Acute Relapsing Pancreatitis - Touch Gastroenterology

Myriam Delhaye is an Associate 

Clinical Director in the 

Medicosurgical Department of 

Gastroenterology (headed by 

Professor Jacques Devière) at the 

Erasme University Hospital. 

Together with the team directed by 

Professor Michel Cremer, she was 

involved in the controversy 

surrounding the clinical significance 

of pancreas divisum and she 

pioneered the use of extracorporeal 

shock wave lithotripsy of bile duct 

and pancreatic stones in 1987. 

Dr Delhaye’s main research interests 

are inflammatory pancreatic 

diseases, pancreatic cystic neoplasms 

and endoscopic therapeutic 

procedures for biliopancreatic 

diseases. She completed a five-year 

academic residency in internal 

medicine with a two-year fellowship 

in gastroenterology at Erasme 

University Hospital. She obtained 

her MD from the Free University of 

Brussels in 1979. 

1 

a report by 

Myriam Delhaye 

Associate Clinical Director, Medicosurgical Department of Gastroenterology, Erasme University Hospital 

Acute relapsing pancreatitis (ARP) represents a 

challenging clinical problem in the field of 

hepatobiliary and pancreatic disorders. It is associated 

with significant morbidity, impairment in quality of 

life and a negative impact on medical costs. Acute 

pancreatitis is a common condition with a reported 

yearly incidence ranging between 300 and 500 

patients per million per year in the Western world. 1 

Without an adequate initial work-up and directed 

therapy, more than half of the patients with an initial 

attack of acute pancreatitis may suffer recurrent 

attacks or develop chronic pancreatitis. 2 

Definitions 

Acute pancreatitis is defined as typical pancreatic 

abdominal pain (mid-epigastric with radiation to the 

back) persisting for several hours, associated with 

elevation of serum amylase or lipase (to more than 

three times the normal levels). 

ARP is defined as two or more well-documented 

separate episodes of pancreatitis (pain and abnormal 

laboratory studies) that resolve between attacks. 3 

Evidence of pancreatitis should be documented by 

computed tomography (CT) or magnetic resonance 

imaging (MRI) during at least one episode. 

Acute idiopathic pancreatitis is a term used when no 

underlying cause has been identified. 

Causes of ARP 

Reference Section 

Acute Relapsing Pancreatitis 

An aetiology can be found in 70% to 80% of patients 

after an attack of acute pancreatitis, with alcohol 

abuse and gallstone disease most often implicated. 4 

Causes of ARP can be classified as follows. 

Toxic/Metabolic Causes 

Alcohol-induced pancreatitis is easily identified based 

on clinical history. 

Hypercalcaemia (due to hyperparathyroidism in 

more than 90% of cases) and hypertriglyceridaemia 

(>1,000mg/dl is usually necessary) are established but 

rare causes of ARP. 5 

Many medications have been implicated as causes of 

acute pancreatitis with a dose-dependent or 

idiosyncratic mechanism for the majority of cases, 4 

but are most often associated with a single episode of 

acute pancreatitis rather than ARP. 

Mechanical Causes 

Mechanical causes can induce a persistent or transient 

obstruction of pancreatic juice flow into the 

duodenum, with a consequent rise in intraductal 

pancreatic pressure. Potential causes of impaired 

pancreatic drainage include: 

• migration of biliary stones, microlithiasis (

Biliary or pancreatic SOD are divided into the 

following three types: 8,10,11 

• Type 1 corresponds to patients with biliary- or 

pancreatic-type pain, elevation of liver function 

tests or pancreatic hydrolases, and dilation of the 

common bile duct (>12mm in diameter) or the 

main pancreatic duct (>5mm in diameter). Type 1 

is considered to be due to a chronic inflammatory 

process (probably secondary to passage of biliary 

lithiasis or microlithiasis through the sphincter), 

which becomes a fibrosis with subsequent stenosis 

of part of or the entire sphincter. 

• Type 2 is considered for patients with biliary- or 

pancreatic-type pain and only one other criterion 

(abnormal laboratory tests or ductal dilation). These 

patients are thought to suffer from a functional 

alteration of the physiological motility of the 

sphincter that causes some delay in the passage of 

biliary or pancreatic juices into the duodenum. 

• Type 3 is reported for patients with only typical 

clinical symptoms. 

Pancreas divisum (PD) is the most common 

congenital variant of the human pancreas occurring 

in 5% to 10% of Caucasian individuals. 12,13 Less than 

5% of the population with PD ever develop 

pancreatic symptoms; subsequently, PD seems to 

have little clinical relevance. 2 

Although controversial, it is postulated that a relative 

outflow obstruction at the site of the minor papilla 

overburdened by draining of the larger dorsal 

pancreas may be the mechanism of pancreatitis in 

some patients with PD and unexplained ARP. 4,14 

However, the frequency of PD is similar in control 

patients, patients with chronic pancreatitis and 

patients with idiopathic pancreatitis. 12,15 

Recruitment bias (greater frequency of PD diagnosis in 

patients referred after unsuccessful opacification of the 

pancreatic ductal system) may have resulted in an 

overestimation of the prevalence of PD in endoscopic 

retrograde cholangio-pancreatography (ERCP) studies 

investigating suspected idiopathic ARP. 16 It has been 

shown that a persistent dilation of the main pancreatic 

duct greater than 3mm at 10 minutes after secretin 

injection assessed during secretin-enhanced magnetic 

resonance cholangio-pancreatography (S-MRCP) is 

correlated with a clinical diagnosis of papillary 

stenosis. 15,17 However, the frequency of such a 

response to secretin suggesting a functional or organic 

stenosis of the major or minor papilla is the same in 

patients with or without PD. 15 Other abnormalities 

that have been associated with ARP include 

anomalous pancreaticobiliary union, choledochocele, 

duodenal duplication cyst and annular pancreas. 18 

BUSINESS BRIEFING: EUROPEAN GASTROENTEROLOGY REVIEW 2005 


Figure 1: Coronal View on T2-weighted MRI, S-MRCP and ERCP of a 

42-year-old Man with Prior Cholecystectomy having Presented with 

10 Attacks of Acute Pancreatitis over Two Years 

A B 

C D 

A 42-year-old man with a history of cholecystectomy presented 10 attacks of acute pancreatitis over two years during which 

he was admitted to hospital five times. This coronal view on T2-weighted MRI (A) and S-MRCP (B) showed a 2cm 

communicating cytic lesion at the junction of body and tail of the pancreas. ERCP demonstrated a normal ductal system in 

the head of the pancreas (C) and a typical branch duct type of intraductal papillary mucinous tumour (IPMT) with intraductal 

filling defect corresponding to mucus (D). A segmental pancreatectomy was performed and pathology revealed a branch duct 

IPMT with in situ carcinoma. 

An isolated, unexplained pancreatic duct stricture 

discovered during the work-up of a first episode of 

acute pancreatitis in a patient over 35 years of age 

without predisposing cause requires exclusion of an 

underlying pancreatic carcinoma. 5 

Intraductal papillary mucinous tumour (IPMT) is the 

most frequent neoplasm associated with ARP. It is an 

intraductal pre-malignant lesion producing mucin that 

blocks the pancreatic duct, thus impeding outflow and 

encouraging bouts of pancreatitis. IPMT is characterised 

by dilation and filling defects of the main pancreatic 

duct or of the branch duct system (see Figure 1). 19 

Miscellaneous Causes 

Genetic diseases can be identified as rare causes of acute 

and recurrent pancreatitis mainly in subjects with early 

onset of pancreatitis and with a history of first- or 

second-degree relatives with unexplained pancreatitis. 4 

These inherited causes are mainly related to cystic 

fibrosis transmembrane conductance regulator gene 

mutations, and trypsinogen-gene mutations. 

Autoimmune pancreatitis is also a rare entity 

characterised by mild pancreatitis associated with 

abnormal laboratory findings (e.g. elevated serum 

immunoglobulin (Ig)G4 levels and presence of autoantibodies), 

imaging studies showing a diffusely 

2

3 


Figure 2: MRI and MRCP Images of a 51-year-old Woman having 

Presented with Seven Attacks of Acute Pancreatitis Since 1998 

A 

B C 

A 51-year-old woman presented seven attacks of acute pancreatitis since 1998. She underwent a cholecystectomy in 

May 2000, but acute pancreatitis recurred, with four attacks during the last 12 months. In this case, there was no alcohol 

abuse, no smoking and no drugs involved. A genetic origin remained possible, as family history was positive for one 

third-degree relative with unexplained ARP. However, genetic testing was negative in the patient. The CT scan showed no 

calcifications. T2-weighted MRI (A) and MRCP before (B) and after (C) secretin injection that were performed one week 

after the last attack of pancreatitis demonstrated a normal pancreatic gland and a normal main pancreatic duct. The 

dynamic response to secretin was also normal with a normal duodenal filling (C). Endoscopic ultrasonography was also 

performed and was normal. A pancreatic SOD type 2 is suspected (based on pancreatic-type pain and increased pancreatic 

hydrolases without dilation of the main pancreatic duct). An ERCP with dual endoscopic sphincterotomy and transient main 

pancreatic duct stenting has been proposed to the patient if another attack occurs. 

swollen pancreas and irregular narrowing of the duct 

due to lymphoplasmacytic infiltration, responding 

favourably to steroid therapy and sometimes 

associated with other autoimmune disorders. 5 

Finally, very rare miscellaneous causes of ARP 

include vascular disorders, infections (e.g. 

tuberculosis, virus and parasite), and tropical 

pancreatitis. 4 Among the patients without an obvious 

cause for ARP, this means that around 20% to 30% of 

all cases with ARP, SOD, PD and occult biliary 

stones and tumours are generally considered as 

aetiological associated factors in 30%, 20%, 20% and 

10%, respectively, leaving only approximately 20% of 

‘idiopathic’ ARP related to genetic, autoimmune, 

infectious and really unknown factors (see Figure 2). 20 

Initial Evaluation Procedures 

History and physical examination are probably the 

most important parts of the initial evaluation to 

search evidence for alcohol abuse, drug-induced 

pancreatitis and a family history of pancreatitis. 

Routine blood tests should include liver function tests 

within 24 to 48 hours of onset of symptoms (a three- 

fold or greater increase in the alanine aminotransferase 

(ALT) level is generally regarded as the best indicator 

of gallstone-induced pancreatitis), and the serum levels 

of calcium and triglyceride soon after admission 

(because of the drop in calcium and triglyceride levels 

due to fasting and administration of intravenous 

fluids). 8 Abdominal U/S is routinely performed in 

patients without previous cholecystectomy in order to 

detect gallbladder stones (with an accuracy of >90%). 

Contrast-enhanced CT scan is usually performed 

either in all patients during their first episode to 

confirm the diagnosis of acute pancreatitis and to 

assess the severity, 8 or only when the attack is severe, 

when the course is complicated, when aetiology 

remains unclear or in the elderly. 2 

Recently, the use of gadolinium-enhanced dynamic 

MRI was found to be comparable with contrastenhanced 

CT for the assessment of the severity of 

acute pancreatitis, while avoiding the use of 

iodinated contrast medium and radiation, and with 

the ability to identify bile duct stones more 

accurately than CT. 21 

S-MRCP should be considered as the first-choice 

procedure in the diagnostic algorithm of ARP (see 

Figure 3), because its diagnostic accuracy in detecting 

the various aetiological lesions of ARP is similar to 

that of ERCP without carrying the risk of potential 

ERCP-related complications. This initial work-up 

during an attack of pancreatitis detects the causes of 

ARP in about 70% of cases. 2 

Further Evaluation Procedures 

If the initial work-up following an attack of 

pancreatitis is negative and successive attacks occur, 

or if the first episode of pancreatitis is moderate to 

severe or occurs after the age of 40 years of age, a 

more extensive evaluation will reveal a diagnosis in 

around two-thirds of this group of patients. 2 

Advanced laboratory analysis may include genetic 

testing in patients younger than 40 years of age, 

tumour markers (carbohydrate antigen (CA) 19–9) 

in patients older than 40 years of age with a positive 

family history or with tobacco use, and serological 

markers of autoimmune pancreatitis if imaging 

studies are compatible with this diagnosis. 

As an additional diagnostic procedure, endoscopic 

ultrasonography (EUS) is able to postulate a cause for 

pancreatitis in approximately one-third of the 

patients with ARP for whom conventional 

evaluation, including transabdominal U/S and 

pancreatic CT with contrast injection, is negative. 22 

Due to its complication rate being lower than that of 

ERCP, EUS should be performed earlier in the 

BUSINESS BRIEFING: EUROPEAN GASTROENTEROLOGY REVIEW 2005

Figure 3: Recommended Algorithm for the Diagnostic Management of ARP 

diagnostic algorithm of ARP, where no evident 

cause is identified after initial evaluation procedures. 

ERCP may be indicated for diagnostic purpose in 

the few patients who suffer two or more attacks of 

acute pancreatitis in whom the aetiology of ARP 

cannot be achieved using high-quality S-MRCP 

and EUS. The aim of diagnostic ERCP is to 

perform ancillary procedures that may improve the 

diagnostic accuracy, such as brush cytology or 

biopsy in suspected neoplasm, minor papilla 

cannulation in suspected PD to clearly demonstrate 

a santorinicele (defined as focal cystic dilation of the 

termination of the dorsal pancreatic duct at the 

minor papilla), 23 sphincter of Oddi manometry in 

suspected SOD or collection of bile in suspected 

occult biliary stones. 7,24 However, ERCP is 

associated with a 3% to 5% complication rate, which 

is much higher in patients with a history of 

pancreatitis and may rise to 30% in cases with 

suspected SOD. 25 Nowadays, sphincter of Oddi 

manometry tends to be replaced by the non-invasive 

S-MRCP, 26 providing information regarding the 

morphology of the pancreatic gland, the dynamics of 

the emptying of the main pancreatic duct and the 

functional status of the exocrine pancreas through 

assessment of the duodenal filling after secretin 

administration. Therefore, ERCP has evolved from 

a diagnostic procedure to an almost exclusively 

therapeutic procedure for the treatment of 


ARP = acute relapsing pancreatitis; Lab = laboratory data; U/S = abdominal ultrasound; CT = computed tomography; S-MRCP = secretin-enhanced magnetic resonance cholangio-pancreatography; EUS = endoscopic 

ultrasonography; MRC = magnetic resonance cholangiography; BD = bile duct; ERCP = endoscopic retrograde cholangio-pancreatography; APBU = anomalous pancreaticobiliary union; CP = chronic pancreatitis; 

SOD = sphincter of Oddi dysfunction; SOM = sphincter of Oddi manometry; IPMT = intraductal papillary mucinous tumor; FNA = fine needle aspiration; PD = pancreas divisum. 

This figure is based on a review of current literature and on the author’s personal experience. 

abnormalities found by less invasive imaging 

techniques such as S-MRCP and EUS. 27 

Management 


{ 

After a negative initial evaluation in patients younger 

than 40 years of age with only one mild episode of 

unexplained acute pancreatitis, expectant approach 

and no further testing is an acceptable management 

strategy, because the medium-term recurrence rate is 

believed to be low and the incidence of malignant 

neoplasm is low in patients with no family history of 

pancreatic cancer and no use of tobacco. 28,29 

However, in patients older than 40 years of age, with 

more than one attack of acute pancreatitis or when 

the initial attack is severe, a systematic identification 

and/or elimination of correctable inciting factors is 

required (see Figure 3). 4 

Occult biliary stones can be demonstrated using 

repeated U/S (for the gallbladder) or EUS (for the 

common bile duct) and treated using endoscopic 

biliary sphincterotomy (EBS) and laparoscopic 

cholecystectomy if the gallbladder is in situ. 

Early ERCP and EBS are safe and beneficial, 

particularly in severe biliary pancreatitis and when 

there is evidence of bile duct obstruction or 

cholangitis (see Figure 4). 30 

4

5 


Figure 4: Potential Treatment Strategies According to the Most Probable Cause of Acute Relapsing Pancreatitis 

ARP = acute relapsing pancreatitis; ERCP = endoscopic retrograde cholangio-pancreatography; EBS = endoscopic biliary sphincterotomy; EUS = endoscopic ultrasonography; MRC = magnetic resonance 

cholangiography; BD = bile duct; UDCA = ursodeoxycholic acid; MPD = main pancreatic duct; APBU = anomalous pancreaticobiliary union; CP = chronic pancreatitis; EPS = endoscopic pancreatic sphincterotomy; 

SOD = sphincter of Oddi dysfunction; ES = endoscopic sphincterotomy; PD = pancreas divisum; S-MRCP = secretin-enhanced magnetic resonance cholangio-pancreatography. 

This figure is based on a review of current literature and on the author’s personal experience. 

Empiric administration of a low-fat diet and oral 

therapy with ursodeoxycholic acid (UDCA) have 

been proposed for patients with suspected biliary 

microlithiasis or sludge before proceeding to more 

technically demanding investigations in high-risk 

patients or patients already cholecystectomised or 

unfit for cholecystectomy. 6,8 

At present, bile analysis and sphincter of Oddi 

manometry are less often performed, because these 

tests are invasive, insensitive and only available at 

tertiary institutions. 11,24 Available data suggest that, 

in suspected pancreatic SOD (on the basis of either 

a basal dilation of the main pancreatic duct or an 

abnormal dynamic response of the pancreatic duct 

at S-MRCP), a dual endoscopic biliary and 

pancreatic sphincterotomy, whether at single or 

separate sessions, yields significantly better response 

than EBS alone. 8,11 

However, the risk of post-sphincterotomy 

pancreatitis is five times higher for this indication 

than for other indications. 31 Placement of a transient 

pancreatic stent might reduce this risk when the 

accessory duct is not patent. 32 This stent usually 

migrates spontaneously, but in case migration does 

not occur, it should be removed for 10 to 14 days 

following dual endoscopic sphincterotomy. 

The selection of patients for treatment of ARP 

associated with PD is difficult, because there is 

currently no diagnostic modality that identifies 

patients who may benefit from dorsal pancreatic 

duct decompression. 13 

S-MRCP could be indicative of true or relative 

stenosis of the minor papilla if prolonged dilation 

of the main pancreatic duct is observed after 

secretin administration. 15 

Endoscopic therapy for patients with ARP 

associated with PD consists of minor papilla 

sphincterotomy, stent insertion or a combination of 

both. 33 The majority of therapeutic trials are small 

retrospective case series with only one randomised 

controlled trial on 19 patients showing a clinical 

benefit after dorsal duct stenting at a mean followup 

of 24 months. 34 Prolonged stenting of the dorsal 

main pancreatic duct should be avoided because of 

the risk of inducing pancreatic damage, mainly 

when the ductal morphology is initially normal. 35 

Therefore, it is recommended that a stent is placed 

after minor papilla sphincterotomy to prevent early 

obstruction secondary to oedema and early 

restenosis, but that the stent is removed in two to 

four weeks if it has not migrated spontaneously into 

the duodenal lumen. 35 


In conclusion, ARP should be evaluated in specialist 

referral centres as diagnosis is time-consuming, 

usually expensive and may expose the patient to a 

substantial morbidity. Future prospective clinical 

trials should define which patients with idiopathic 

ARP (whether or not it is associated with 

References 



anatomical variants) are most likely to benefit from 

endoscopic intervention. These studies should allow 

appropriate patient selection and the development 

of novel, effective, preventive and therapeutic 

strategies to improve the clinical condition of 

these patients. ■ 

1. Andersson R, Andersson B, Haraldsen P, Drewsen G, Eckerwall G, “Incidence, management and recurrence rate of acute 

pancreatitis”, Scand. J. Gastroenterol. (2004);39: pp. 891–894. 

2. Khalid A, Slivka A, “Approach to idiopathic recurrent pancreatitis”, Gastrointest. Endoscopy Clin. N. Am. 

(2003);13: pp. 695–716. 

3. Tarnasky P R, Hawes R H, “Endoscopic diagnosis and therapy of unexplained (idiopathic) acute pancreatitis”, 

Gastrointest. Endoscopy Clin. N. Am. (1998);8: pp. 13–37. 

4. Somogyi L, Martin S P, Venkatesan T, Ulrich II C D, “Recurrent acute pancreatitis: an algorithmic approach to 

identification and elimination of inciting factors”, Gastroenterology (2001);120: pp. 708–717. 

5. Bank S, Indaram A, “Causes of acute and recurrent pancreatitis. Clinical considerations and clues to diagnosis”, 

Gastroenterol. Clin. N. Am. (1999);28: pp. 572–589. 

6. Testoni P A, Caporuscio S, Bagnolo F, Lella F, “Idiopathic recurrent pancreatitis: long-term results after ERCP, endoscopic 

sphincterotomy, or ursodeoxycholic acid treatment”, Am. J. Gastroenterol. (2000);95: pp. 1,702–1,707. 

7. Lee S P, Nicholls J F, Park H Z, “Biliary sludge as a cause of acute pancreatitis”, N. Engl. J. Med. (1992);326: pp. 

589–593. 

8. Levy M J, Geenen J E, “Idiopathic acute recurrent pancreatitis”, Am. J. Gastroenterol. (2001);96: pp. 2,540–2,555. 

9. Chen J W C, Saccone G T P, Toouli J, “Sphincter of Oddi dysfunction and acute pancreatitis”, Gut (1998);43: pp. 

305–308. 

10. Hogan W J, Sherman S, Pasricha P, Carr-Locke D L, “Sphincter of Oddi manometry”, Gastrointest. Endosc. 

(1997);45: pp. 342–348. 

11. Petersen B T, “Sphincter of Oddi dysfunction, part 2: evidence-based review of the presentations with ‘objective’ pancreatic 

findings (types I and II) and of presumptive type III”, Gastrointest. Endosc. (2004);59: pp. 670–687. 

12. Delhaye M, Engelholm L, Cremer M, “Pancreas divisum: congenital anatomic variant or anomaly? Contribution of 

endoscopic retrograde dorsal pancreatography”, Gastroenterology (1985);89: pp. 951–958. 

13. Klein S D, Affronti J P, “Pancreas divisum, an evidence-based review: part I, pathophysiology”, Gastrointest. Endosc. 

(2004);60: pp. 419–425. 

14. Cotton P B, “Congenital anomaly of pancreas divisum as cause of obstructive pain and pancreatitis”, Gut (1980);21: pp. 

105–114. 

15. Matos C, Metens T, Devière J, Delhaye M, Le Moine O, Cremer M, “Pancreas divisum: evaluation with secretinenhanced 

magnetic resonance cholangiopancreatography”, Gastrointest. Endosc. (2001),53: pp. 728–733. 

16. Delhaye M, Engelholm L, Cremer M, “Pancreas divisum: controversial clinical significance”, Dig. Dis. (1988);6: pp. 

30–39. 

17. Matos C, Metens T, Devière J, Nicaise N, Braudé P, Van Yperen G, Cremer M, Struyven J, “Pancreatic duct: 

morphologic and functional evaluation with dynamic MR pancreatography after secretin stimulation”, Radiology 

(1997);203: pp. 435–441. 

18. Delhaye M, Matos C, Devière J, “Acute relapsing pancreatitis. Congenital variants: diagnosis, treatment, outcomes”, J. 

Pancreas (2001);2: pp. 373–381. 

19. Farrell J J, Brugge W R, “Intraductal papillary mucinous tumor of the pancreas”, Gastrointest. Endosc. (2002);55: pp. 

701–714. 

20. Coyle W J, Pineau B C, Tarnasky P R, Knapple W L, Aabakken L, Hoffman B J, Cunningham J T, Hawes R H, 

Cotton P B, “Evaluation of unexplained acute and acute recurrent pancreatitis using endoscopic retrograde 

cholangiopancreatography, sphincter of Oddi manometry and endoscopic ultrasound”, Endoscopy (2002);34: pp. 617–623. 

21. Arvanitakis M, Delhaye M, De Maertelaere V, Bali M, Winant C, Coppens E, Jeanmart J, Zalcman M, Van Gansbeke 

D, Devière J, Matos C, “Computed tomography and magnetic resonance imaging in the assessment of acute pancreatitis”, 

Gastroenterology (2004);126: pp. 715–723. 

22. Yusoff I F, Raymond G, Sahai A V, “A prospective comparison of the yield of EUS in primary vs. recurrent idiopathic 

acute pancreatitis”, Gastrointest. Endosc. (2004);60: pp. 673–678. 

23. Costamagna G, Ingrosso M, Tringali A, Multignani M, Manfredi R, “Santorinicele and recurrent acute pancreatitis in 

pancreas divisum: diagnosis with dynamic secretin-stimulated magnetic resonance cholangiopancreatography and endoscopic 

treatment”, Gastrointest. Endosc. (2000);52: pp. 262–267. 

6

7 


24. Kaw M, Brodmerkel G J, “ERCP, biliary crystal analysis, and sphincter of Oddi manometry in idiopathic recurrent 

pancreatitis”, Gastrointest. Endosc. (2002);55: pp. 157–162. 

25. ASGE guideline, “Complications of ERCP”, Gastrointest. Endosc. (2003);57: pp. 633–638. 

26. Mariani A, Curioni S, Zanello A, Passaretti S, Masci E, Rossi M, Del Maschio A, Testoni P A, “Secretin MRCP and 

endoscopic pancreatic manometry in the evaluation of sphincter of Oddi function: a comparative pilot study in patients with 

idiopathic recurrent pancreatitis”, Gastrointest. Endosc. (2003);58: pp. 847–852. 

27. ASGE guideline, “The role of ERCP in diseases of the biliary tract and the pancreas”, Gastrointest. Endosc. (2005);62: 

pp. 1–8. 

28. Ballinger A B, Barnes E, Alstead E M, Fairclough P D, “Is intervention necessary after a first episode of acute idiopathic 

pancreatitis?”, Gut (1996);38: pp. 293–295. 

29. Draganov P, Forsmark C E, “‘Idiopathic’ pancreatitis”, Gastroenterology (2005);128: pp. 756–763. 

30. Sharma V, Howden C, “Meta-analysis of randomised controlled trials of endoscopic retrograde cholangiopancreatography and 

endoscopic sphincterotomy for the treatment of acute biliary pancreatitis”, Am. J. Gastroenterol. (1999);94: pp. 

3,211–3,214. 

31. Freeman M L, Nelson D B, Sherman S, Haber G B, Herman M E, Dorsher P J, Moore J P, Fennerty M B, Ryan M 

E, Shaw M J, Lande J D, Pheley A M, “Complications of endoscopic biliary sphincterotomy”, N. Engl. J. Med. 

(1996);335: pp. 909–918. 

32. Tarnasky P R, Palesch Y Y, Cunningham J T, Mauldin P D, Cotton P B, Hawes R H, “Pancreatic stenting prevents 

pancreatitis after biliary sphincterotomy in patients with sphincter of Oddi dysfunction”, Gastroenterology (1998);115: 

pp. 1,518–1,524. 

33. Cohen S A, Siegel J H, “Pancreas divisum. Endoscopic therapy”, Surg. Clin. N. Am. (2001);81: pp. 467–477. 

34. Lans J I, Geenen J E, Johanson J F, Hogan W J, “Endoscopic therapy in patients with pancreas divisum and acute 

pancreatitis: a prospective, randomized, controlled clinical trial”, Gastrointest. Endosc. (1992);38: pp. 430–434. 

35. Gerke H, Byrne M F, Stiffler H L, Obando J V, Mitchell R M, Jowell P S, Branch M S, Baillie J, “Outcome of 

endoscopic minor papillotomy in patients with symptomatic pancreas divisum”, J. Pancreas (2004);5: pp. 122–131.

Acute Relapsing Pancreatitis - Touch Gastroenterology

Create successful ePaper yourself

Delete template?

Save as template?