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Open Access Review
Rare Causes of Acute Pancreatitis: Drugs, Eosinophilia, and Autoimmunity

Mauro Turrin *

Former Department of Internal Medicine, Ospedali Riuniti Padova Sud “Madre Teresa di Calcutta”, Monselice (Padova), Italy

Correspondence: Mauro Turrin

Academic Editor:  Prashanth Rawla

Special Issue: Pancreatitis: New Insights into Etiology, Pathogenesis, Diagnosis, Management and Complications

Received: March 15, 2019 | Accepted: August 20, 2019 | Published: August 29, 2019

OBM Hepatology and Gastroenterology 2019, Volume 3, Issue 3, doi:10.21926/obm.hg.1903034

Recommended citation: Turrin M. Rare Causes of Acute Pancreatitis: Drugs, Eosinophilia, and Autoimmunity. OBM Hepatology and Gastroenterology 2019;3(3):20; doi:10.21926/obm.hg.1903034.

© 2019 by the authors. This is an open access article distributed under the conditions of the Creative Commons by Attribution License, which permits unrestricted use, distribution, and reproduction in any medium or format, provided the original work is correctly cited.


Background: Among the rarest causes of acute pancreatitis, in addition to the drugs (DIAP), there are eosinophilic pancreatitis (EP) and autoimmune pancreatitis (AIP).

Methods: We surveyed on PUBMED the descriptions of clinical cases of eosinophilic pancreatitis appeared from 1990 to June 2019 and those related to new drugs responsible for acute pancreatitis.

Results: We found forty reports on eosinophilic pancreatitis associated or not with hypereosinophilia and gastro-intestinal manifestations. There are several reports on drugs implicated in acute pancreatitis.

Conclusions: Here we discuss the importance of hypereosinophilia in EP and IgG–4 increase in Type 1 AIP. Differential diagnosis with pancreatic neoplasms and therapy schedules are also discussed as well.


Acute pancreatitis; drug-induced pancreatitis; eosinophilic pancreatitis; autoimmune pancreatitis; immunoglobulin G4-related disease 

1. Introduction

Eosinophilic pancreatitis (EP) is a very rare disease. In the list of rare diseases compiled by Orphanet register [1], this term does not appear. The list includes autoimmune type 1 pancreatitis at no. 280302 (Synonym: lymphoplasmocytic sclerosing pancreatitis or IgG4-related pancreatitis) and type 2 at no. 280315 (Synonym: duct-centric pancreatitis). However, their prevalence is not defined and at no. 103919, undefined autoimmune pancreatitis (AIP) has been placed.

EP is a benign form, it is accompanied in 80% of cases with peripheral eosinophilia and can be associated with idiopathic hypereosinophilic syndrome (HIES), which is defined as a non-clonal lymphoproliferative multisystem disease characterized by persistent eosinophilia and associated with infiltration and damage to the eosinophilia-associated organ.

 It is characterized by a persistent eosinophil count >1,500/μL for more than six months (normal: <500/μL), the absence of etiology identifiable by eosinophilia, and the presence of signs and other symptoms associated with the organs such as heart, lungs, gastrointestinal tract, skin, and nervous system. It is often associated, in up to 85% of patients, with eosinophilic gastroenteritis (EoG) [102].

In the Orphanet register [1] the "hypereosinophilic syndrome with undetermined significance" (HEUS) is classified at the number 3260 (phenotype MIM number: 607685). Its prevalence is unknown and the age of onset is between 20 and 50 years with male/female ratio = 4–9:1.

The forms of EP described in the literature [2,3,4,5,6,7,8,9,10,11,13,14,15,16,17,18,19,20,21,22,24,25,26,27,28] do not present a particular clinical picture, and in most cases, they were treated surgically because they  were detected as pseudocystic tumor like forms [2,3,4,5,6,8,9,13,14,15,29,106].  Eosinophilic pancreatitis often occurs in an acute form.

In the frequent cases associated with hypereosinophilia, the diagnosis is suggestive but must be confirmed by biopsy and also to exclude autoimmune pancreatitis.

Autoimmune pancreatitis (AIP) is a fibro-inflammatory disease that accounts for 4.6–5% of chronic pancreatitis. It presents a widespread or focal involvement of the pancreas, progressive in nature, which is manifested by jaundice, associated or not to pancreatic mass. It is currently included in the hyper-IgG4 pathology group.

Acute pancreatitis can depend on several causes (Table 1).

Table 1 Etiology of acute pancreatitis. Modified from earlier studies [49,50].

Eosinophilic pancreatitis is not reported in this table.

About 2% cases of acute pancreatitis are caused by drugs. In 85–95% of these cases, the resolution is spontaneous and occurs in 3–7 days. The drugs with the highest incidence of pancreatitis are:

- didanosine (analog of inosina, used in HIV–1 therapy): 23%;

- azathioprine, 6-mercaptopurine and mesalazine: 3–5%;

- ACE-inhibitors and sartans: 1–2%.

Regarding the intake of losartan (associated or not with hydrochlorothiazide), there are only three reports in PubMed related to six cases of acute pancreatitis induced by this drug [40,42,43,44].

The most recent drugs included in the list of those associated with acute pancreatitis are statins, the latest atypical antipsychotics, dipeptidyl peptidase-4 inhibitors (DPP–4, incretin) [48,51], GLP–1 Agonists [52,53], SGLT2 inhibitors [54,55], and vedolizumab [58].

Among antibiotics, in addition to tetracyclines and tigecycline [61], at least four cases of acute pancreatitis from amoxicillin + ac clavulanate have been reported in the literature [62].

Regarding oral metronidazole, used for the eradication of Helicobacter pylori, in a recent Swedish large population-based case-control study [62], it was associated with an increased risk of acute pancreatitis within 30 days of exposure to both single and combined regimens (with amoxicillin).

As for statins, the association had already been detected years ago in several studies and clinical cases [45,47] and was confirmed by a 2015 epidemiological study [46]. The latter study found that the use of HMG-CoA reductase is associated with an increased rate of incidence of acute pancreatitis, especially during the first year of use.

Most of the reports related to the ARBs and ACE inhibitors indicated in Table 1 confirmed the injurious action of the drug for rechallenge. Regarding DPP–4 inhibitors (incretin), the incidence of acute pancreatitis was found to significantly increased in diabetic patients treated with gliptins compared to control groups with a difference in absolute risk of 0.13%. This increase translates into one or two additional cases of acute pancreatitis per 1,000 patients treated for two years [51]. The third common cause of acute pancreatitis is hypertriglyceridemia [73], accounting for up to 10% of all cases (hypertriglyceridemia-induced acute pancreatitis: HTGP). Among the drugs implicated in acute pancreatitis, thiazides, estrogen (clomiphene), tipranavir/ritonavir, tamoxifen [56], olanzapine, mirtazapine [57], isotretinoin [104] mainly act through the hypertriglyceridemia they cause.

Chronic familial pancreatitis (Orpha code 676) is a very rare form of chronic infantile pancreatitis, with a prevalence of 1–9/1,000,000, with autosomal dominant transmission, and its age of onset varies from infancy to adolescence.

Hereditary pancreatitis (or autosomal dominant hereditary pancreatitis) has a high risk of pancreatic cancer.

2. Differential Diagnosis

In the case of marked persistent hypereosinophilia, non-intense pain, rapid resolution, normal pancreas on CT scan and the exclusion of other associated pathologies, it could be acute eosinophilic pancreatitis in the normal pancreatic form.

There are eight diagnostic criteria for this disease (Box 1).

For the detection of eosinophilia, eosinophilic pancreatitis is considered for the differential diagnosis with some other pathologies, as indicated in Table 2.

Table 2 Pathologies with which eosinophilic pancreatitis is considered for the differential diagnosis.

In most cases of EP, there is the simultaneous involvement of the gastrointestinal tract in the prevalent form (up to 85% of patients) of eosinophilic gastroenteritis (EoG), an association that can also appear later during the disease [2,17].

There are only two reports in the literature documenting a prolonged time gap between previous eosinophilic gastroenteritis and acute eosinophilic pancreatitis [18,26].

Eosinophilic fibrosis of the pancreas has been described in the context of eosinophil multi-visceral fibrosis [14,75]. The EP should be differentiated from chronic pancreatitis associated with idiopathic hypereosinophilic syndrome [HIES].                                      

 A condition of hypereosinophilia associated with chronic pancreatitis has been described in two articles, reporting a total of 51 cases [12,23]. An Indian study, performed in 2018 on a population of 114 cases of chronic pancreatitis, found the presence of peripheral eosinophilia in 24.5% of patients, predominantly women [79].

EP is considered by some authors to be a variant of autoimmune pancreatitis [8,10] in the context of IgG4-related systemic diseases (Table 3) [80].

Table 3 Spectrum of IgG4-related systemic diseases. Modified from Stone et al. [80].

 In EP, pancreatic CT scan may be normal (Balthazar score = 0) [21,25,26], may present pancreatic duct dilatation, or may frequently manifest a pseudocyst or pseudotumoral form [3,4,5,6,7,9,13,14,15,29].

The histological features of eosinophilic pancreatitis have two distinct forms:

- widespread eosinophilic infiltration in pancreatic ducts, in the acini and interstitium with phlebitis and eosinophilic arteritis, and with the minimal presence of lymphocytes and plasma cells;

- intense and localized eosinophilic infiltrate with pseudocyst formation [8,16].     

A systematic search of PubMed for original and review articles in English published during 1990 to June 2019 was performed using keywords and text related to EP and AIP, which included “eosinophilic pancreatitis”, “autoimmune pancreatitis”, “diagnosis”, “case reports”, “IgG4-related disease”, “rare causes”, and “recurrent acute pancreatitis”.

There were total 40 reports of EP appearing from  the following countries: USA [7,8,14,15,18,25,28,78,100], Turkey [3,17], China [16,22], Korea [13,21], France [9,11,77,101], India [6,27], Japan [20,24,106], Denmark [18], UK [5], Brazil [29], Italy [26], and Tunisia [76].                  

If IgG4 is elevated, more than twice of the upper limit of the normal value (usually IgG4 is around 5–6%, with normal values up to 135 mg/dL), it could be autoimmune pancreatitis.

The diagnostic criteria for the AIP are indicated in Box 2.

The criteria for the diagnosis of autoimmune pancreatitis (HISORt criteria [81,82]):

Autoimmune pancreatitis is classified into type 1, type 2, and type NOS (not otherwise specified). AIP type 1 is a more severe condition than the other subtypes [89].

The clinical manifestations and epidemiological and histological features of autoimmune pancreatitis are described in Tables 4 and 5.

Table 4 Clinical manifestations of autoimmune pancreatitis (AIP).

Table 5 Epidemiological and histological features of the two forms of autoimmune pancreatitis (AIP), type 1 and type 2. Modified from Shimosegawa et al. [83].

The most common morphological aspect, detected in 85% of patients, is given by a pancreatic mass or by the enlargement of the entire pancreas [84]. Therefore, the confirmatory diagnosis is made by pancreatic biopsy.

Some recent studies from Japan have shown that with the minimally invasive technique of the needle aspiration under echo-endoscopic guidance [29,85], it is possible to formulate very accurate histopathological diagnosis.

In the differential diagnosis, with non-invasive technique, between autoimmune pancreatitis and pancreatic cancer, the use of contrast-enhanced harmonic endoscopic ultrasound (CEH-EUS) was found to be useful [86].

If it is important to make the differential diagnosis with pancreatic neoplasia [81], the possible association of AIP, in the presence or during the remission phase, with pancreatic cancer [87,88] should be considered.

Furthermore, the detection of certain antibodies may help in the diagnosis of AIP:

- anti-plasminogen-binding protein-peptide antibodies (anti-PBP),

- anti-carbonic anhydrase II antibodies (anti-CA-II),

- anti-carbonic anhydrase IV antibodies (anti-CA-IV), and

- anti-lactoferrin antibodies (anti-LF).

Anti-PBP antibodies were found positive in 94% of cases AIP in comparison to the absence in the control patients [90].

The pathologic differential diagnosis of Immunoglobulin G4-related disease is indicated in Table 6.

Table 6 Conditions that can mimic IgG4-related disease histopathologically. Adapted from  Bledsoe et al. [91].

3. Therapy

The therapy of autoimmune pancreatitis involves the use of glucocorticoids.

In the literature, different dosages and durations of the therapies have been empolyed:

A. Prednisolone: 30–40 mg/day for 2–4 weeks with doses of 5 mg/day every 2–4 weeks up to 5 mg/day; maintenance dose: 2.5–5 mg/day [92];

B. Prednisolone: 0.5 mg/kg body weight/day for two weeks [93];

C. Prednisone: 40 mg/day for 4–6 weeks with 5 mg weekly doses per week for a total of 11 weeks (initial treatment in IgG4-associated cholangitis) [94].

It is also possible to use immunomodulatory drugs, such as azathioprine, in case of Ig4-associated cholangitis (2 mg/kg/day for 1–3 years). In the event of steroid failure or relapse or AIP without IgG4-cholangitis, the monoclonal anti-CD20 antibody, rituximab, can be administered [95]. Recently, a clarification on the treatment of autoimmune type 1 and type 2 pancreatitis has been published by Okazaki et al. in January 2017 [96].

For the treatment of IgG4-related disease, an international consensus was published in 2015 that analyzed various pharmacological options reported so far [97]. In the study,  in addition to cortisone therapy, the role of conventional steroid-sparing drugs was defined (azathioprine, mycophenolate mofetil, 6-mercaptopurine, methotrexate, tacrolimus, and cyclophosphamide) and the use of rituximab was suggested as a depletor of B cells.

A study from Italy in 2015 [98] reported methotrexate as a promising, safe and low-cost agent to maintain glucocorticoid-induced remission of IgG4-related disease with systemic involvement.

Regarding the IgG-4 sclerosing cholangitis, the Japanese guidelines [99] were published in February 2019, which defined, among other things, the classification of the same in four subtypes, the relationship with the inflammatory hepatic pseudotumors, the development of cholangiocarcinoma, algorithms for diagnosis and treatment, and the differential diagnosis with primary sclerosing cholangitis (PSC).            

The most common therapy of eosinophilic pancreatitis involves the use of prednisolone 40 mg/day [17,19] for 2–3 weeks. Caglar et al. described a scheme that suggests the use of prednisone 40 mg/day for six weeks with ketotifen 500 mg/day, with a dose of 4 mg every two weeks to a maintenance dose of 16 mg/day [17].

Maeshima et al. instead described a scheme with prednisolone 30 mg/day + montelukast 10 mg/day for one month [20]. However, there are currently no reliable data to establish the duration of therapy. It is also possible to make the use of alternatives of steroids, such as sodium cromoglycate [11,17], ketotifen [11], montelukast [11,20], azathioprine, and hydroxyurea.

4. Conclusions

  • The number of drugs involved in acute pancreatitis is constantly increasing.
  • Eosinophilic pancreatitis is a very rare but benign pathology as only about forty cases have been described in the literature. It is often associated with hypereosinophilia and eosinophilic gastroenteritis.
  • It is considered a variant of autoimmune pancreatitis. The diagnosis requires an instrumental technique (ultrasound, CT, MRCP, EUS, and also ERCP) up to biopsy, considering the frequent initial pseudo-diagnosis of pancreatic neoplasia and the consequent lack of preoperative suspicion. The therapy involves the use of corticosteroids.
  • Autoimmune pancreatitis is a rare disease that is classified into three forms: type 1, type 2, and type NOS. Type 1 is associated with the involvement of multiple organs in the IgG4-related disease. It may occur in a tumor-like form or may also be associated with pancreatic neoplasia. A dosage of IgG4 is helpful in the diagnosis that in any case will need instrumental analysis up to the pancreatic biopsy.

Therapeutic options include cortisone, steroid-sparing drugs, immunomodulatory agents, and the monoclonal antibody, rituximab.

Author Contributions

Single author.


No funding resources and grant.

Competing Interests

The author have declared that no competing interests exist

Glossary Abbreviations

CT: Computed tomography

EUS: Endoscopic ultrasound

CEH-EUS: Contrast-enhanced harmonic endoscopic ultrasound

EUS-FNA: Endoscopic ultrasound-guided fine needle aspiration

ERCP: Endoscopic retrograde cholangiopancreatography

MRI: Magnetic Resonance Imaging

MRCP: Magnetic Resonance Cholangiopancreatography

EGID: Eosinophilic Gastrointestinal Disordes

EoG: Eosinophilic Gastroenteritis

EoE: Eosinophilic Esophagitis

EoC: Eosinophilic Colitis

PCE: Primary Colonic Eosinophilia

EP: Eosinophilic Pancreatitis

AIP: Autoimmune Pancreatitis

DIP: Drug Induced Pancreatitis

HE: Hypereosinophilia

HES: Hypereosinophilic Syndrome

HEUS: Hypereosinophilic Syndrome of Unknown Significance

HEFA: Hereditary (familial) HE

HER: Secondary (reactive) HE

IHES: Idiopathic Hypereosinophilic Syndrome

HTGP: Hypertriglyceridemia-induced acute pancreatitis


  1. Orphanet report series - Prevalence of rare diseases: Bibliographic data. 2019 January 1. http://www.orpha.net/orphacom/cahiers/docs/GB/Prevalence_of_rare_diseases_by_alphabetical_list.pdf
  2. Sheikh RA, Prindiville TP, Pecha RE, Ruebner BH. Unusual presentations of eosinophilic gastroenteritis: Case series and review of literature. World J Gastroenterol. 2009; 15: 2156-2161. https://doi.org/10.3748/wjg.15.2156 [CrossRef]
  3. Cay A, Imamoglu M, Cobanoglu U. Eosinophilic pancreatitis mimicking pancreatic neoplasia. Can J Gastroenterol. 2006, 20: 361-364. https://doi.org/10.1155/2006/386918 [CrossRef]
  4. Euscher E, Vaswani K, Frankel W. Eosinophilic pancreatitis: a rare entity that can mimic a pancreatic neoplasm. Ann Diagn Pathol. 2000; 4: 379-385. [CrossRef]
  5. Christopher V, Thompson MH, Hughes S. Eosinophilic gastroenteritis mimicking pancreatic cancer. Postgrad Med J. 2002; 78: 498-499. https://doi.org/10.1136/pmj.78.922.498 [CrossRef]
  6. Rakesh K, Banerjee R, Gupta R, Ramji C, Pradeep R, Rao GV, et al. Eosinophilic pancreatitis with pseudocyst. Indian J Gastroenterol. 2007; 26: 136-137.
  7. Polyak S, Smith TA, Mertz H. Eosinophilic gastroenteritis causing pancreatitis and pancreaticobiliary ductal dilation. Dig Dis Sci. 2002; 47: 1091-1095. [CrossRef]
  8. Abraham SC, Leach S, Yeo CJ, Cameron JL, Murakata LA, Boitnott JK, et al. Eosinophilic pancreatitis and increased eosinophils in the pancreas. Am J Surg Pathol. 2003; 27: 334-342. https://doi.org/10.1097/00000478-200303000-00006 [CrossRef]
  9. Barthet M, Hastier P, Buckley MJ, Bernard JP, Sastre B, Baroni JL, et al. Eosinophilic pancreatitis mimicking pancreatic neoplasia: EUS and ERCP findings - is non-surgical diagnosis possible? Pancreas. 1998; 17: 419-422. https://doi.org/10.1097/00006676-199811000-00014 [CrossRef]
  10. Sah RP, Pannala R, Zhang L, GrahamRP, Sugumar A, Chari ST. Eosinophilia and allergic disorders in autoimmune pancreatitis. Am J Gastroenterol. 2010; 105: 2485-2491. https://doi.org/10.1038/ajg.2010.236 [CrossRef]
  11. Bastid C, Sahel J, Choux R, Payan mJ, Sarles H. Eosinophilic pancreatitis: report of a case. Pancreas. 1990; 5: 104-107. https://doi.org/10.1097/00006676-199001000-00016 [CrossRef]
  12. Tokoo M, Oguchi H, Kawa S, Homma T, Nagata A. Eosinophilia associated with chronic pancreatitis: An analysis of 122 patients with definite chronic pancreatitis. Am J Gastroenterol. 1992; 87: 455-460.
  13. Song JW, Kim MH, Seo WJ, Oh DR, Kim GD, Moon SH, et al. A case of eosinophilic pancreatitis. Korean J Gastroenterol. 2003; 42: 444-449.
  14. Stevens T, Mackey R, Falk GW, Bennet A, Henderson JM. Eosinophilic pancreatitis presenting as a pancreatic mass with obstructive jaundice. Gastrointest Endosc. 2006; 63: 525-527. https://doi.org/10.1016/j.gie.2005.10.005 [CrossRef]
  15. Kakodkar S, Omar H, Cabrera J, Chi K. Eosinophilic pancreatitis diagnosed with endoscopic ultrasound. ACG Case Rep J. 2015; 2: 239-241. https://doi.org/10.14309/crj.2015.71 [CrossRef]
  16. Tian L, Fu P, Dong X, Qi J, Zhu H. Eosinophilic pancreatitis: Three case reports and literature review. Mol Clin Oncol. 2016; 4: 559-562. https://doi.org/10.3892/mco.2016.760 [CrossRef]
  17. Çăglar E, Karişmaz K, Dobrucali A. A case of eosinophilic gastroenteritis mimicking gastric lymphoma associated with pancreatitis due to duodenal involvement. Turk J Gastroenterol. 2012; 23: 585-589. https://doi.org/10.4318/tjg.2012.0436 [CrossRef]
  18. Lyngbaek S, Adamsen S, Aru A, Bergenfeldt M. Recurrent acute pancreatitis due to eosinophilic gastroenteritis. Case report and literature review. JOP. 2006; 7: 211-217.
  19. Le Connie D, Nguyen H. Eosinophilic gastroenteritis, ascites, and pancreatitis: A case report and review of the literature. South Med J. 2004; 97: 905-906. https://doi.org/10.1097/01.SMJ.0000139403.55785.1C [CrossRef]
  20. Maeshima A, Murakami H, Sadakata H, Saitoh T, Matsushima T, Tamura J, et al. Eosinophilic gastroenteritis presenting with acute pancreatitis. J Med. 1997; 28: 265-272.
  21. Baek MS, Mok YM, Han WC, Kim YS. A patient with eosinophilic gastroenteritis presenting with acute pancreatitis and ascites. Gut Liver. 2014; 8: 224-227. [CrossRef]
  22. Zhu B, Bai H, Wu J. A patient with eosinophilic gastroenteritis presenting with acute pancreatitis. Chinese J Pediatr. 2015; 53: 542-543.
  23. Wang Q, Lu CM, Guo T, Qian JM. et al. Eosinophilia associated with chronic pancreatitis. Pancreas. 2009; 38: 149-153. https://doi.org/10.1097/MPA.0b013e31818d8ecc. [CrossRef]
  24. Suzuki S, Homma T, Kurokawa M, Matsukura S, Adachi M, Wakabayashi K, et al. Eosinophilic gastroenteritis due to cow’s milk allergy presenting with acute pancreatitis. Int Arch Allergy Immunol. 2012; 158: 75-82. https://doi.org/10.1159/000337782 [CrossRef]
  25. Tse KY, Christiansen SC. Eosinophilic gastroenteritis due to egg allergy presenting as acute pancreatitis. Allergy Rhinol (Providence). 2015; 6: e80-e81. [CrossRef]
  26. Turrin M, Martinelli S. Acute pancreatitis at quick resolution. Merit of…Eosinophils? Intern Emerg Med. 2016 (suppl): S107-S108. https://doi.org/10.13140/RG.2.2.22484.04480 [CrossRef]
  27. Javid Bhat K, Bhat S, Dutt K, Gupta S, Jeelani Samoon H. Chronic diarrhea, eosinophilic ascites, acute pancreatitis and deep venous thrombosis: A case report. Caspian J Intern Med. 2014; 5: 182-186.
  28. Reppucci J, Chang M, Hughes S, Liu Xiuli. Eosinophilic pancreatitis: A rare cause of recurrent acute pancreatitis. Case Rep Gastroenterol. 2017; 11: 120-126. DOI: 10.1159/000457788. [CrossRef]
  29. De Moura DTH, Rocha RSP, Jukemura J, Brunaldi VO, Guedes HG, Torrez FRA, et al. A rare non-oncological pancreatic mass: Eosinophilic pancreatitis diagnosis through EUS-FNA. Endosc Int Open. 2019; 7: E151–E154. https://doi.org/10.1055/a-0806-7099 [CrossRef]
  30. Tilkemeier P, Thompson RD. Acute pancreatitis possibly related to enalapril. N Engl J Med. 1988; 318: 1275-1276. https://doi.org/10.1056/NEJM198805123181914 [CrossRef]
  31. Martin T, Taupignon A, Graf E, Perrin D. Pancreatitis and hepatitis in a patient treated with enalapril maleate. A cas report. Therapie. 1989; 44: 449-450.
  32. Gonzalez Ramallo VJ, Muiňo Miguez A, Torres Segovia FJ. Necrotizing pancreatitis and enalapril. Eur J Med. 1992; 1: 123.
  33. Maringhini A, Termini A, Patti R, Ciambra M, Biffarella P, Pagliaro L. Enalapril-associated acute pancreatitis: Recurrence after rechallenge. Am J Gastroenterol. 1997; 92: 166-167.
  34. Carnovale A, Esposito P, Bassano P, Russo L, Uomo G. Enalapril-induced acute recurrent pancreatitis. Dig Liver Dis. 2003; 35: 55-57. https://doi.org/10.1016/S1590-8658(02)00012-9 [CrossRef]
  35. Kanbay M, Selcuk H, Yilmaz U, Boyacioglu S. Recurrent acute pancreatitis probably secondary to lisinopril. South Med J. 2006; 99: 1388-1389. [CrossRef]
  36. Maliekal J, Drake CF. Acute pancreatitis associated with the use of lisinopril. Ann Pharmacother. 1993; 27: 1465-1466. https://doi.org/10.1177/106002809302701211 [CrossRef]
  37. Gershon T, Olshaker JS. Acute pancreatitis following lisinopril rechallenge. Am J Emerg Med. 1998; 16: 523-524. https://doi.org/10.1016/S0735-6757(98)90009-2 [CrossRef]
  38. Kanbay M, Korkmaz M, Yilmaz U, Gur G, Boyacioglu. Acute pancreatitis due to ramipril therapy. Postgrad Med J. 2004; 80: 617-618; https://doi.org/10.1136/pgmj.2003.018119 [CrossRef]
  39. Famularo G, Minisola G, Nicotra GD, De Simone C. Acute pancreatitis associated with irbesartan therapy. Pancreas. 2005; 13: 294-295. [CrossRef]
  40. Fisher AA, Bassett ML. Acute pancreatitis associated with angiotensin II receptor antagonists. Ann Pharmacother. 2002; 36: 1883-1886. [CrossRef]
  41. Cann B, Sali M, Batman A, Yilmaz H, Korkmaz U, Celebi A, et al. Valsartan-induced acute pancreatitis. Inter Med. 2014; 53: 703-705. https://doi.org/10.2169/internalmedicine.53.0667 [CrossRef]
  42. Bosch X. Losartan-induced acute pancreatitis. Ann Intern Med. 1997; 127: 1043-1044. https://doi.org/10.7326/0003-4819-127-11-199712010-00031 [CrossRef]
  43. Birck R, Keim V, Fiedler F, van der Woude FJ, Rohmeiss P. Pancreatitis after losartan. Lancet. 1998; 351: 1178. https://doi.org/10.1016/S0140-6736(05)79122-4 [CrossRef]
  44. Arellano L, Altaba A, Santamaria C, García-Vicente JA. Acute pancreatitis in a patient treated with losartan. Aten Primaria. 2014; 46: 316-317. https://doi.org/10.1016/j.aprim.2014.02.003 [CrossRef]
  45. Kaurich T. Drug-induced acute pancreatitis. Proc (Bayl Univ Med Cent). 2008; 21: 77-81. [CrossRef]
  46. Kuoppala J, Pulkkinen J, Kastannen H, Kiviniemi V, Jyrkkä J, Enlund H, et al. Use of statins and the risk of acute pancreatitis: A population-based case-control study. Pharmacoepidemiol Drug Saf. 2015; 24: 1085-1092. https://doi.org/10.1002/pds.3858 [CrossRef]
  47. Lai SW, Lin CL, Liao KF. Rosuvastatin and risk of acute pancreatitis in a population-based case-control study. Int J Cardiol. 2015; 187: 417-420. https://doi.org/ 10.1016/j.ijcard.2015.03.373 [CrossRef]
  48. DeVries JH, Rosenstok J. DPP-4 inhibitor-related pancreatitis: Rare but real! Diabetes Care. 2017; 40: 163-164. https://doi.org/10.2337/dci16-0035 [CrossRef]
  49. Badalov N, Baradarian R, Iswara K, Li J, Steinberg W, Tenner S. Drug-induced acute pancreatitis: An evidence-based review. Clin Gastroenterol Hepatol. 2007; 5: 648-661. [CrossRef]
  50. Turrin M, Martinelli S. Eosinophilic pancreatitis and autoimmune pancreatitis: Comparison, differential diagnosis, and treatment. CMI. 2017; 11: 23-30. [CrossRef]
  51. Tkač I, Raz I. Combined analysis of three large interventional trials with gliptins indicates increased incidence of acute pancreatitis in patients with type 2 diabetes. Diabetes Care. 2017; 40: 284-286. https://doi.org/10.2337/dc15-1707 [CrossRef]
  52. Montilla S, Marchesini G, Sammarco A, Trotta MP, Siviero PD, Tomino C, et al. Drug utilization, safety, and effectiveness of exenatide, sitagliptin, and vildagliptin for type 2 diabetes in the real world: data from the italian AIFA Anti-diabetics monitoring registry. Nutr Metab Cardiovasc Dis. 2014; 24: 1346-1353. https://doi.org/10.1016/j.numecd.2014.07.014. [CrossRef]
  53. Anderson SL, Trujillo JM. Association of pancreatitis with glucagon-like peptide-1 agonist use. Ann Pharmacoter. 2010; 44: 904-909. https://doi.org/10.1345/aph.1M676. [CrossRef]
  54. Srivali N, Thongprayoon C, Cheungpasitporn W, Ungprasert P. Acute pancreatitis in the use of canagliflozin: A rare side-effect of the novel therapy for type 2 diabetes mellitus. J Basic Clin Pharm. 2015; 6: 101-102. https://doi.org/10.4103/0976-0105.160753 [CrossRef]
  55. Chowdhary M, Kabbani AA, Chhabra A. Canagliflozin-induced pancreatitis: A rare side effect of a new drug. Ther Clin Risk Manag. 2015; 11: 991-994. https://doi.org/10.2147/TCRM.S86641 [CrossRef]
  56. Kataria PSC, Kendre PP, Patel AA, Bohra MZ, Tahiliani N.Tamoxifen induced pancreatitis: An unusual complication of commonly used drug. J Clin Diagn Res. 2017; 11: XD05-XD06. https://doi.org/10.7860/JCDR/2017/27440.10467.
  57. Bowers RD, Valanejad SM, Holombo AA. Mirtazapine-induced pancreatitis - a case report. J Pharm Pract. 2018; 1: 897190018760645. https:// doi.org/10.1177/0897190018760645. [CrossRef]
  58. Picardo S, So K, Venugopal K, Chin M. Vedolizumab-induced acute pancreatitis: The first reported clinical case. BMJ Case Rep. 2018; pii: bcr-2017-222554. https://doi.org/10.1136/bcr-2017-222554 [CrossRef]
  59. Murtaza G, Fagah A, Konowitz N, Lu H, Kuruvilla A, Adhikari S. Acute pancreatitis related to chemothe rapy drug. World J Oncol. 2017; 8: 18-19. https://doi.org/10.14740/wjon1006e. [CrossRef]
  60. Kawakami H, Kubota Y, Ban T, Shibata N, Hosokawa A. Lenvatinib-induced acute pancreatitis associated with a pancreatic pseudocyst and splenic pseudoaneurysms. Pancreas. 2018; 47: e34-e35. https://doi.org/ 10.1097/MPA.0000000000001061 [CrossRef]
  61. Akhter S, Krishnan P, Kaul P. Tigecycline-associated acute pancreatitis. Am J Ther. 2018; 25: e749-e750. https:// doi.org/10.1097/MJT.0000000000000763. [CrossRef]
  62. Chams S, Sayegh SE, Hamdon M, Kumar S, Tegeltija V. Amoxicillin/clavulanic acid-induced pancreatitis: Case report. BMC Gastroenterol. 2018; 18: 122. [CrossRef]
  63. Barbulescu A, Oskarsson V, Lindblad M, Ljung R, Brooke HL. Oral metronidazole use and risk of acute pancreatitis: A population-based case-control study. Clin Epidemiol. 2018; 10: 1573-1581. https://doi.org/ 0.2147/CLEP.S159702. [CrossRef]
  64. Kikuchi I, Miyata N, Yoshimura Y, Miyamoto K, Tachikawa N. Methimazole-induced acute pancreatitis: A case report. Clin J Gastroenterol. 2019; 12: 239-242. https://doi.org/ 10.1007/s12328-018-0926-5. [CrossRef]
  65. J Mercogliano C, Khan M, Ahmad M. A case of probable Amiodarone-induced pancreatitis in the treatment of atrial fibrillation: A literature review and case report. J Community Hosp Intern Med Perspect. 2017; 7: 369-371. https://doi.org/10.1080/20009666.2017.1403829. [CrossRef]
  66. García Gavilán MD, Moreno García AM, Rosales Zabal JM, Navarro Jarabo JM, Sánchez Cantos A. Case of drug-induced acute pancreatitis produced by horsetail infusions. Rev Espo Enferm Dig. 2017; 109: 301-304. https://doi.org/10.17235/reed.2017.4157/2015. [CrossRef]
  67. Makrides C, Koukouvas M, Achillews G, Tsikkos S, Vounou E, Symeonides M, et al. Methomyl-induced severe acute pancreatitis: Possible etiological association. JOP. 2005; 6: 166-171.
  68. Falcão de Campos C, de Carvalho M. Riluzole-induced recurrent pancreatitis. J Clin Neurosci 2017; 45: 153-154. https://doi.org/10.1016/j.jocn.2017.08.032. [CrossRef]
  69. Rawla P, Raj JP. Doxycycline-induced acute pancreatitis: A rare adverse event. Gastroenterology Res. 2017; 10: 244-246. https://doi.org/10.1474/gr838w [CrossRef]
  70. Raiss H, El Amarti L, Tigaud JD, Layachi M, Bruyas A, Boutayeb S, et al. Probable paclitaxel-induced pancreatitis: Uncommon case report and literature review. J Gastrointest Oncol. 2017; 8: E80-E83. https://doi.org/10.21037/jgo.2017.08.06. [CrossRef]
  71. Barkin JA, Nemeth Z, Saluja AK, Barkin JS. Cannabis-induced acute pancreatitis: A systematic review. Pancreas. 2017; 46: 1035-1038. https://doi.org/10.1097/MPA.0000000000000873. [CrossRef]
  72. Culetto A, Bournet B, Buscail L. Clinical profile of cannabis-associated acute pancreatitis. Dig Liver Dis. 2017; 49: 1284-1285. https://doi.org/10.1016/j.dld.2017.08.040. [CrossRef]
  73. de Petris N, Amodio A, Frulloni L. Hypertriglyceridemic pancreatitis: Epidemiology, pathophysiology and clinical management. United European Gastroenterol J. 2018; 6: 649–655. https://doi.org:10.1177/2050640618755002 [CrossRef]
  74. Guler S, Cimen S, MacDonald F, et al. Eosinophilic pancreatitis. In: Di Giovanni G, Marcoz P (editors). Rare Diseases. New York: Nova Science Publishers; 2014.
  75. Gullo L, Golfieri R, Orcioni GE, Pileri S. Multivisceral eosinophilic fibrosis: A new clinical presentation. Eur J Gastroenterol Hepatol. 2000; 12: 1037-1039. [CrossRef]
  76. Atig A, Ben Jazia E, Alaoua A, Khalifa M, Ghannouchi N, Braham A, et al. Acute pancreatitis due to idiopathic hypereosinophilic syndrome: A case report. Acta Endosc. 2011: 41: 26-28. [CrossRef]
  77. Roy-Peaud F, Paccalin M, Le Moal G, Landron C, Roblot P, Becq-Giraudon B. Eosinophilic Pancreatitis. Presse Med. 2002; 31: 25.
  78. Abdalgani MM, Irani AMA. Hypereosinophilic syndrome presenting as acute pancreatitis. J Allergy Clin Immunol. 2013; 131: Suppl AB 121. https://doi.org/10.1016/j.jaci.2012.12.1103 [CrossRef]
  79. Vutukuru VR, Rao RRV, Mathai V, Settipalli S. Relevance of peripheral eosinophilia in chronic pancreatitis. Int Surg J. 2019; 6: 523-529. https://doi.org/10.18203/2349-2902.isj20190396 [CrossRef]
  80. Stone JH, Khosroshahi A, Deshpande V, Chan JK, Heathcote JG, Aalberse R, et al. Recommendations for the nomenclature of IgG4-related disease and its individual organ system manifestations. Arthritis Rheum. 2012; 64: 3061-3067. https://doi.org/10.1002/art.34593 [CrossRef]
  81. Chari ST, Takahashi N, Levy MJ, Smyrk TC, Clain JE, Pearson RK, et al. A diagnostic strategy to distinguish autoimmune pancreatitis from pancreatic cancer. Clin Gastroenterol Hepatol. 2009; 7: 1097-1103. [CrossRef]
  82. Schneider A, Michaely H, Rückert F, Weiss C, Ströbel P, Belle S, et al. Diagnosing autoimmune pancreatitis with the Unifying-Autoimmune-Pancreatitis-Criteria. Pancreatology. 2017; 17: 381-394. https://doi.org/10.1016/j.pan.2017.03.005. [CrossRef]
  83. Shimosegawa T, Chari ST, Frulloni L, Kamisawa T, Kawa S, Mino-Kenudson M, et al. International consensus diagnostic criteria for autoimmune pancreatitis: Guidelines of the International Association of Pancreatology. Pancreas. 2011; 40: 352-358. [CrossRef]
  84. Raina A, Yadav D, Krasinskas AM, McGrath KM, Khalid A, Sanders M, et al. Evaluation and management of autoimmune pancreatitis: Experience at a large US center. Am J Gastroenterol. 2009; 104: 2295-2306. https://doi.org/10.1038/ajg.2009.325 [CrossRef]
  85. Kanno A, Masamune A, Fujishima F, Iwashita T, Kodama Y, Katanuma A, et al. Diagnosis of autoimmune pancreatitis by EUS guided FNA using a 22-gauge needle: A prospective multicenter study. Gastrointest Endosc. 2016; 84: 797-804. [CrossRef]
  86. Cho MK, Moon SH, Song TJ, Kim RE, Oh DW, Park DH, et al. Contrast-enhanced endoscopic ultrasound for differentially diagnosing autoimmune pancreatitis and pancreatic cancer. Gut Liver. 2018; 12: 591-596. https://doi.org/10.5009/gnl17391 [CrossRef]
  87. Ghazale A, Chari S. Is autoimmune pancreatitis a risk factor for pancreatic cancer? Pancreas. 2007; 35: 376. https://doi.org/10.1097/MPA.0b013e318073ccb8 [CrossRef]
  88. Pezzilli R, Vecchiarelli S, Di Marco MC, Serra C, Santini D, Calculli L, et al. Pancreatic ductal adenocarcinoma associated with autoimmune pancreatitis. Case Rep Gastroenetrol. 2011; 5: 378-385; https://doi.org/10.1159/000330291 [CrossRef]
  89. Amodio A, Campagnola P, Trevisan V, Brozzi L, Granato A, De Marchi G, et al. IGG4-related pancreatitis: Clinical and radiological characteristics and therapeutic implications in 153 patients. Dig Liver Dis. 2018; 50: e87. https://doi.org/10.1016/S1590-8658(18)30311-6 [CrossRef]
  90. Frulloni L, Lunardi C, Simone R, Dolcino M, Scattolini C, Falconi M, et al. Identification of a novel antibody associated with autoimmune pancreatitis. N Engl J Med. 2009; 361: 2135-2142. https://doi.org/10.1056/NEJMoa0903068 [CrossRef]
  91. Bledsoe JR, Della-Torre E, Rovati L, Desphande V. IgG4-related disease: Review of the histopathologic features, differential diagnosis, and therapeutic approach. APMIS. 2018; 126: 459-476. https:// doi.org/10.1111/apm.12845 [CrossRef]
  92. Hirano K, Tada M, Isayama H, Yagioka H, Sasaki T, Kogure H, et al. Long-term prognosis of autoimmune pancreatitis with and without corticosteroid treatment. Gut. 2007; 56: 1719-1724. https://doi.org/10.1136/gut.2006.115246 [CrossRef]
  93. Moon SH, Kim MH, Park DH, Hwang CY, Park SJ, Lee SS, et al. Is a 2-week steroid trial after initial negative investigation for malignancy useful in differentiating autoimmune pancreatitis from pancreatic cancer? A prospective outcome study. Gut. 2008; 57: 1704. https://doi.org/10.1136/gut.2008.150979 [CrossRef]
  94. Ghazale A, Chari ST, Zhang L, Smyrk TC, Takahashi N, Levy MY, et al. Immunoglobulin G4-associated cholangitis: clinical profile and response to therapy. Gastroenterology. 2008; 134: 706-715. http://dx.doi.org/10.1053/j.gastro.2007.12.009 [CrossRef]
  95. Hart PA, Topazian MD, Witzig TE, Clain JE, Gleeson FC, Klebig RR, et al. Treatment of relapsing autoimmune pancreatitis with immunomodulators and rituximab: The Mayo Clinic experience. Gut. 2013; 62: 1607-1615. https://doi.org/10.1136/gutjnl-2012-302886 [CrossRef]
  96. Okazaki K, Chari ST, Frulloni L, Lerch MM, Kamisawa T, Kawa S, et al. International consensus for the treatment of autoimmune pancreatitis. Pancreatology. 2017; 17: 1-6. https://doi.org/10.1016/j.pan.2016.12.003 [CrossRef]
  97. Khosroshahi A, Wallace ZS, Crowe JL, Akamizu T, Azumi A, Carruthers MN, et al. International consensus guidance statement on the management and treatment of IgG4-related disease. Arthritis Rheum.2015; 67: 1688-1699. https://doi.org/10.1002/art.39132 [CrossRef]
  98. Della-Torre E, Campochiaro C, Bozzolo EP, Dagna L, Scotti R, Nicoletti R, et al. Methotrexate for maintenance of remission in IgG4-related disease. Rheumatology. 2015; 54; 1934-1936. https://doi.org/10.1093/rheumatology/kev244 [CrossRef]
  99. Kamisawa T, Nakazawa T, Tazuma S, Zen Y, Tanaka A, Ohara H, et al. Clinical practice guidelines for IgG4-related sclerosing cholangitis. J Hepatobiliary Pancreat Sci. 2019; 26: 9-42. https://doi.org/ 10.1002/jhbp.596 [CrossRef]
  100. Abdalgani MM, Irani Anne-Marie A. Hypereosinophilic syndrome presenting as acute pancreatitis. J Allergy Clin Immunol. 2013; 131: 121. [CrossRef]
  101. Bellaiche G, Fontaine H, Choudat L, Lusina D, Ley G, Slama JL. Pancreatic involvement, ascites and diarrhea in idiopathic hypereosinophilic syndrome. Gastroenterol Clin Biol. 1997; 21: 519-522. https://doi.org/GCB-07-1997-21-6-7-0399-8320-101019-ART96 [CrossRef]
  102. Sunkara T, Rawla P, Yarlagadda KS, Gaduputi V. Eosinophilic gastroenteritis: Diagnosis and clinical perspectives. Clin Exp Gastroenterol. 2019; 12: 239-253. https:// doi.org/10.2147/CEG.S173130 [CrossRef]
  103. Rawla P, Sunkara T, Thandra KC, Gaduputi V. Hypertriglyceridemia-induced pancreatitis: Update review of current treatment and preventive strategies. Clin J Gastroenterol 2018; 11: 441-448. https://doi.org/10.1007/s12328-018-0881-1. [CrossRef]
  104. Opel D, Kramer ON, Chevalier M, Bigby M, Albrecht J. Not every patient needs a triglyceride check, but all can get pancreatitis: A systematic review and clinical characterization of isotretinoin‐associated pancreatitis. Br J Dermatol. 2017; 177: 960-966. https://doi.org/10.111/bjd.15207 [CrossRef]
  105. Rawla P, Bandaru SS, Vellipuram AR. Review of infectious etiology of acute pancreatitis. Gastroenterology Res. 2017; 10: 153-158. https://doi.org/ 10.14740/gr858w. [CrossRef]
  106. Yasuoka Y, Yoshida A, Nakajyou T, Yamamoto T, Abe Y. A case report of eosinophilic pancreatitis presenting as inflammatory pancreatic tumor. Jpn J Gastroenterol Surg. 2008; 41: 1953-1959. [CrossRef]
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