and non-alcoholic duct destructive chronic pancreatitis. There are also a large number of case reports employing descriptive terminology such as pancreatitis associated with Sjögren's syndrome, primary sclerosing cholangitis, or inflammatory bowel disease. Some of the earliest cases were reported as pancreatic pseudotumor or pseudolymphoma.[ citation needed ]

Related Research Articles

<span class="mw-page-title-main">Pancreas</span> Organ of the digestive system and endocrine system of vertebrates

The pancreas is an organ of the digestive system and endocrine system of vertebrates. In humans, it is located in the abdomen behind the stomach and functions as a gland. The pancreas is a mixed or heterocrine gland, i.e., it has both an endocrine and a digestive exocrine function. 99% of the pancreas is exocrine and 1% is endocrine. As an endocrine gland, it functions mostly to regulate blood sugar levels, secreting the hormones insulin, glucagon, somatostatin and pancreatic polypeptide. As a part of the digestive system, it functions as an exocrine gland secreting pancreatic juice into the duodenum through the pancreatic duct. This juice contains bicarbonate, which neutralizes acid entering the duodenum from the stomach; and digestive enzymes, which break down carbohydrates, proteins and fats in food entering the duodenum from the stomach.

<span class="mw-page-title-main">Pancreatitis</span> Inflammation of the pancreas

Pancreatitis is a condition characterized by inflammation of the pancreas. The pancreas is a large organ behind the stomach that produces digestive enzymes and a number of hormones. There are two main types: acute pancreatitis, and chronic pancreatitis.

<span class="mw-page-title-main">Pancreatic cancer</span> Type of endocrine gland cancer

Pancreatic cancer arises when cells in the pancreas, a glandular organ behind the stomach, begin to multiply out of control and form a mass. These cancerous cells have the ability to invade other parts of the body. A number of types of pancreatic cancer are known.

<span class="mw-page-title-main">Autoimmune hepatitis</span> Chronic, autoimmune disease of the liver

Autoimmune hepatitis, formerly known as lupoid hepatitis, plasma cell hepatitis, or autoimmune chronic active hepatitis, is a chronic, autoimmune disease of the liver that occurs when the body's immune system attacks liver cells, causing the liver to be inflamed. Common initial symptoms may include fatigue, nausea, muscle aches, or weight loss or signs of acute liver inflammation including fever, jaundice, and right upper quadrant abdominal pain. Individuals with autoimmune hepatitis often have no initial symptoms and the disease may be detected by abnormal liver function tests and increased protein levels during routine bloodwork or the observation of an abnormal-looking liver during abdominal surgery.

<span class="mw-page-title-main">Primary biliary cholangitis</span> Autoimmune disease of the liver

Primary biliary cholangitis (PBC), previously known as primary biliary cirrhosis, is an autoimmune disease of the liver. It results from a slow, progressive destruction of the small bile ducts of the liver, causing bile and other toxins to build up in the liver, a condition called cholestasis. Further slow damage to the liver tissue can lead to scarring, fibrosis, and eventually cirrhosis.

<span class="mw-page-title-main">Endoscopic retrograde cholangiopancreatography</span> Use of endoscopy and fluoroscopy to treat and diagnose digestive issues.

Endoscopic retrograde cholangiopancreatography (ERCP) is a technique that combines the use of endoscopy and fluoroscopy to diagnose and treat certain problems of the biliary or pancreatic ductal systems. It is primarily performed by highly skilled and specialty trained gastroenterologists. Through the endoscope, the physician can see the inside of the stomach and duodenum, and inject a contrast medium into the ducts in the biliary tree and pancreas so they can be seen on radiographs.

<span class="mw-page-title-main">Primary sclerosing cholangitis</span> Medical condition

Primary sclerosing cholangitis (PSC) is a long-term progressive disease of the liver and gallbladder characterized by inflammation and scarring of the bile ducts, which normally allow bile to drain from the gallbladder. Affected individuals may have no symptoms or may experience signs and symptoms of liver disease, such as yellow discoloration of the skin and eyes, itching, and abdominal pain.

<span class="mw-page-title-main">Acute pancreatitis</span> Medical condition

Acute pancreatitis (AP) is a sudden inflammation of the pancreas. Causes, in order of frequency, include: a gallstone impacted in the common bile duct beyond the point where the pancreatic duct joins it; heavy alcohol use; systemic disease; trauma; and, in children, mumps. Acute pancreatitis may be a single event; it may be recurrent; or it may progress to chronic pancreatitis and/or pancreatic failure.

<span class="mw-page-title-main">Chronic pancreatitis</span> Medical condition

Chronic pancreatitis is a long-standing inflammation of the pancreas that alters the organ's normal structure and functions. It can present as episodes of acute inflammation in a previously injured pancreas, or as chronic damage with persistent pain or malabsorption. It is a disease process characterized by irreversible damage to the pancreas as distinct from reversible changes in acute pancreatitis. Tobacco smoke and alcohol misuse are two of the most frequently implicated causes, and the two risk factors are thought to have a synergistic effect with regards to the development of chronic pancreatitis. Chronic pancreatitis is a risk factor for the development of pancreatic cancer.

<span class="mw-page-title-main">Gastrointestinal disease</span> Medical condition

Gastrointestinal diseases refer to diseases involving the gastrointestinal tract, namely the esophagus, stomach, small intestine, large intestine and rectum; and the accessory organs of digestion, the liver, gallbladder, and pancreas.

Retroperitoneal fibrosis or Ormond's disease is a disease featuring the proliferation of fibrous tissue in the retroperitoneum, the compartment of the body containing the kidneys, aorta, renal tract, and various other structures. It may present with lower back pain, kidney failure, hypertension, deep vein thrombosis, and other obstructive symptoms. It is named after John Kelso Ormond, who rediscovered the condition in 1948.

<span class="mw-page-title-main">Exocrine pancreatic insufficiency</span> Human disease

Exocrine pancreatic insufficiency (EPI) is the inability to properly digest food due to a lack or reduction of digestive enzymes made by the pancreas. EPI can occur in humans and is prevalent in many conditions such as cystic fibrosis, Shwachman–Diamond syndrome, different types of pancreatitis, multiple types of diabetes mellitus, advanced renal disease, older adults, celiac disease, IBS-D, IBD, HIV, alcohol-related liver disease, Sjogren syndrome, tobacco use, and use of somatostatin analogues.

<span class="mw-page-title-main">Eosinophilic gastroenteritis</span> Medical condition

Eosinophilic gastroenteritis, also known as eosinophilic enteritis, is a rare and heterogeneous condition characterized by patchy or diffuse eosinophilic infiltration of gastrointestinal (GI) tissue, first described by Kaijser in 1937. Presentation may vary depending on location as well as depth and extent of bowel wall involvement and usually runs a chronic relapsing course. It can be classified into mucosal, muscular and serosal types based on the depth of involvement. Any part of the GI tract can be affected, and isolated biliary tract involvement has also been reported. The stomach is the organ most commonly affected, followed by the small intestine and the colon.

<span class="mw-page-title-main">Sphincter of Oddi dysfunction</span> Medical condition

Sphincter of Oddi dysfunction refers to a group of functional disorders leading to abdominal pain due to dysfunction of the Sphincter of Oddi: functional biliary sphincter of Oddi and functional pancreatic sphincter of Oddi disorder. The sphincter of Oddi is a sphincter muscle, a circular band of muscle at the bottom of the biliary tree which controls the flow of pancreatic juices and bile into the second part of the duodenum. The pathogenesis of this condition is recognized to encompass stenosis or dyskinesia of the sphincter of Oddi ; consequently the terms biliary dyskinesia, papillary stenosis, and postcholecystectomy syndrome have all been used to describe this condition. Both stenosis and dyskinesia can obstruct flow through the sphincter of Oddi and can therefore cause retention of bile in the biliary tree and pancreatic juice in the pancreatic duct.

Multifocal fibrosclerosis and idiopathic fibrosclerosis are disorders of unknown aetiology, characterised by fibrous lesions (co-)occurring at a variety of sites. Known manifestations include retroperitoneal fibrosis, mediastinal fibrosis and Riedel's thyroiditis.

<span class="mw-page-title-main">Idiopathic sclerosing mesenteritis</span> Medical condition

Idiopathic sclerosing mesenteritis (ISM) is a rare disease of the small intestine, characterized by chronic inflammation and eventual fibrosis of the mesentery. It has also been called mesenteric lipodystrophy, or retractile mesenteritis.

<span class="mw-page-title-main">IgG4-related disease</span> Medical condition

IgG4-related disease (IgG4-RD), formerly known as IgG4-related systemic disease, is a chronic inflammatory condition characterized by tissue infiltration with lymphocytes and IgG4-secreting plasma cells, various degrees of fibrosis (scarring) and a usually prompt response to oral steroids. In approximately 51–70% of people with this disease, serum IgG4 concentrations are elevated during an acute phase.

Chronic sclerosing sialadenitis is a chronic (long-lasting) inflammatory condition affecting the salivary gland. Relatively rare in occurrence, this condition is benign, but presents as hard, indurated and enlarged masses that are clinically indistinguishable from salivary gland neoplasms or tumors. It is now regarded as a manifestation of IgG4-related disease.

Pancreaticobiliary maljunction(PBM) is a congenital malformation where the pancreatic and bile ducts meet outside of the duodenum. There are two varieties of PBM: one with biliary dilatation and the other without. When an abnormally long common channel is visible on direct cholangiography, such as endoscopic retrograde cholangiopancreatography or magnetic resonance cholangiopancreatography, PBM is diagnosed.

<span class="mw-page-title-main">IgG4-related prostatitis</span> Medical condition

IgG4-related prostatitis is prostate involvement in men with IgG4-related disease (IgG4-RD), which is an emerging fibroinflammatory disease entity which is characterised (i) by a tendency to mass forming lesions in multiple sites of the body and (ii) by usually a prompt response to steroid therapy.

References

  1. ↑ Rose, Noel R.; Mackay, Ian R. (2006). The autoimmune diseases (4th ed.). Academic Press. p.  783. ISBN   978-0-12-595961-2.
  2. ↑ Stone, John H.; Khosroshahi, Arezou; Deshpande, Vikram; Chan, John K. C.; Heathcote, J. Godfrey; Aalberse, Rob; Azumi, Atsushi; Bloch, Donald B.; Brugge, William R.; Carruthers, Mollie N.; Cheuk, Wah; Cornell, Lynn; Castillo, Carlos Fernandez-Del; Ferry, Judith A.; Forcione, David; Klöppel, Günter; Hamilos, Daniel L.; Kamisawa, Terumi; Kasashima, Satomi; Kawa, Shigeyuki; Kawano, Mitsuhiro; Masaki, Yasufumi; Notohara, Kenji; Okazaki, Kazuichi; Ryu, Ji Kon; Saeki, Takako; Sahani, Dushyant; Sato, Yasuharu; Smyrk, Thomas; Stone, James R.; Takahira, Masayuki; Umehara, Hisanori; Webster, George; Yamamoto, Motohisa; Yi, Eunhee; Yoshino, Tadashi; Zamboni, Giuseppe; Zen, Yoh; Chari, Suresh (2012). "Recommendations for the nomenclature of IgG4-related disease and its individual organ system manifestations". Arthritis & Rheumatism. 64 (10): 3061–7. doi:10.1002/art.34593. PMC   5963880 . PMID   22736240.
  3. 1 2 Sah, Raghuwansh P.; Chari, Suresh T.; Pannala, Rahul; Sugumar, Aravind; Clain, Jonathan E.; Levy, Michael J.; Pearson, Randall K.; Smyrk, Thomas C.; Petersen, Bret T.; Topazian, Mark D.; Takahashi, Naoki; Farnell, Michael B.; Vege, Santhi S. (2010). "Differences in Clinical Profile and Relapse Rate of Type 1 Versus Type 2 Autoimmune Pancreatitis". Gastroenterology. 139 (1): 140–8, quiz e12–3. doi: 10.1053/j.gastro.2010.03.054 . PMID   20353791.
  4. 1 2 3 4 5 6 Nagpal, Sajan Jiv Singh; Sharma, Ayush; Chari, Suresh T. (September 2018). "Autoimmune Pancreatitis". American Journal of Gastroenterology. 113 (9): 1301. doi:10.1038/s41395-018-0146-0. PMID   29910463. S2CID   49268848.
  5. 1 2 Kamisawa, Terumi; Takuma, Kensuke; Egawa, Naoto; Tsuruta, Koji; Sasaki, Tsuneo (July 2010). "Autoimmune pancreatitis and IgG4-related sclerosing disease". Nature Reviews Gastroenterology & Hepatology. 7 (7): 401–409. doi:10.1038/nrgastro.2010.81. PMID   20548323. S2CID   3039273.
  6. ↑ Frulloni, Lucca; Lunardi, Claudio; Simone, Rita; Scattolini, Chiara; Falconi, Massimo; Benini, Luigi; Vantini, Italo; Corrocher, Roberto; Puccetti, Antonio (November 2009). "Identification of a novel antibody associated with autoimmune pancreatitis". New England Journal of Medicine. 361 (22): 2135–42. doi: 10.1056/NEJMoa0903068 . PMID   19940298.
  7. ↑ Buijs, Jorie; Cahen, Djuna; van Heerde, Marianne; Hansen, Bettina; van Buuren, Henk; Peppelenbosch, Maikel; Fuhler, Gwenny; Bruno, Marco (November 2016). "Testing for Anti-PBP Antibody Is Not Useful in Diagnosing Autoimmune Pancreatitis". American Journal of Gastroenterology. 111 (11): 1650–54. doi:10.1038/ajg.2016.241. PMID   27325222. S2CID   21363945.
  8. 1 2 Khandelwal, Ashish; Shanbhogue, Alampady Krishna; Takahashi, Naoki; Sandrasegaran, Kumaresan; Prasad, Srinivasa R. (2014). "Recent Advances in the Diagnosis and Management of Autoimmune Pancreatitis". American Journal of Roentgenology. 202 (5): 1007–21. doi:10.2214/AJR.13.11247. PMID   24758653.
  9. ↑ Kamisawa, T.; Okazaki, K.; Kawa, S. (2008). "Diagnostic criteria for autoimmune pancreatitis in Japan". World Journal of Gastroenterology. 14 (32): 4992–4994. doi: 10.3748/wjg.14.4992 . PMC   2742924 . PMID   18763279.
  10. ↑ Okazaki, Kazuichi; Uchida, Kazushige; Matsushita, Mitsunobu; Takaoka, Makoto (2007). "How to diagnose autoimmune pancreatitis by the revised Japanese clinical criteria". Journal of Gastroenterology. 42 (Suppl 18): 32–8. doi:10.1007/s00535-007-2049-5. PMID   17520221. S2CID   24338875.
  11. ↑ O'Reilly, Derek A; Malde, Deep J; Duncan, Trish; Rao, Madhu; Filobbos, Rafik (2014). "Review of the diagnosis, classification and management of autoimmune pancreatitis". World Journal of Gastrointestinal Pathophysiology. 5 (2): 71–81. doi: 10.4291/wjgp.v5.i2.71 . PMC   4025075 . PMID   24891978.
  12. ↑ Lin, Lien-Fu; Huang, Pi-Teh; Ho, Ka-Sic; Tung, Jai-Nien (2008). "Autoimmune Chronic Pancreatitis". Journal of the Chinese Medical Association. 71 (1): 14–22. doi: 10.1016/S1726-4901(08)70067-4 . PMID   18218555. S2CID   23254447.
  13. 1 2 Law, R.; Bronner, M.; Vogt, D.; Stevens, T. (2009). "Autoimmune pancreatitis: A mimic of pancreatic cancer". Cleveland Clinic Journal of Medicine. 76 (10): 607–15. doi: 10.3949/ccjm.76a.09039 . PMID   19797461.
  14. ↑ Hart, Phil; Chari, Suresh (2013). "Immunomodulators and Rituximab in the Management of Autoimmune Pancreatitis". Pancreapedia. doi: 10.3998/panc.2013.20 .
  15. ↑ Chari, Suresh T.; Smyrk, Thomas C.; Levy, Michael J.; Topazian, Mark D.; Takahashi, Naoki; Zhang, Lizhi; Clain, Jonathan E.; Pearson, Randall K.; Petersen, Bret T.; Vege, Santhi Swaroop (2006). "Diagnosis of Autoimmune Pancreatitis: The Mayo Clinic Experience". Clinical Gastroenterology and Hepatology. 4 (8): 1010–6, quiz 934. doi:10.1016/j.cgh.2006.05.017. PMID   16843735.
  16. ↑ Okazaki, K (November 2003). "Autoimmune pancreatitis is increasing in Japan". Gastroenterology. 125 (5): 1557–8. doi: 10.1016/j.gastro.2003.09.011 . PMID   14628815.
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