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Copyright ©2010 Baishideng. All rights reserved.
World J Gastrointest Endosc. May 16, 2010; 2(5): 165-178
Published online May 16, 2010. doi: 10.4253/wjge.v2.i5.165
Endoscopic retrograde cholangiopancreatography associated pancreatitis: A 15-year review
Kevin E Woods, Department of Medicine, Gastrointestinal Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, United States
Field F Willingham, Department of Medicine, Division of Gastroenterology, Emory University School of Medicine, Atlanta, GA 30322, United States
Author contributions: Woods KE and Willingham FF performed the analysis and synthesis of the literature and wrote and approved the final version.
Correspondence to: Field F Willingham, MD, MPH, Director of Endoscopy, Emory University School of Medicine, 1365 Clifton Road, NE, Building B STE 1200, Atlanta, GA 30322, United States. field.willingham@emoryhealthcare.org
Telephone: +1-404-7783184 Fax:-+1-404-7782925
Received: January 15, 2010
Revised: April 29, 2010
Accepted: May 6, 2010
Published online: May 16, 2010

Abstract

The aim of this article is to review the literature regarding post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis. We searched for and evaluated all articles describing the diagnosis, epidemiology, pathophysiology, morbidity, mortality and prevention of post-ERCP pancreatitis (PEP) in adult patients using the PubMed database. Search terms included endoscopic retrograde cholangiopancreatography, pancreatitis, ampulla of vater, endoscopic sphincterotomy, balloon dilatation, cholangiography, adverse events, standards and utilization. We limited our review of articles to those published between January 1, 1994 and August 15, 2009 regarding human adults and written in the English language. Publications from the reference sections were reviewed and included if they were salient and fell into the time period of interest. Between the dates queried, seventeen large (> 500 patients) prospective and four large retrospective trials were conducted. PEP occurred in 1%-15% in the prospective trials and in 1%-4% in the retrospective trials. PEP was also reduced with pancreatic duct stent placement and outcomes were improved with endoscopic sphincterotomy compared to balloon sphincter dilation in the setting of choledocholithiasis. Approximately 34 pharmacologic agents have been evaluated for the prevention of PEP over the last fifteen years in 63 trials. Although 22 of 63 trials published during our period of review suggested a reduction in PEP, no pharmacologic therapy has been widely accepted in clinical use in decreasing the development of PEP. In conclusion, PEP is a well-recognized complication of ERCP. Medical treatment for prevention has been disappointing. Proper patient selection and pancreatic duct stenting have been shown to reduce the complication rate in randomized clinical trials.

Key Words: Cholangiopancreatography endoscopic retrograde, Adverse effects, Pancreatitis, Prevention and control/therapy, Risk assessment, Risk factors, Ampulla of vater, Sphincter of oddi, Humans



INTRODUCTION

The first endoscopic pancreatogram was obtained in 1968, and in 1974, biliary sphincterotomy was first described[1-2]. This was followed by the first report of papillotomy for the management of choledocholithiasis[3] and in subsequent years, numerous endoscopic techniques evolved to address pancreaticobiliary disease. As computerized axial tomography and magnetic resonance imaging have improved, endoscopic retrograde cholangiopancreatography (ERCP) has evolved from primarily a diagnostic procedure into primarily a therapeutic procedure.

As the indications for ERCP have increased, a greater focus on recognizing and preventing complications has emerged. Asymptomatic hyperamylasemia, cardiopulmonary depression, hypoxia, aspiration, intestinal perforation, bleeding, cholangitis, adverse medication reactions, sepsis, acute pancreatitis and death all are recognized complications of ERCP. Post-ERCP pancreatitis (PEP) remains the leading cause of morbidity and mortality post procedure and has been at the center of studies designed to improve procedural outcomes[4-9].

Over the last 15 years, in large prospective trials the overall and pancreatitis complication rates following ERCP have ranged from 2.4% to 15.9%[10-13] and 1.0% to 15.1%[14-16] respectively. Some studies have suggested that lower rates of PEP can be achieved; however the incidence of pancreatitis remains high particularly in at-risk patient populations. Pancreatitis continues to be the major cause of post-procedure morbidity and mortality[17-22] (Table 1).

Table 1 Clinical trials evaluating the incidence of overall complications and post-ERCP pancreatitis.
AuthorCountryYear publishednNo. ERCPOverall complications (%)Post-ERCP pancreatitis (%)
Large prospective trials
Wang[20]China2009269131787.924.31
Kapral[62]Austrian2008NRa313212.605.10
Dundee[23]Australia20075637005.713.71
Williams[24]United Kingdom2007456152345.001.60
Bhatia[25]India200614971497NRa3.80
Cheng 2006 and Sherman 2003b[111,154]United States20061115NRaNRa15.10
Andriulli[59]Italy200411271050NRNRa4.80
Christensen[13]Denmark2004NRa117715.903.80
BarthetFrance20026581159NRa3.50
Vandervoort[10]United States20021223122311.207.20
Freeman[58]United States2001NRa1963NRa6.70
Masci[35]Italy2001210320444.951.80
DePalma[27]Italy1999535NRaNRa5.30
Deans[11]United Kingdom199795810002.401.00
Johnson[28]United States19971979NRaNRa 10.40
Freeman[29]United States and Canada19962347NRa9.805.40
Loperfido[12]Italy19952769NRa4.001.30
Large retrospective trials
Cotton[29]United States200911497NRa4.002.60
Lukens[30]United States2009260639243.120.97
Andriulli[31]Italy200716855NRa6.853.47
Cheon[60]United States2007987214331NRa4.00
DIAGNOSIS OF PEP

PEP has been defined as the presence of new pancreatic-type abdominal pain associated with at least a threefold increase in serum amylase concentration occurring 24 h after an ERCP, with pain severe enough to require admission to the hospital or to extend an admitted patient’s length of stay. This definition was developed in 1991 based upon approximately 15 000 procedures evaluated during a consensus workshop. The severity of PEP was defined according to length of stay (mild pancreatitis 2-3 d, moderate pancreatitis 4-10 d and severe pancreatitis more than 10 d or intensive care admission or local complications secondary to pancreatitis)[23]. This consensus definition has not been uniformly adopted and many studies published after 1991 have used different criteria to define PEP and classify severity.

Several studies have challenged the serum amylase threshold of three times the upper limit of normal, arguing that this definition is not always consistent with the clinical and morphological features of pancreatitis[24-30]. Variations in the published studies regarding the criteria for serum amylase elevationhave included twice[28-31], four times[10,32-33] and five times[25-26,33-35] the upper limit of the normal.

In regard to the severity of PEP, there is also heterogeneity in criteria used in published studies. Some authors have used the Atlanta criteria published in 1993 to define severity[36-38]. The Atlanta criteria incorporate systemic complications of PEP by integrating the Acute Physiologic and Chronic Health Evaluation (APACHE) II classification and the Ranson’s criteria to define the severity[38-40]. An APACHE II score greater than 8 or a Ranson’s score with 3 or more of 11 criteria would be defined as severe PEP. Some studies have used the APACHE II classification alone to grade the severity of PEP[41]. Other studies have used combinations of criteria to define the presence and severity of PEP or have established unique definitions[31,36,42-45]. The heterogeneity of criteria in the literature on PEP hinders direct comparison of the published clinical trials.

PATHOPHYSIOLOGY OF PEP

The pathophysiology of PEP is not well understood. Mechanical, hydrostatic, chemical, enzymatic, allergic, thermal, cytokine and microbiological factors have all been proposed as causes[37,46-49]. Many studies suggest that PEP results from mechanical trauma with injury of the papilla or pancreatic sphincter causing swelling of the pancreatic duct and obstruction to the flow of pancreatic enzymes. This hypothesis remains controversial and no consensus related to the pathogenesis of PEP has been established.

The cascade of events leading to acute pancreatitis has been characterized in three phases. The first phase is characterized by premature activation of trypsin within the pancreatic acinar cells[50]. The second phase is characterized by intrapancreatic inflammation. The third phase is characterized by extrapancreatic inflammation[50]. Inflammation in the second and third phases has been described in a four step process with (1) activation of inflammatory cells; (2) chemoattraction of activated inflammatory cells; (3) activation of adhesion molecules resulting in binding of inflammatory cells to the endothelium; and (4) migration of activated inflammatory cells into areas of inflammation[50]. Recent studies have evaluated proinflammatory markers (TNF, IL-1, IL-6, IL-8, PAF and IL-10) in the setting of PEP[51-54]. While three randomized control trials suggested a protective effect using low and high dose (4 μg/kg and 20 μg/kg) interleukin 10 given intravenously 15-30 min prior to ERCP[14], subsequent studies using similar IL-10 protocols did not support these findings[55-56]. Though not demonstrated to date, modulation of proinflammatory pathways could represent an appealing goal for studies evaluating PEP and the systemic inflammatory response.

PROCEDURAL RELATED FACTORS ASSOCIATED WITH PEP

Although the triggers of the inflammatory cascade are not yet well understood, procedural and patient- related factors have been clearly associated with the incidence of PEP. ERCP is the most technically difficult endoscopic procedure performed in both inpatient and outpatient settings by trainees and experienced endoscopists. While trauma to the duodenum or papilla during endoscopy without cannulation rarely causes pancreatitis, cannulation of the papilla, especially in moderate to difficult cases, has been associated with high rates of PEP[7]. Procedures involving multiple (> 1-4) or failed attempts at cannulation, multiple pancreatic injections (≥ 2-5), pancreatic acinarization and prolonged cannulation time (> 10 min) have been associated with PEP. Operator experience, ampullary balloon dilation, pre-cut access sphincterotomy, endoscopic sphincterotomy (ES), sphincter of Oddi manometry, distal common bile duct diameters of ≤ 1 cm, presence of a pancreatic stricture, papillectomy and procedures not involving stone removal have also been associated with higher risks for developing PEP[10,12,20,29,35,46,57-60] (Table 2).

Table 2 Patient and procedural risk factors associated with post-ERCP pancreatitis.
Patient related factors
Female sex
Young age
History of or suspected sphincter of oddi dysfunction
History of pancreatitis, recurrent pancreatitis or post-ERCP pancreatitis
Procedure related factors
Difficult or multiple cannulation attempts
Multiple pancreatic contrast injections
Pancreatic acinarization
Precut sphincterotomy
Endoscopic papillary balloon dilation
Sphincter of oddi manometry
Distal common bile duct diameter ≤ 1 cm
Presence of a pancreatic stricture
Procedures not involving stone removal
OPERATOR EXPERIENCE

While there is no established mandate for procedure volume for competence in ERCP, a prospective study published in 1996 to evaluate the number of supervised ERCPs a physician must perform to achieve procedural competence was reported to be at least 180 procedures[61]. In the United States, the American Society for Gastrointestinal Endoscopy and the American College of Gastroenterology have published quality indicators for ERCP. It is expected that competent endoscopists will be able to perform sphincterotomy, clear the common bile duct of stones, provide relief of biliary obstruction and successfully place stents for bile leaks in ≥ 85% of cases[62].

There have been few studies published in regard to operator experience in ERCP and this issue remains controversial. A recent study in Austria demonstrated a case volume exceeding 50 ERCPs per year had higher success and lower overall complication rates[63]. It is generally agreed that the case mix at high volume and academic referral centers may include a greater proportion of difficult and high-risk cases which may confound the relationship between experience and complication rates.

While operator experience is felt to be critical for high quality outcomes, many large prospective and retrospective trials have not shown consistent data correlating inexperience with PEP. Higher rates of bleeding have been reported after endoscopic sphincterotomy with a mean case volume of < 1 per wk[19] and trainee involvement was associated with severe or fatal complications in a recent retrospective analysis[64]. A large prospective trial however, found that case volume had no effect on the incidence of PEP[29]. A prospective survey of ERCP in the United Kingdom in 2007 based on self reported surveys demonstrated that 15% of all credentialed endoscopists performed less than 50 ERCPs per year as compared to 61% of those in training with 11% of deaths with endoscopists performing less than 50 ERCPs per year. Although the rates of PEP were low at 1.5%, the success rates for bile duct stone extraction and biliary stent placement were 62% and 73% respectively. The authors summarized that in the UK there is a need for fewer operators and greater experience in those performing therapeutic endoscopy[65]. In the same year, a study in France showed no risk associated with operator inexperience[66].

CANNULATION TECHNIQUES

Cannulation techniques to access the pancreatic and biliary ducts include the use of sphincterotomes or straight or curved catheters with guide-wires or contrast injection. When an initial attempt at cannulation fails, access may be achieved after placement of a pancreatic guide-wire or stent to help guide the endoscopist towards the common bile duct and away from the pancreatic duct. Precut access papillotomy is frequently employed in referral centers when conventional approaches fail. Rare or experimental techniques such as the use of endoscopic scissors or endoscopic dissection with a cotton swab have been reported but are rarely employed in clinical practice[67].

Compared to standard catheters, the use of sphincterotomes may reduce failed attempts to obtain biliary access, decrease time required to cannulate the common bile duct and decrease the rate of PEP[68-69]. Selective sphinctertome cannulation with a guide wire may be associated with a reduced rate of PEP compared to cannulation with contrast injection[68-72] (Table 3). In 2008, a large prospective controlled trial randomized 430 patients into sphincterotome plus guide-wire versus conventional cannulation arms. The series demonstrated a significantly higher rate of cannulation with guide-wires but failed to show a significant difference in the rate of PEP between the two approaches[73]. The authors reported an 8.8%-14.9% increased risk of PEP after greater than 4 attempts at the papilla, highlighting the importance of cannulation with fewer attempts. These findings are consistent with previous studies[10,73].

Table 3 Frequency of post-ERCP pancreatitis - conventional contrast based cannulation versus guide-wire cannulation in randomized trials.
Rate of pancreatitis
AuthorYear publishedCountrynCC (%)GWC (%)P value
Lee[72]2009Korea30011.302.000.001
Bailey[73]2008Australia4307.906.200.48
Artifon[70]2007Brazil and United States30016.608.600.037
Lella[69]2004Italy3924.100.00< 0.01
Cortas[68]1999Canada4710.305.60NRa
PANCREATIC DUCT INJECTION

Multiple pancreatic duct injections (≥ 2-5)[10,20,29,59] and pancreatic acinarization[12,20,35] have been recognized as risk factors for PEP. Differences in the osmolality and ionicity of contrast media have been studied with varying results in terms of impact on PEP[30,33,60,74-76]. A recent meta-analysis of thirteen randomized controlled trials indicated there was no significant difference between high and low- osmolality contrast media[76]. Earlier studies suggested that there was a decreased risk of PEP with the use of non–ionic contrast agents[74], however this has not been consistently demonstrated[75]. One large retrospective analysis of 14 331 ERCPs suggested that less opacification of the pancreatic duct, head versus tail, resulted in significantly lower rates of PEP[60]. Although there is heterogeneity, clinical trial data suggest that hydrostatic pressure may play a role in the development of pancreatitis.

PANCREATIC DUCT STENTING

The theory that PEP is caused by pancreatic duct obstruction is supported by the majority of randomized controlled trials that demonstrate a decreased incidence of pancreatitis in high risk patients with the placement of a pancreatic duct stent[18,77-84]. In the three largest studies published to date evaluating the rate of pancreatitis with pancreatic duct stent placement, there were significant differences with decreased rates of PEP of 10.4%, 14.8% and 52.3%[17,78-79]. While pancreatic duct stenting has been shown to decrease the risk of PEP, it has not been able to prevent it. Despite stent placement, pancreatitis occurs in 2.0%-14% of cases[78-79,81,83-84] and some studies fail to demonstrate a statistically significant protective effect[60,83-84] (Table 4).

Table 4 Randomized controlled trials evaluating the effect of pancreatic duct stenting on prevention of post-ERCP pancreatitis.
AuthorCountryYear publishednRate of post-ERCP pancreatitis
P value
Without stent (%)With stent (%)
Tsuchiya[84]Japan20076412.503.10NRa
Sofuni[78]Japan200720113.603.200.02
Harewood[77]United States20051933.000.000.02
Fazel[85]United States20037428.005.00< 0.05
Tarnasky[18]United States19988026.007.000.03
Smithline[87]United States19939318.0014.000.299
BILIARY STONE EXTRACTION

In the setting of choledocholithiasis, endoscopic papillary balloon dilatation (EPBD), ES and mechanical lithotripsy are the techniques used to extract obstructing stones. There have been multiple studies that have established the increased rate of PEP with EPBD ranging from 4.9%-20.0% versus 0.42%-10.0% with ES[85-88]. Prospective trials support this observation; however it is difficult to generalize the findings given the many factors that contribute to procedural complications[89-93] (Table 5). Balloon dilation may also be required in some clinical settings. If a patient has had a prior sphincterotomy and has limited remaining tissue for incision, balloon dilation may be necessary to enlarge the bile duct insertion and enable stone extraction.

Table 5 Frequency of post-ERCP pancreatitis - endoscopic sphincterotomy vs endoscopic papillary balloon dilation in randomized studies.
AuthorYear publishedCountrynRate of pancreatitis
P value
ES (%)EPBD (%)
DiSario[98]b2004United States2370.8315.38< 0.05
Fujita[87]2003Japan2822.8010.90< 0.05
Vlavianos[92]2003United Kingdom2021.014.86NRa
Arnold[89]2001Germany6010.0020.00NRa
Bergman[99]1997The Netherlands2026.936.93NRa
PATIENT-RELATED RISK FACTORS ASSOCIATED WITH PEP

Given the high risk of PEP in certain populations, identifying a clear indication is critical in reducing the complication rate. It has been well recognized that ERCP is riskiest in patients who need it the least[21,94]. Large prospective trials have demonstrated that female gender, age less than 60-70 years, suspected SOD and recurrent or prior PEP were associated with a higher risk of PEP[10,12,20,29,35,57,95] (Table 2). Though widely accepted, there has been some heterogeneity across studies. For example, one smaller trial suggested an age of less than 50 as a significant risk factor[95]. A recent large retrospective study of 16 855 patients demonstrated the highest rates of PEP were associated with patients with SOD but there was no significant increase in younger patients or in women[64]. Alternatively, a meta-analysis evaluating five patient- related risk factors demonstrated a relative risk of SOD of 4.09 (95% CI 1.93 to 3.12; P < 0.001) and female gender of 2.23 (95% CI 1.75 to 2.84; P < 0.001)[96]. One study demonstrated a 10 fold increase in the development of PEP in patients with SOD[97].

Some factors may be protective as well. Studies have suggested that the absence of chronic pancreatitis[58], the presence of obesity[98], older age (> 80)[99] and a history of alcohol consumption or cigarette smoking may be associated with a decreased risk of PEP[100]. Proper patient selection and identification of patients at higher risk is the most effective means of reducing the incidence of PEP.

PHARMACOLOGIC AGENTS EVALUATED IN PREVENTION/REDUCITON OF PEP

There has been great interest in the affect of pharmacologic agents on PEP. Preventing cellular injury and pancreatic tissue auto-digestion may involve blocking the premature activation of proteolytic enzymes within the acinar cells[19,101-109]. Though conceptually straightforward, the goal of blocking this activation has been difficult to achieve. Multiple trials have been performed with a goal of reducing the incidence or severity of PEP. Approximately 34 (Table 6) pharmacologic agents and procedures (e.g. topical application of pharmacologic agents injected or sprayed on to the papilla) have been evaluated for potential prevention of PEP in controlled trials. Most clinical trials have been disappointing and a minority of studies has demonstrated benefit (Table 7)[14,15,31,34,42-45,55,56,59,96,110-161].

Table 6 Pharmacologic agents evaluated for potential reduction/prevention of post-ERCP pancreatitis.
Pharmacologic agentRCT showed benefit
AllopurinolYes
CephtazidimeYes
DiclofenacYes
GabexateYes
Glyceryl trinitrateYes
HydrocortisoneYes
IndomethacinYes
Interleukin-10 (IL-10)Yes
Nafamostat mesylateYes
OctreotideYes
SomatostatinYes
UlinastatinYes
Anticholinergic drugsNo
AprotininNo
Botulinum toxinNo
CalcitoninNo
EpinephrineNo
Fresh frozen plazmaNo
GlucagonNo
H-2 BlockerNo
HeparinNo
LidocaineNo
MethylprednisoloneNo
N-aceytyl cysteine (NAC)No
Natural beta-caroteneNo
NifedipineNo
NitroglycerinNo
Parenteral nutritionNo
PentoxifyllineNo
PrednisoneNo
Recombinant PAF acetylhydrolase (rPAF-AH)No
SeleniumNo
SemapimodNo
Table 7 Randomized controlled trails of pharmacologic agents evaluated for reduction or prevention of post-ERCP pancreatitis.
Rate of post-ERCP pancreatitis (%)
AgentAuthorFactor studiednOverallControlInterventionP value
Allopurinol
Martinez–Torres[110]Allopurinol 300 mg PO at 15 h; 300 mg PO at 3 h before ERCP170NRa9.402.300.049
Romagnuolo[111]bAllopurinol 300 mg PO at 1 h before ERCP586NRa4.105.500.440
Katsinelos[112]Allopurinol 600 mg PO at 15 h; 600 mg PO at 3 h before ERCP24310.2017.803.20< 0.001
Mosler[113]Allopurinol 600 mg PO at 4 h; 300 mg PO at 1 h before ERCP34612.5512.1412.960.520
Budzynska[114]Allopurinol 200 mg PO at 15 h; 200 mg PO at 3 h before ERCP30010.707.9012.100.320
Beta-carotene
Lavy[115]Natural beta-carotene 2 g at 12 h before ERCP3219.609.6010.00NRa
Botulinum toxin
Gorelick[116]Botulinum toxin injection after biliary sphincterotomy26NRa43.0025.000.340
Cephtazidime
Raty[117]Cephtazidime 2g IV 30 min before ERCP321NRa9.382.580.009
Hydrocortisone
Kwanngern[118]Hydrocortisone 100 mg IV at 1 h before ERCP1206.6711.861.640.031
Manolakopoulos[119]bHydrocortisone 100 mg IV at 30 min before ERCP34010.0013.007.100.380
De Palma[31]Hydrocortisone 100 mg IV immediately before ERCP5295.304.905.70NS
Prednisone
Sherman[120]bPrednisone 40 mg PO at 15 h and at 3 h before ERCP111515.0713.6016.600.190
Budzynska[114]Prednisone 40 mg at 15 h; 40 mg at 3 h before ERCP10.707.9012.000.330
Methylprednisolone
Dumot[43]Methylprednisolone 125 mg IV immediately before ERCP286NRa8.7012.400.340
Heparin
Barkay[42]Unfractionated heparin 5000 IU SC 20-30 min before ERCP106NRa7.407.80NS
Rabenstein[121]Low molecular weight heparin Certoparin 3000 IU SC the day before ERCP4488.508.818.140.870
Interlukin-10
Sherman[56]bIL-10 8 μg/kg IV 15-30 min before ERCP30517.3814.3015.400.830
IL-10 20 μg/kg IV 15-30 min before ERCP22.000.140
Deviere[14]IL-10 4 μg/kg IV 30 min before ERCP14429.9024.4010.410.046
IL-10 20 μg/kg IV 30 min before ERCP6.810.017
Dumot[55]IL-10 8 μg/kg IV 15 min before ERCP20010.009.1010.900.650
N-acetyl cystine
Milewski[122]NAC 600 mg IV BID × 2 d after ERCP1069.4311.767.27NS
Katsinelos[123]NAC 70 mg/kg 2 h before and 35 mg/kg 4 h intervals for 24 h after procedure24910.809.6012.10> 0.500
Nifedipine
Prat[124]Nifedipine 20 mg PO 3-6 h before ERCP15515.5017.70 13.20NS
Sand[125]Nifedipine 20 mg PO q 8 h the day of ERCP1663.614.004.00NRa
Nitroglycerin
Hao[126]Glyceryl trinitrate 5 mg IV and 100 mg vitamin C 5 min before ERCP maneuvers7416.2025.007.900.012
Beauchant[127]bNitroglycerin bolus of 0.1 mg, then 35 g/kg/min IV for 6 h after ERCP20812.0015.0010.000.260
Kaffes[128]Transdermal glyceryl trinitrate patch (15 mg) precordial area 30-40 min before ERCP318NRa7.407.70NS
Moreto[129]Transdermal glyceryl trinitrate patch (15 mg) precordial area 30-40 min before ERCP1449.0015.004.000.030
Sudhindran[130]Glyceryl trinitrate 2 mg SL 5 min before ERCP18613.0018.008.00< 0.050
Diclofenac
Khoshbaten[131]Diclofenac 100 mg PR immediately after ERCP10015.0026.004.00< 0.010
Cheon[132]Diclofenac 50 mg at 30-90 min before and at 4-6 h after ERCP20716.4016.7016.20NS
Murray[44]Diclofenac 100 mg PR immediately after ERCP22011.0015.456.360.049
Indomethacin
Sotoudehmanesh[133]Indomethacin 100 mg PR after ERCP4424.986.783.16OR 0.4 (0.2 - 1.1)
Octreotide
Kisli[134]Octreotide 0.1 mg gtt 60 min before ERCP and continued during and after ERCP120NRa11.4915.15NS
Li[135]bOctreotide 0.3 mg gtt 1 h before -6 h after ERCP; then 0.1 mg SC; 12 h later 0.1 mg SC8323.855.262.420.046
Thomopoulos[136]Octreotide 500 μg TID starting 24 h before ERCP20110.898.902.000.03
Testoni[137]bOctreotide 200 μg TID × 24 h before ERCP114NRa14.3012.00NS
Hardt[138]Octreotide 200 μg SC the night before ERCP94NRaNRaNRaNS
Duvnjak[139]Octreotide 0.5 mg SC 60 min before ERCP209NRa9.523.85NS
Arvanitidis[140]Octreotide 0.1 mg SC 30 min before; 8 h and 16 h after ERCP7310.9511.1110.81NS
Tulassay[45]bOctreotide 0.1 mg SC 45 min after ERCP11997.846.005.90NS
Arcidiacono[141]Octreotide 0.1 mg SC 120 and 30 min before; 4 h after ERCP1516.62NRaNRaNS
Baldazzi[142]Octreotide 0.1 mg SC 45 min before; 6 h after ERCP100NRaNRaNRaNRa
Testoni[143]Octreotide 0.2 mg SC before ERCP60NRaNRaNRaNS
Testoni[34]Octreotide 200 μg TID × 3 d before ERCP60NRaNRaNRaNS
Gabexate
Ueki[144]Gabexate 600 mg IV 60-90 min before and 22 h after ERCP682.90NRa2.90NS
Manes[145]bGabexate mesylate 500 mg within 1 h before ERCP6085.609.403.90< 0.01
Gabexate mesylate 500 mg within 1h after ERCP3.40< 0.01
Xiong[146]Gabexate 300 mg IV 30 min before gtt until 4 h after ERCP2006.7010.503.100.04
Fujishiro[151]bGabexate 900 mg/1500 mL gtt for 13 h beginning 1 h before ERCP139NRaNRa4.30NS
Andriulli[59]bGabexate 500 mg 30 min before gtt until 6 h after ERCP11275.604.805.80NS
Masci[96]bGabexate 500 mg IV 30 min before gtt until 6.5 h after ERCP and 1 g IV for 13 h after ERCP4341.802.201.40NS
Andriulli[147]bGabexate 500 mg IV 30 min before and 2 h after ERCP5798.606.508.10NS
Cavallini[148]bGabexate 1 g IV 30-90 min before gtt until 12 h after ERCP4185.008.002.000.03
Nafamostat mesylate
Choi[149]Nafamostat mesylate 20 mg gtt 1 h before and for 24 h after ERCP7045.407.403.300.018
Ulinastatin
Yoo[150]Ulinastatin 100 000 U gtt after ERCP for 5.5 h2276.205.606.700.715
Ueki[144]Ulinastatin 150 000 units 60-90 min before & for 22 h after ERCP682.902.902.90NS
Fujishiro[151]bUlinastatin 150 000 units 1 h before, during; 11 h after ERCP6.50NS
Ulinastatin 50 000 units8.50NS
Tsujino[152]bUlinastatin 150 000 U gtt 10 min before ERCP4065.177.402.900.041
Pentoxifylline
Kapetanos[153]Pentoxifylline 400 mg PO TID before ERCP3204.383.005.600.28
Recombinant PAF acetylhydrolase
Sherman[154]bRecombinant PAF acetylhydrolase (rPAF-AH) 1 mg/kg gtt < 1 h before ERCP60017.6019.6017.500.59
Recombinant PAF acetylhydrolase (rPAF-AH) 5 mg/kg gtt < 1 h before ERCP15.900.34
Semapimod
van Westerloo[155]Semapimod IV 50 mg/100 mL glucose gtt 1 h before ERCP24211.9814.889.090.117
Somatostatin
Lee[156]bSomatostatin 3 mg in 500 mL NS gtt 12 h starting 30min before ERCP3916.659.603.600.02
Andriulli[59]bSomatostatin 750 μg IV 30 min before and continued for 6 h after ERCP6.30NS
Arvanitidis[157]Somatastatin 4 μg/kg gtt 12 h on identification of the papilla and before introduction of the catheter372NRa9.801.70< 0.05
Somatostatin 3 mg gtt 12 h on identification of the papilla and before introduction of the catheter1.70< 0.05
Poon[158]Somatostatin 250 mg IV bolus immediately after ERCP270NRa13.304.400.01
Andriulli[147]bSomatastatin 750 μg IV 30 min before and 2 h after ERCP11.50NS
Poon[159]Somatostatin 3 mg in 500 mL NS gtt for 12 h starting 30 min before ERCP2205.9110.003.000.03
Bordas[160]Natural somatostatin 4 mg/kg IV on identification of the papilla and before introduction of the catheter160NRa10.002.50< 0.05
Topical spray on papilla
Matsushita[15]Epinephrine (10 mL of 0.02%) sprayed on papilla before cannulation3701.102.160.000.123
Schwartz[161]Lidocaine (10 mL of 1%) sprayed on the major papilla before cannulation2944.083.044.320.73

Allopurinol has been shown in two of five prospective trials to decrease the incidence of PEP[110,112]. In these trials showing benefits, allopurinol was given in 300 mg or 600 mg doses at 15 h and 3 h prior to ERCP. When reviewing other studies of allopurinol, these effects were not significant in patients dosed on a different 4 h and 1 h regimen and with varying dose concentrations of allopurinol[111,113,114]. This may suggest that not only the dose but timing of allopurinol administration is important in the reduction of PEP. Diclofenac, a non steroidal anti-inflammatory drug, was evaluated in three trials. With diclofenac 100 mg PR dosed immediately after ERCP, the incidence of PEP was decreased[44,131] but a trial evaluating diclofenac 50 mg PO at 30-90 min prior to ERCP and up to 4-6 h post ERCP showed no decrease in PEP[132]. In regard to glyceryl trinitrate[129], hydrocortisone[118] and interleukin-10[14], all agents were shown in one randomized control trial to show benefit. However in studies with larger numbers of patients[31,56,128] these findings were found to be statistically insignificant.

Gabexate[145,146,148], octreotide[135,136], somatostatin[156,159] and ulinastatin[152] have all been reported to show a reduction in PEP. However there have been studies evaluating each of these agents with similar designs that report no significant reduction in the incidence of PEP. These differences could be explained by the selection of patients, number of patients, clinical presentation and timing of administration or dosage of the agent under investigation.

While the use of allopurinol, cephtazidime, diclofenac, gabexate, glyceryl trinitrate, hydrocortisone, indomethacin, interleukin-10, nafamostat mesylate, octreotide, somatostatin and ulinastatin have shown promise in clinical trials, there is currently no accepted pharmacologic intervention to prevent pancreatitis and in some cases (gabexate, nafamostat and somatostatin) the pharmacologic agent is not approved for use in some countries. Nevertheless, pharmacologic prevention remains an active area of research.

MANAGEMENT OF PEP

Once mild or moderate PEP has occurred it usually quickly resolves with conservative therapy. Although there are no specific guidelines for the treatment of PEP, a recent study demonstrated that a protocol-based management strategy was associated with less severe pancreatitis, shorter lengths of hospital stay, need for fewer imaging studies and less use of antibiotics[102]. Practice guidelines for acute pancreatitis treatment are available and may be applicable to PEP as well[50].

In patients with persistent or severe PEP, two important markers of severity are multisystem organ failure and pancreatic necrosis, both of which require aggressive management[23]. Early identification of organ failure, pancreatic necrosis, perforation (especially in the setting of endoscopic sphincterotomy), biliary damage/ leak and pancreatic fluid collections are important clinical branch points, potentially requiring more intensive intervention. Checking serum transaminases, amylase and lipase is not routinely recommended post- ERCP. If assessed, elevations are commonly observed post procedure. These elevations are likely secondary to intermittent biliary, pancreatic or papillary obstruction. 46% of patients in a recent study were reported to have elevated liver test elevations after ERCP and only 5.4% of them had PEP[103]. Asymptomatic elevations are not an indication for a change in management and repeat ERCP is performed only with a clear indication.

Although there is controversy related to enteral feeding during treatment of acute pancreatitis, patients who are unlikely to resume oral nutrition within five days require nutritional support which can be provided via TPN or enteral routes. There appears to be some advantages to enteral feeding and a recent study found that initiating oral nutrition after mild acute pancreatitis with a low fat soft diet appeared to be safe but did not result in a shorter length of hospitalization[104].

CONCLUSION

Acute pancreatitis is the most common complication after ERCP. The pathophysiology is not well understood but theories regarding mechanical, hydrostatic, chemical, enzymatic, allergic, thermal, cytokine and microbiological factors have been proposed. While trauma during endoscopy without cannulation rarely causes pancreatitis, procedural factors involving cannulation, access and pancreaticobiliary drainage have been associated with PEP. Although operator experience is important in high quality outcomes, many large prospective and retrospective trials have not shown consistent data associating inexperience with increased incidence, perhaps due to the importance of case-mix in outcome. Patient-related risk factors are well recognized with Sphincter of Oddi dysfunction and a history of PEP conferring additional risk in the post-procedure setting. However, obesity, older age, alcohol consumption and cigarette smoking may be protective. Approximately 34 pharmacologic agents have been evaluated and 63 clinical trials have been performed in an effort to identify an agent to prevent PEP. Over the last 15 years, no pharmacologic agent has been accepted in reducing PEP due to a lack of reproducibility, heterogeneity in outcomes and/or limitations in study design. Proper patient selection and identification of risk factors pre-procedure is the most effective means of reducing the incidence of PEP.

Footnotes

Peer reviewers: Tony CK Tham, MD, Consultant Gastroenterologist, Ulster Hospital, Dundonald, Belfast BT16 1RH, Northern Ireland, United Kingdom; Everson Luiz de Almeida Artifon, MD, PhD, FASGE, University of Sao Paulo School of Medicine, Rua Guimaraes Passos, Vila Mariana, Sao Paulo 04107030, Brazil

S- Editor Zhang HN L- Editor Roemmele A E- Editor Liu N

References
1.  McCune WS, Shorb PE, Moscovitz H. Endoscopic cannulation of the ampulla of vater: a preliminary report. Ann Surg. 1968;167:752-756.  [PubMed]  [DOI]  [Cited in This Article: ]
2.  Peel AL, Hermon-Taylor J, Ritchie HD. Technique of transduodenal exploration of the common bile duct. Duodenoscopic appearances after biliary sphincterotomy. Ann R Coll Surg Engl. 1974;55:236-244.  [PubMed]  [DOI]  [Cited in This Article: ]
3.  Zimmon DS, Falkenstein DB, Kessler RE. Endoscopic papillotomy for choledocholithiasis. N Engl J Med. 1975;293:1181-1182.  [PubMed]  [DOI]  [Cited in This Article: ]
4.  Zimmon DS, Falkenstein DB, Riccobono C, Aaron B. Complications of endoscopic retrograde cholangiopancreatography. Analysis of 300 consecutive cases. Gastroenterology. 1975;69:303-309.  [PubMed]  [DOI]  [Cited in This Article: ]
5.  Bilbao MK, Dotter CT, Lee TG, Katon RM. Complications of endoscopic retrograde cholangiopancreatography (ERCP). A study of 10,000 cases. Gastroenterology. 1976;70:314-320.  [PubMed]  [DOI]  [Cited in This Article: ]
6.  Skude G, Wehlin L, Maruyama T, Ariyama J. Hyperamylasaemia after duodenoscopy and retrograde cholangiopancreatography. Gut. 1976;17:127-132.  [PubMed]  [DOI]  [Cited in This Article: ]
7.  Deschamps JP, Allemand H, Janin Magnificat R, Camelot G, Gillet M, Carayon P. Acute pancreatitis following gastrointestinal endoscopy without ampullary cannulation. Endoscopy. 1982;14:105-106.  [PubMed]  [DOI]  [Cited in This Article: ]
8.  Odes HS, Novis BN, Barbezat GO, Bank S. Effect of calcitonin on the serum amylase levels after endoscopic retrograde cholangiopancreatography. Digestion. 1977;16:180-184.  [PubMed]  [DOI]  [Cited in This Article: ]
9.  Börsch G, Bergbauer M, Nebel W, Sabin G. [Effect of somatostatin on amylase level and pancreatitis rate following ERCP]. Med Welt. 1984;35:109-112.  [PubMed]  [DOI]  [Cited in This Article: ]
10.  Vandervoort J, Soetikno RM, Tham TC, Wong RC, Ferrari AP Jr, Montes H, Roston AD, Slivka A, Lichtenstein DR, Ruymann FW. Risk factors for complications after performance of ERCP. Gastrointest Endosc. 2002;56:652-656.  [PubMed]  [DOI]  [Cited in This Article: ]
11.  Deans GT, Sedman P, Martin DF, Royston CM, Leow CK, Thomas WE, Brough WA. Are complications of endoscopic sphincterotomy age related? Gut. 1997;41:545-548.  [PubMed]  [DOI]  [Cited in This Article: ]
12.  Loperfido S, Angelini G, Benedetti G, Chilovi F, Costan F, De Berardinis F, De Bernardin M, Ederle A, Fina P, Fratton A. Major early complications from diagnostic and therapeutic ERCP: a prospective multicenter study. Gastrointest Endosc. 1998;48:1-10.  [PubMed]  [DOI]  [Cited in This Article: ]
13.  Christensen M, Matzen P, Schulze S, Rosenberg J. Complications of ERCP: a prospective study. Gastrointest Endosc. 2004;60:721-731.  [PubMed]  [DOI]  [Cited in This Article: ]
14.  Devière J, Le Moine O, Van Laethem JL, Eisendrath P, Ghilain A, Severs N, Cohard M. Interleukin 10 reduces the incidence of pancreatitis after therapeutic endoscopic retrograde cholangiopancreatography. Gastroenterology. 2001;120:498-505.  [PubMed]  [DOI]  [Cited in This Article: ]
15.  Matsushita M, Takakuwa H, Shimeno N, Uchida K, Nishio A, Okazaki K. Epinephrine sprayed on the papilla for prevention of post-ERCP pancreatitis. J Gastroenterol. 2009;44:71-75.  [PubMed]  [DOI]  [Cited in This Article: ]
16.  Gottlieb K, Sherman S. ERCP and biliary endoscopic sphincterotomy-induced pancreatitis. Gastrointest Endosc Clin N Am. 1998;8:87-114.  [PubMed]  [DOI]  [Cited in This Article: ]
17.  Fogel EL, Eversman D, Jamidar P, Sherman S, Lehman GA. Sphincter of Oddi dysfunction: pancreaticobiliary sphincterotomy with pancreatic stent placement has a lower rate of pancreatitis than biliary sphincterotomy alone. Endoscopy. 2002;34:280-285.  [PubMed]  [DOI]  [Cited in This Article: ]
18.  Tarnasky PR, Palesch YY, Cunningham JT, Mauldin PD, Cotton PB, Hawes RH. Pancreatic stenting prevents pancreatitis after biliary sphincterotomy in patients with sphincter of Oddi dysfunction. Gastroenterology. 1998;115:1518-1524.  [PubMed]  [DOI]  [Cited in This Article: ]
19.  Silviera ML, Seamon MJ, Porshinsky B, Prosciak MP, Doraiswamy VA, Wang CF, Lorenzo M, Truitt M, Biboa J, Jarvis AM. Complications related to endoscopic retrograde cholangiopancreatography: a comprehensive clinical review. J Gastrointestin Liver Dis. 2009;18:73-82.  [PubMed]  [DOI]  [Cited in This Article: ]
20.  Wang P, Li ZS, Liu F, Ren X, Lu NH, Fan ZN, Huang Q, Zhang X, He LP, Sun WS. Risk factors for ERCP-related complications: a prospective multicenter study. Am J Gastroenterol. 2009;104:31-40.  [PubMed]  [DOI]  [Cited in This Article: ]
21.  Cohen S, Bacon BR, Berlin JA, Fleischer D, Hecht GA, Loehrer PJ Sr, McNair AE Jr, Mulholland M, Norton NJ, Rabeneck L. National Institutes of Health State-of-the-Science Conference Statement: ERCP for diagnosis and therapy, January 14-16, 2002. Gastrointest Endosc. 2002;56:803-809.  [PubMed]  [DOI]  [Cited in This Article: ]
22.  Brugge WR, Van Dam J. Pancreatic and biliary endoscopy. N Engl J Med. 1999;341:1808-1816.  [PubMed]  [DOI]  [Cited in This Article: ]
23.  Cotton PB, Lehman G, Vennes J, Geenen JE, Russell RC, Meyers WC, Liguory C, Nickl N. Endoscopic sphincterotomy complications and their management: an attempt at consensus. Gastrointest Endosc. 1991;37:383-393.  [PubMed]  [DOI]  [Cited in This Article: ]
24.  Testoni PA, Bagnolo F, Caporuscio S, Lella F. Serum amylase measured four hours after endoscopic sphincterotomy is a reliable predictor of postprocedure pancreatitis. Am J Gastroenterol. 1999;94:1235-1241.  [PubMed]  [DOI]  [Cited in This Article: ]
25.  Testoni PA, Cicardi M, Bergamaschini L, Guzzoni S, Cugno M, Buizza M, Bagnolo F, Agostoni A. Infusion of C1-inhibitor plasma concentrate prevents hyperamylasemia induced by endoscopic sphincterotomy. Gastrointest Endosc. 1995;42:301-305.  [PubMed]  [DOI]  [Cited in This Article: ]
26.  Testoni PA, Bagnolo F. Pain at 24 hours associated with amylase levels greater than 5 times the upper normal limit as the most reliable indicator of post-ERCP pancreatitis. Gastrointest Endosc. 2001;53:33-39.  [PubMed]  [DOI]  [Cited in This Article: ]
27.  Testoni PA, Bagnolo F, Natale C, Primignani M. Incidence of post-endoscopic retrograde-cholangiopancreatography/sphincterotomy pancreatitis depends upon definition criteria. Dig Liver Dis. 2000;32:412-418.  [PubMed]  [DOI]  [Cited in This Article: ]
28.  Weiner GR, Geenen JE, Hogan WJ, Catalano MF. Use of corticosteroids in the prevention of post-ERCP pancreatitis. Gastrointest Endosc. 1995;42:579-583.  [PubMed]  [DOI]  [Cited in This Article: ]
29.  Freeman ML, Nelson DB, Sherman S, Haber GB, Herman ME, Dorsher PJ, Moore JP, Fennerty MB, Ryan ME, Shaw MJ. Complications of endoscopic biliary sphincterotomy. N Engl J Med. 1996;335:909-918.  [PubMed]  [DOI]  [Cited in This Article: ]
30.  Johnson GK, Geenen JE, Johanson JF, Sherman S, Hogan WJ, Cass O. Evaluation of post-ERCP pancreatitis: potential causes noted during controlled study of differing contrast media. Midwest Pancreaticobiliary Study Group. Gastrointest Endosc. 1997;46:217-222.  [PubMed]  [DOI]  [Cited in This Article: ]
31.  De Palma GD, Catanzano C. Use of corticosteriods in the prevention of post-ERCP pancreatitis: results of a controlled prospective study. Am J Gastroenterol. 1999;94:982-985.  [PubMed]  [DOI]  [Cited in This Article: ]
32.  Sherman S, Ruffolo TA, Hawes RH, Lehman GA. Complications of endoscopic sphincterotomy. A prospective series with emphasis on the increased risk associated with sphincter of Oddi dysfunction and nondilated bile ducts. Gastroenterology. 1991;101:1068-1075.  [PubMed]  [DOI]  [Cited in This Article: ]
33.  Sherman S, Hawes RH, Rathgaber SW, Uzer MF, Smith MT, Khusro QE, Silverman WB, Earle DT, Lehman GA. Post-ERCP pancreatitis: randomized, prospective study comparing a low- and high-osmolality contrast agent. Gastrointest Endosc. 1994;40:422-427.  [PubMed]  [DOI]  [Cited in This Article: ]
34.  Testoni PA, Lella F, Bagnolo F, Caporuscio S, Cattani L, Colombo E, Buizza M. Long-term prophylactic administration of octreotide reduces the rise in serum amylase after endoscopic procedures on Vater’s papilla. Pancreas. 1996;13:61-65.  [PubMed]  [DOI]  [Cited in This Article: ]
35.  Masci E, Toti G, Mariani A, Curioni S, Lomazzi A, Dinelli M, Minoli G, Crosta C, Comin U, Fertitta A. Complications of diagnostic and therapeutic ERCP: a prospective multicenter study. Am J Gastroenterol. 2001;96:417-423.  [PubMed]  [DOI]  [Cited in This Article: ]
36.  Abid GH, Siriwardana HP, Holt A, Ammori BJ. Mild ERCP-induced and non-ERCP-related acute pancreatitis: two distinct clinical entities? J Gastroenterol. 2007;42:146-151.  [PubMed]  [DOI]  [Cited in This Article: ]
37.  Chen CC, Wang SS, Lu RH, Lu CC, Chang FY, Lee SD. Early changes of serum proinflammatory and anti-inflammatory cytokines after endoscopic retrograde cholangiopancreatography. Pancreas. 2003;26:375-380.  [PubMed]  [DOI]  [Cited in This Article: ]
38.  Bradley EL 3rd. A clinically based classification system for acute pancreatitis. Summary of the International Symposium on Acute Pancreatitis, Atlanta, Ga, September 11 through 13, 1992. Arch Surg. 1993;128:586-590.  [PubMed]  [DOI]  [Cited in This Article: ]
39.  Knaus WA, Zimmerman JE, Wagner DP, Draper EA, Lawrence DE. APACHE-acute physiology and chronic health evaluation: a physiologically based classification system. Crit Care Med. 1981;9:591-597.  [PubMed]  [DOI]  [Cited in This Article: ]
40.  Ranson JH, Rifkind KM, Roses DF, Fink SD, Eng K, Spencer FC. Prognostic signs and the role of operative management in acute pancreatitis. Surg Gynecol Obstet. 1974;139:69-81.  [PubMed]  [DOI]  [Cited in This Article: ]
41.  Bhatia V, Garg PK, Tandon RK, Madan K. Endoscopic retrograde cholangiopancreatography-induced acute pancreatitis often has a benign outcome. J Clin Gastroenterol. 2006;40:726-731.  [PubMed]  [DOI]  [Cited in This Article: ]
42.  Barkay O, Niv E, Santo E, Bruck R, Hallak A, Konikoff FM. Low-dose heparin for the prevention of post-ERCP pancreatitis: a randomized placebo-controlled trial. Surg Endosc. 2008;22:1971-1976.  [PubMed]  [DOI]  [Cited in This Article: ]
43.  Dumot JA, Conwell DL, O’Connor JB, Ferguson DR, Vargo JJ, Barnes DS, Shay SS, Sterling MJ, Horth KS, Issa K. Pretreatment with methylprednisolone to prevent ERCP-induced pancreatitis: a randomized, multicenter, placebo-controlled clinical trial. Am J Gastroenterol. 1998;93:61-65.  [PubMed]  [DOI]  [Cited in This Article: ]
44.  Murray B, Carter R, Imrie C, Evans S, O’Suilleabhain C. Diclofenac reduces the incidence of acute pancreatitis after endoscopic retrograde cholangiopancreatography. Gastroenterology. 2003;124:1786-1791.  [PubMed]  [DOI]  [Cited in This Article: ]
45.  Tulassay Z, Döbrönte Z, Prónai L, Zágoni T, Juhász L. Octreotide in the prevention of pancreatic injury associated with endoscopic cholangiopancreatography. Aliment Pharmacol Ther. 1998;12:1109-1112.  [PubMed]  [DOI]  [Cited in This Article: ]
46.  Sherman S, Lehman GA. ERCP- and endoscopic sphincterotomy-induced pancreatitis. Pancreas. 1991;6:350-367.  [PubMed]  [DOI]  [Cited in This Article: ]
47.  Pezzilli R, Romboli E, Campana D, Corinaldesi R. Mechanisms involved in the onset of post-ERCP pancreatitis. JOP. 2002;3:162-168.  [PubMed]  [DOI]  [Cited in This Article: ]
48.  Messmann H, Vogt W, Holstege A, Lock G, Heinisch A, von Fürstenberg A, Leser HG, Zirngibl H, Schölmerich J. Post-ERP pancreatitis as a model for cytokine induced acute phase response in acute pancreatitis. Gut. 1997;40:80-85.  [PubMed]  [DOI]  [Cited in This Article: ]
49.  Oezcueruemez-Porsch M, Kunz D, Hardt PD, Fadgyas T, Kress O, Schulz HU, Schnell-Kretschmer H, Temme H, Westphal S, Luley C. Diagnostic relevance of interleukin pattern, acute-phase proteins, and procalcitonin in early phase of post-ERCP pancreatitis. Dig Dis Sci. 1998;43:1763-1769.  [PubMed]  [DOI]  [Cited in This Article: ]
50.  Banks PA, Freeman ML. Practice guidelines in acute pancreatitis. Am J Gastroenterol. 2006;101:2379-2400.  [PubMed]  [DOI]  [Cited in This Article: ]
51.  Kilciler G, Musabak U, Bagci S, Yesilova Z, Tuzun A, Uygun A, Gulsen M, Oren S, Oktenli C, Karaeren N. Do the changes in the serum levels of IL-2, IL-4, TNFalpha, and IL-6 reflect the inflammatory activity in the patients with post-ERCP pancreatitis? Clin Dev Immunol. 2008;2008:481560.  [PubMed]  [DOI]  [Cited in This Article: ]
52.  Sultan S, Baillie J. What are the predictors of post-ERCP pancreatitis, and how useful are they? JOP. 2002;3:188-194.  [PubMed]  [DOI]  [Cited in This Article: ]
53.  Demols A, Deviere J. New frontiers in the pharmacological prevention of post-ERCP pancreatitis: the cytokines. JOP. 2003;4:49-57.  [PubMed]  [DOI]  [Cited in This Article: ]
54.  Pande H, Thuluvath P. Pharmacological prevention of post-endoscopic retrograde cholangiopancreatography pancreatitis. Drugs. 2003;63:1799-1812.  [PubMed]  [DOI]  [Cited in This Article: ]
55.  Dumot JA, Conwell DL, Zuccaro G Jr, Vargo JJ, Shay SS, Easley KA, Ponsky JL. A randomized, double blind study of interleukin 10 for the prevention of ERCP-induced pancreatitis. Am J Gastroenterol. 2001;96:2098-2102.  [PubMed]  [DOI]  [Cited in This Article: ]
56.  Sherman S, Cheng CL, Costamagna G, Binmoeller KF, Puespoek A, Aithal GP, Kozarek RA, Chen YK, Van Steenbergen W, Tenner S. Efficacy of recombinant human interleukin-10 in prevention of post-endoscopic retrograde cholangiopancreatography pancreatitis in subjects with increased risk. Pancreas. 2009;38:267-274.  [PubMed]  [DOI]  [Cited in This Article: ]
57.  Williams EJ, Taylor S, Fairclough P, Hamlyn A, Logan RF, Martin D, Riley SA, Veitch P, Wilkinson ML, Williamson PR. Risk factors for complication following ERCP; results of a large-scale, prospective multicenter study. Endoscopy. 2007;39:793-801.  [PubMed]  [DOI]  [Cited in This Article: ]
58.  Freeman ML, DiSario JA, Nelson DB, Fennerty MB, Lee JG, Bjorkman DJ, Overby CS, Aas J, Ryan ME, Bochna GS. Risk factors for post-ERCP pancreatitis: a prospective, multicenter study. Gastrointest Endosc. 2001;54:425-434.  [PubMed]  [DOI]  [Cited in This Article: ]
59.  Andriulli A, Solmi L, Loperfido S, Leo P, Festa V, Belmonte A, Spirito F, Silla M, Forte G, Terruzzi V. Prophylaxis of ERCP-related pancreatitis: a randomized, controlled trial of somatostatin and gabexate mesylate. Clin Gastroenterol Hepatol. 2004;2:713-718.  [PubMed]  [DOI]  [Cited in This Article: ]
60.  Cheon YK, Cho KB, Watkins JL, McHenry L, Fogel EL, Sherman S, Lehman GA. Frequency and severity of post-ERCP pancreatitis correlated with extent of pancreatic ductal opacification. Gastrointest Endosc. 2007;65:385-393.  [PubMed]  [DOI]  [Cited in This Article: ]
61.  Jowell PS, Baillie J, Branch MS, Affronti J, Browning CL, Bute BP. Quantitative assessment of procedural competence. A prospective study of training in endoscopic retrograde cholangiopancreatography. Ann Intern Med. 1996;125:983-989.  [PubMed]  [DOI]  [Cited in This Article: ]
62.  Baron TH, Petersen BT, Mergener K, Chak A, Cohen J, Deal SE, Hoffinan B, Jacobson BC, Petrini JL, Safdi MA. Quality indicators for endoscopic retrograde cholangiopancreatography. Am J Gastroenterol. 2006;101:892-897.  [PubMed]  [DOI]  [Cited in This Article: ]
63.  Kapral C, Duller C, Wewalka F, Kerstan E, Vogel W, Schreiber F. Case volume and outcome of endoscopic retrograde cholangiopancreatography: results of a nationwide Austrian benchmarking project. Endoscopy. 2008;40:625-630.  [PubMed]  [DOI]  [Cited in This Article: ]
64.  Cotton PB, Garrow DA, Gallagher J, Romagnuolo J. Risk factors for complications after ERCP: a multivariate analysis of 11,497 procedures over 12 years. Gastrointest Endosc. 2009;70:80-88.  [PubMed]  [DOI]  [Cited in This Article: ]
65.  Williams EJ, Taylor S, Fairclough P, Hamlyn A, Logan RF, Martin D, Riley SA, Veitch P, Wilkinson M, Williamson PJ. Are we meeting the standards set for endoscopy? Results of a large-scale prospective survey of endoscopic retrograde cholangio-pancreatograph practice. Gut. 2007;56:821-829.  [PubMed]  [DOI]  [Cited in This Article: ]
66.  Vitte RL, Morfoisse JJ. Evaluation of endoscopic retrograde cholangiopancreatography procedures performed in general hospitals in France. Gastroenterol Clin Biol. 2007;31:740-749.  [PubMed]  [DOI]  [Cited in This Article: ]
67.  Freeman ML, Guda NM. ERCP cannulation: a review of reported techniques. Gastrointest Endosc. 2005;61:112-125.  [PubMed]  [DOI]  [Cited in This Article: ]
68.  Cortas GA, Mehta SN, Abraham NS, Barkun AN. Selective cannulation of the common bile duct: a prospective randomized trial comparing standard catheters with sphincterotomes. Gastrointest Endosc. 1999;50:775-779.  [PubMed]  [DOI]  [Cited in This Article: ]
69.  Lella F, Bagnolo F, Colombo E, Bonassi U. A simple way of avoiding post-ERCP pancreatitis. Gastrointest Endosc. 2004;59:830-834.  [PubMed]  [DOI]  [Cited in This Article: ]
70.  Artifon EL, Sakai P, Cunha JE, Halwan B, Ishioka S, Kumar A. Guidewire cannulation reduces risk of post-ERCP pancreatitis and facilitates bile duct cannulation. Am J Gastroenterol. 2007;102:2147-2153.  [PubMed]  [DOI]  [Cited in This Article: ]
71.  Ito K, Fujita N, Noda Y, Kobayashi G, Obana T, Horaguchi J, Takasawa O, Koshita S, Kanno Y. Pancreatic guidewire placement for achieving selective biliary cannulation during endoscopic retrograde cholangio-pancreatography. World J Gastroenterol. 2008;14:5595-5600; discussion 5599.  [PubMed]  [DOI]  [Cited in This Article: ]
72.  Lee TH, Park do H, Park JY, Kim EO, Lee YS, Park JH, Lee SH, Chung IK, Kim HS, Park SH. Can wire-guided cannulation prevent post-ERCP pancreatitis? A prospective randomized trial. Gastrointest Endosc. 2009;69:444-449.  [PubMed]  [DOI]  [Cited in This Article: ]
73.  Bailey AA, Bourke MJ, Williams SJ, Walsh PR, Murray MA, Lee EY, Kwan V, Lynch PM. A prospective randomized trial of cannulation technique in ERCP: effects on technical success and post-ERCP pancreatitis. Endoscopy. 2008;40:296-301.  [PubMed]  [DOI]  [Cited in This Article: ]
74.  Barkin JS, Casal GL, Reiner DK, Goldberg RI, Phillips RS, Kaplan S. A comparative study of contrast agents for endoscopic retrograde pancreatography. Am J Gastroenterol. 1991;86:1437-1441.  [PubMed]  [DOI]  [Cited in This Article: ]
75.  Johnson GK, Geenen JE, Bedford RA, Johanson J, Cass O, Sherman S, Hogan WJ, Ryan M, Silverman W, Edmundowicz S. A comparison of nonionic versus ionic contrast media: results of a prospective, multicenter study. Midwest Pancreaticobiliary Study Group. Gastrointest Endosc. 1995;42:312-316.  [PubMed]  [DOI]  [Cited in This Article: ]
76.  George S, Kulkarni AA, Stevens G, Forsmark CE, Draganov P. Role of osmolality of contrast media in the development of post-ERCP pancreatitis: a metanalysis. Dig Dis Sci. 2004;49:503-508.  [PubMed]  [DOI]  [Cited in This Article: ]
77.  Harewood GC, Pochron NL, Gostout CJ. Prospective, randomized, controlled trial of prophylactic pancreatic stent placement for endoscopic snare excision of the duodenal ampulla. Gastrointest Endosc. 2005;62:367-370.  [PubMed]  [DOI]  [Cited in This Article: ]
78.  Sofuni A, Maguchi H, Itoi T, Katanuma A, Hisai H, Niido T, Toyota M, Fujii T, Harada Y, Takada T. Prophylaxis of post-endoscopic retrograde cholangiopancreatography pancreatitis by an endoscopic pancreatic spontaneous dislodgement stent. Clin Gastroenterol Hepatol. 2007;5:1339-1346.  [PubMed]  [DOI]  [Cited in This Article: ]
79.  Freeman ML. Pancreatic stents for prevention of post-endoscopic retrograde cholangiopancreatography pancreatitis. Clin Gastroenterol Hepatol. 2007;5:1354-1365.  [PubMed]  [DOI]  [Cited in This Article: ]
80.  Tarnasky PR. Mechanical prevention of post-ERCP pancreatitis by pancreatic stents: results, techniques, and indications. JOP. 2003;4:58-67.  [PubMed]  [DOI]  [Cited in This Article: ]
81.  Fazel A, Quadri A, Catalano MF, Meyerson SM, Geenen JE. Does a pancreatic duct stent prevent post-ERCP pancreatitis? A prospective randomized study. Gastrointest Endosc. 2003;57:291-294.  [PubMed]  [DOI]  [Cited in This Article: ]
82.  Simmons DT, Petersen BT, Gostout CJ, Levy MJ, Topazian MD, Baron TH. Risk of pancreatitis following endoscopically placed large-bore plastic biliary stents with and without biliary sphincterotomy for management of postoperative bile leaks. Surg Endosc. 2008;22:1459-1463.  [PubMed]  [DOI]  [Cited in This Article: ]
83.  Smithline A, Silverman W, Rogers D, Nisi R, Wiersema M, Jamidar P, Hawes R, Lehman G. Effect of prophylactic main pancreatic duct stenting on the incidence of biliary endoscopic sphincterotomy-induced pancreatitis in high-risk patients. Gastrointest Endosc. 1993;39:652-657.  [PubMed]  [DOI]  [Cited in This Article: ]
84.  Tsuchiya T, Itoi T, Sofuni A, Itokawa F, Kurihara T, Ishii K, Tsuji S, Kawai T, Moriyasu F. Temporary pancreatic stent to prevent post endoscopic retrograde cholangiopancreatography pancreatitis: a preliminary, single-center, randomized controlled trial. J Hepatobiliary Pancreat Surg. 2007;14:302-307.  [PubMed]  [DOI]  [Cited in This Article: ]
85.  Arnold JC, Benz C, Martin WR, Adamek HE, Riemann JF. Endoscopic papillary balloon dilation vs. sphincterotomy for removal of common bile duct stones: a prospective randomized pilot study. Endoscopy. 2001;33:563-567.  [PubMed]  [DOI]  [Cited in This Article: ]
86.  Disario JA. Endoscopic balloon dilation for extraction of bile duct stones: the devil is in the details. Gastrointest Endosc. 2003;57:282-285.  [PubMed]  [DOI]  [Cited in This Article: ]
87.  Fujita N, Maguchi H, Komatsu Y, Yasuda I, Hasebe O, Igarashi Y, Murakami A, Mukai H, Fujii T, Yamao K. Endoscopic sphincterotomy and endoscopic papillary balloon dilatation for bile duct stones: A prospective randomized controlled multicenter trial. Gastrointest Endosc. 2003;57:151-155.  [PubMed]  [DOI]  [Cited in This Article: ]
88.  Vlavianos P, Chopra K, Mandalia S, Anderson M, Thompson J, Westaby D. Endoscopic balloon dilatation versus endoscopic sphincterotomy for the removal of bile duct stones: a prospective randomised trial. Gut. 2003;52:1165-1169.  [PubMed]  [DOI]  [Cited in This Article: ]
89.  Song SY, Lee KS, Na KJ, Ahn BH. Tension pneumothorax after endoscopic retrograde pancreatocholangiogram. J Korean Med Sci. 2009;24:173-175.  [PubMed]  [DOI]  [Cited in This Article: ]
90.  García-Cano J. Fatal pancreatitis after endoscopic balloon dilation for extraction of common bile duct stones in an 80-year-old woman. Endoscopy. 2007;39 Suppl 1:E132.  [PubMed]  [DOI]  [Cited in This Article: ]
91.  Mao Z, Zhu Q, Wu W, Wang M, Li J, Lu A, Sun Y, Zheng M. Duodenal perforations after endoscopic retrograde cholangiopancreatography: experience and management. J Laparoendosc Adv Surg Tech A. 2008;18:691-695.  [PubMed]  [DOI]  [Cited in This Article: ]
92.  Margantinis G, Sakorafas GH, Kostopoulos P, Kontou S, Tsiakos S, Arvanitidis D. Post-ERCP/endoscopic sphincterotomy duodenal perforation is not always a surgical emergency. Dig Liver Dis. 2006;38:434-436.  [PubMed]  [DOI]  [Cited in This Article: ]
93.  Park DH, Kim MH, Lee SK, Lee SS, Choi JS, Song MH, Seo DW, Min YI. Endoscopic sphincterotomy vs. endoscopic papillary balloon dilation for choledocholithiasis in patients with liver cirrhosis and coagulopathy. Gastrointest Endosc. 2004;60:180-185.  [PubMed]  [DOI]  [Cited in This Article: ]
94.  Cotton PB. ERCP is most dangerous for people who need it least. Gastrointest Endosc. 2001;54:535-536.  [PubMed]  [DOI]  [Cited in This Article: ]
95.  Christoforidis E, Goulimaris I, Kanellos I, Tsalis K, Demetriades C, Betsis D. Post-ERCP pancreatitis and hyperamylasemia: patient-related and operative risk factors. Endoscopy. 2002;34:286-292.  [PubMed]  [DOI]  [Cited in This Article: ]
96.  Masci E, Mariani A, Curioni S, Testoni PA. Risk factors for pancreatitis following endoscopic retrograde cholangiopancreatography: a meta-analysis. Endoscopy. 2003;35:830-834.  [PubMed]  [DOI]  [Cited in This Article: ]
97.  Tarnasky P, Cunningham J, Cotton P, Hoffman B, Palesch Y, Freeman J, Curry N, Hawes R. Pancreatic sphincter hypertension increases the risk of post-ERCP pancreatitis. Endoscopy. 1997;29:252-257.  [PubMed]  [DOI]  [Cited in This Article: ]
98.  Deenadayalu VP, Blaut U, Watkins JL, Barnett J, Freeman M, Geenen J, Ryan M, Parker H, Frakes JT, Fogel EL. Does obesity confer an increased risk and/or more severe course of post-ERCP pancreatitis?: a retrospective, multicenter study. J Clin Gastroenterol. 2008;42:1103-1109.  [PubMed]  [DOI]  [Cited in This Article: ]
99.  Lukens FJ, Howell DA, Upender S, Sheth SG, Jafri SM. ERCP in the very elderly: outcomes among patients older than eighty. Dig Dis Sci. 2010;55:847-851.  [PubMed]  [DOI]  [Cited in This Article: ]
100.  Debenedet AT, Raghunathan TE, Wing JJ, Wamsteker EJ, DiMagno MJ. Alcohol use and cigarette smoking as risk factors for post-endoscopic retrograde cholangiopancreatography pancreatitis. Clin Gastroenterol Hepatol. 2009;7:353-8e4.  [PubMed]  [DOI]  [Cited in This Article: ]
101.  Cooper ST, Slivka A. Incidence, risk factors, and prevention of post-ERCP pancreatitis. Gastroenterol Clin North Am. 2007;36:259-276, vii-viii.  [PubMed]  [DOI]  [Cited in This Article: ]
102.  Reddy N, Wilcox CM, Tamhane A, Eloubeidi MA, Varadarajulu S. Protocol-based medical management of post-ERCP pancreatitis. J Gastroenterol Hepatol. 2008;23:385-392.  [PubMed]  [DOI]  [Cited in This Article: ]
103.  Silverman WB, Thompson RA. Management of asymptomatically/minimally symptomatic post-ERCP serum liver test elevations: first do no harm. Dig Dis Sci. 2002;47:1498-1501.  [PubMed]  [DOI]  [Cited in This Article: ]
104.  Jacobson BC, Vander Vliet MB, Hughes MD, Maurer R, McManus K, Banks PA. A prospective, randomized trial of clear liquids versus low-fat solid diet as the initial meal in mild acute pancreatitis. Clin Gastroenterol Hepatol. 2007;5:946-951; quiz 886.  [PubMed]  [DOI]  [Cited in This Article: ]
105.  Dundee PE, Chin-Lenn L, Syme DB, Thomas PR. Outcomes of ERCP: prospective series from a rural centre. ANZ J Surg. 2007;77:1013-1017.  [PubMed]  [DOI]  [Cited in This Article: ]
106.  Barthet M, Lesavre N, Desjeux A, Gasmi M, Berthezene P, Berdah S, Viviand X, Grimaud JC. Complications of endoscopic sphincterotomy: results from a single tertiary referral center. Endoscopy. 2002;34:991-997.  [PubMed]  [DOI]  [Cited in This Article: ]
107.  Andriulli A, Loperfido S, Napolitano G, Niro G, Valvano MR, Spirito F, Pilotto A, Forlano R. Incidence rates of post-ERCP complications: a systematic survey of prospective studies. Am J Gastroenterol. 2007;102:1781-1788.  [PubMed]  [DOI]  [Cited in This Article: ]
108.  Disario JA, Freeman ML, Bjorkman DJ, Macmathuna P, Petersen BT, Jaffe PE, Morales TG, Hixson LJ, Sherman S, Lehman GA. Endoscopic balloon dilation compared with sphincterotomy for extraction of bile duct stones. Gastroenterology. 2004;127:1291-1299.  [PubMed]  [DOI]  [Cited in This Article: ]
109.  Bergman JJ, Rauws EA, Fockens P, van Berkel AM, Bossuyt PM, Tijssen JG, Tytgat GN, Huibregtse K. Randomised trial of endoscopic balloon dilation versus endoscopic sphincterotomy for removal of bileduct stones. Lancet. 1997;349:1124-1129.  [PubMed]  [DOI]  [Cited in This Article: ]
110.  Martinez-Torres H, Rodriguez-Lomeli X, Davalos-Cobian C, Garcia-Correa J, Maldonado-Martinez JM, Medrano-Muñoz F, Fuentes-Orozco C, Gonzalez-Ojeda A. Oral allopurinol to prevent hyperamylasemia and acute pancreatitis after endoscopic retrograde cholangiopancreatography. World J Gastroenterol. 2009;15:1600-1606.  [PubMed]  [DOI]  [Cited in This Article: ]
111.  Romagnuolo J, Hilsden R, Sandha GS, Cole M, Bass S, May G, Love J, Bain VG, McKaigney J, Fedorak RN. Allopurinol to prevent pancreatitis after endoscopic retrograde cholangiopancreatography: a randomized placebo-controlled trial. Clin Gastroenterol Hepatol. 2008;6:465-471; quiz 371.  [PubMed]  [DOI]  [Cited in This Article: ]
112.  Katsinelos P, Kountouras J, Chatzis J, Christodoulou K, Paroutoglou G, Mimidis K, Beltsis A, Zavos C. High-dose allopurinol for prevention of post-ERCP pancreatitis: a prospective randomized double-blind controlled trial. Gastrointest Endosc. 2005;61:407-415.  [PubMed]  [DOI]  [Cited in This Article: ]
113.  Mosler P, Sherman S, Marks J, Watkins JL, Geenen JE, Jamidar P, Fogel EL, Lazzell-Pannell L, Temkit M, Tarnasky P. Oral allopurinol does not prevent the frequency or the severity of post-ERCP pancreatitis. Gastrointest Endosc. 2005;62:245-250.  [PubMed]  [DOI]  [Cited in This Article: ]
114.  Budzyńska A, Marek T, Nowak A, Kaczor R, Nowakowska-Dulawa E. A prospective, randomized, placebo-controlled trial of prednisone and allopurinol in the prevention of ERCP-induced pancreatitis. Endoscopy. 2001;33:766-772.  [PubMed]  [DOI]  [Cited in This Article: ]
115.  Lavy A, Karban A, Suissa A, Yassin K, Hermesh I, Ben-Amotz A. Natural beta-carotene for the prevention of post-ERCP pancreatitis. Pancreas. 2004;29:e45-e50.  [PubMed]  [DOI]  [Cited in This Article: ]
116.  Gorelick A, Barnett J, Chey W, Anderson M, Elta G. Botulinum toxin injection after biliary sphincterotomy. Endoscopy. 2004;36:170-173.  [PubMed]  [DOI]  [Cited in This Article: ]
117.  Räty S, Sand J, Pulkkinen M, Matikainen M, Nordback I. Post-ERCP pancreatitis: reduction by routine antibiotics. J Gastrointest Surg. 2001;5:339-345; discussion 345.  [PubMed]  [DOI]  [Cited in This Article: ]
118.  Kwanngern K, Tiyapattanaputi P, Wanitpukdeedecha M, Navicharern P. Can a single dose corticosteroid reduce the incidence of post-ERCP pancreatitis? A randomized, prospective control study. J Med Assoc Thai. 2005;88 Suppl 4:S42-S45.  [PubMed]  [DOI]  [Cited in This Article: ]
119.  Manolakopoulos S, Avgerinos A, Vlachogiannakos J, Armonis A, Viazis N, Papadimitriou N, Mathou N, Stefanidis G, Rekoumis G, Vienna E. Octreotide versus hydrocortisone versus placebo in the prevention of post-ERCP pancreatitis: a multicenter randomized controlled trial. Gastrointest Endosc. 2002;55:470-475.  [PubMed]  [DOI]  [Cited in This Article: ]
120.  Sherman S, Blaut U, Watkins JL, Barnett J, Freeman M, Geenen J, Ryan M, Parker H, Frakes JT, Fogel EL. Does prophylactic administration of corticosteroid reduce the risk and severity of post-ERCP pancreatitis: a randomized, prospective, multicenter study. Gastrointest Endosc. 2003;58:23-29.  [PubMed]  [DOI]  [Cited in This Article: ]
121.  Rabenstein T, Fischer B, Wiessner V, Schmidt H, Radespiel-Tröger M, Hochberger J, Mühldorfer S, Nusko G, Messmann H, Schölmerich J. Low-molecular-weight heparin does not prevent acute post-ERCP pancreatitis. Gastrointest Endosc. 2004;59:606-613.  [PubMed]  [DOI]  [Cited in This Article: ]
122.  Milewski J, Rydzewska G, Degowska M, Kierzkiewicz M, Rydzewski A. N-acetylcysteine does not prevent post-endoscopic retrograde cholangiopancreatography hyperamylasemia and acute pancreatitis. World J Gastroenterol. 2006;12:3751-3755.  [PubMed]  [DOI]  [Cited in This Article: ]
123.  Katsinelos P, Kountouras J, Paroutoglou G, Beltsis A, Mimidis K, Zavos C. Intravenous N-acetylcysteine does not prevent post-ERCP pancreatitis. Gastrointest Endosc. 2005;62:105-111.  [PubMed]  [DOI]  [Cited in This Article: ]
124.  Prat F, Amaris J, Ducot B, Bocquentin M, Fritsch J, Choury AD, Pelletier G, Buffet C. Nifedipine for prevention of post-ERCP pancreatitis: a prospective, double-blind randomized study. Gastrointest Endosc. 2002;56:202-208.  [PubMed]  [DOI]  [Cited in This Article: ]
125.  Sand J, Nordback I. Prospective randomized trial of the effect of nifedipine on pancreatic irritation after endoscopic retrograde cholangiopancreatography. Digestion. 1993;54:105-111.  [PubMed]  [DOI]  [Cited in This Article: ]
126.  Hao JY, Wu DF, Wang YZ, Gao YX, Lang HP, Zhou WZ. Prophylactic effect of glyceryl trinitrate on post-endoscopic retrograde cholangiopancreatography pancreatitis: a randomized placebo-controlled trial. World J Gastroenterol. 2009;15:366-368.  [PubMed]  [DOI]  [Cited in This Article: ]
127.  Beauchant M, Ingrand P, Favriel JM, Dupuychaffray JP, Capony P, Moindrot H, Barthet M, Escourrou J, Plane C, Barrioz T. Intravenous nitroglycerin for prevention of pancreatitis after therapeutic endoscopic retrograde cholangiography: a randomized, double-blind, placebo-controlled multicenter trial. Endoscopy. 2008;40:631-636.  [PubMed]  [DOI]  [Cited in This Article: ]
128.  Kaffes AJ, Bourke MJ, Ding S, Alrubaie A, Kwan V, Williams SJ. A prospective, randomized, placebo-controlled trial of transdermal glyceryl trinitrate in ERCP: effects on technical success and post-ERCP pancreatitis. Gastrointest Endosc. 2006;64:351-357.  [PubMed]  [DOI]  [Cited in This Article: ]
129.  Moretó M, Zaballa M, Casado I, Merino O, Rueda M, Ramírez K, Urcelay R, Baranda A. Transdermal glyceryl trinitrate for prevention of post-ERCP pancreatitis: A randomized double-blind trial. Gastrointest Endosc. 2003;57:1-7.  [PubMed]  [DOI]  [Cited in This Article: ]
130.  Sudhindran S, Bromwich E, Edwards PR. Prospective randomized double-blind placebo-controlled trial of glyceryl trinitrate in endoscopic retrograde cholangiopancreatography-induced pancreatitis. Br J Surg. 2001;88:1178-1182.  [PubMed]  [DOI]  [Cited in This Article: ]
131.  Khoshbaten M, Khorram H, Madad L, Ehsani Ardakani MJ, Farzin H, Zali MR. Role of diclofenac in reducing post-endoscopic retrograde cholangiopancreatography pancreatitis. J Gastroenterol Hepatol. 2008;23:e11-e16.  [PubMed]  [DOI]  [Cited in This Article: ]
132.  Cheon YK, Cho KB, Watkins JL, McHenry L, Fogel EL, Sherman S, Schmidt S, Lazzell-Pannell L, Lehman GA. Efficacy of diclofenac in the prevention of post-ERCP pancreatitis in predominantly high-risk patients: a randomized double-blind prospective trial. Gastrointest Endosc. 2007;66:1126-1132.  [PubMed]  [DOI]  [Cited in This Article: ]
133.  Sotoudehmanesh R, Khatibian M, Kolahdoozan S, Ainechi S, Malboosbaf R, Nouraie M. Indomethacin may reduce the incidence and severity of acute pancreatitis after ERCP. Am J Gastroenterol. 2007;102:978-983.  [PubMed]  [DOI]  [Cited in This Article: ]
134.  Kisli E, Baser M, Aydin M, Guler O. The role of octreotide versus placebo in the prevention of post-ERCP pancreatitis. Hepatogastroenterology. 2007;54:250-253.  [PubMed]  [DOI]  [Cited in This Article: ]
135.  Li ZS, Pan X, Zhang WJ, Gong B, Zhi FC, Guo XG, Li PM, Fan ZN, Sun WS, Shen YZ. Effect of octreotide administration in the prophylaxis of post-ERCP pancreatitis and hyperamylasemia: A multicenter, placebo-controlled, randomized clinical trial. Am J Gastroenterol. 2007;102:46-51.  [PubMed]  [DOI]  [Cited in This Article: ]
136.  Thomopoulos KC, Pagoni NA, Vagenas KA, Margaritis VG, Theocharis GI, Nikolopoulou VN. Twenty-four hour prophylaxis with increased dosage of octreotide reduces the incidence of post-ERCP pancreatitis. Gastrointest Endosc. 2006;64:726-731.  [PubMed]  [DOI]  [Cited in This Article: ]
137.  Testoni PA, Bagnolo F, Andriulli A, Bernasconi G, Crotta S, Lella F, Lomazzi A, Minoli G, Natale C, Prada A. Octreotide 24-h prophylaxis in patients at high risk for post-ERCP pancreatitis: results of a multicenter, randomized, controlled trial. Aliment Pharmacol Ther. 2001;15:965-972.  [PubMed]  [DOI]  [Cited in This Article: ]
138.  Hardt PD, Kress O, Fadgyas T, Doppl W, Schnell-Kretschmer H, Wüsten O, Klör HU. Octreotide in the prevention of pancreatic damage induced by endoscopic sphincterotomy. Eur J Med Res. 2000;5:165-170.  [PubMed]  [DOI]  [Cited in This Article: ]
139.  Duvnjak M, Supanc V, Simicević VN, Hrabar D, Troskot B, Smirci-Duvnjak L, Bekavac-Beslin M. Use of octreotide-acetate in preventing pancreatitis-like changes following therapeutic endoscopic retrograde cholangiopancreatography. Acta Med Croatica. 1999;53:115-118.  [PubMed]  [DOI]  [Cited in This Article: ]
140.  Arvanitidis D, Hatzipanayiotis J, Koutsounopoulos G, Frangou E. The effect of octreotide on the prevention of acute pancreatitis and hyperamylasemia after diagnostic and therapeutic ERCP. Hepatogastroenterology. 1998;45:248-252.  [PubMed]  [DOI]  [Cited in This Article: ]
141.  Arcidiacono R, Gambitta P, Rossi A, Grosso C, Bini M, Zanasi G. The use of a long-acting somatostatin analogue (octreotide) for prophylaxis of acute pancreatitis after endoscopic sphincterotomy. Endoscopy. 1994;26:715-718.  [PubMed]  [DOI]  [Cited in This Article: ]
142.  Baldazzi G, Conti C, Spotti EG, Arisi GP, Scevola M, Gobetti F, Agliardi CM, Galasso P, Bonomi E, Bianchi F. [Prevention of post-ERCP acute pancreatitis with octreotide]. G Chir. 1994;15:359-362.  [PubMed]  [DOI]  [Cited in This Article: ]
143.  Testoni PA, Lella F, Bagnolo F, Buizza M, Colombo E. Controlled trial of different dosages of octreotide in the prevention of hyperamylasemia induced by endoscopic papillosphincterotomy. Ital J Gastroenterol. 1994;26:431-436.  [PubMed]  [DOI]  [Cited in This Article: ]
144.  Ueki T, Otani K, Kawamoto K, Shimizu A, Fujimura N, Sakaguchi S, Matsui T. Comparison between ulinastatin and gabexate mesylate for the prevention of post-endoscopic retrograde cholangiopancreatography pancreatitis: a prospective, randomized trial. J Gastroenterol. 2007;42:161-167.  [PubMed]  [DOI]  [Cited in This Article: ]
145.  Manes G, Ardizzone S, Lombardi G, Uomo G, Pieramico O, Porro GB. Efficacy of postprocedure administration of gabexate mesylate in the prevention of post-ERCP pancreatitis: a randomized, controlled, multicenter study. Gastrointest Endosc. 2007;65:982-987.  [PubMed]  [DOI]  [Cited in This Article: ]
146.  Xiong GS, Wu SM, Zhang XW, Ge ZZ. Clinical trial of gabexate in the prophylaxis of post-endoscopic retrograde cholangiopancreatography pancreatitis. Braz J Med Biol Res. 2006;39:85-90.  [PubMed]  [DOI]  [Cited in This Article: ]
147.  Fujishiro H, Adachi K, Imaoka T, Hashimoto T, Kohge N, Moriyama N, Suetsugu H, Kawashima K, Komazawa Y, Ishimura N. Ulinastatin shows preventive effect on post-endoscopic retrograde cholangiopancreatography pancreatitis in a multicenter prospective randomized study. J Gastroenterol Hepatol. 2006;21:1065-1069.  [PubMed]  [DOI]  [Cited in This Article: ]
148.  Andriulli A, Clemente R, Solmi L, Terruzzi V, Suriani R, Sigillito A, Leandro G, Leo P, De Maio G, Perri F. Gabexate or somatostatin administration before ERCP in patients at high risk for post-ERCP pancreatitis: a multicenter, placebo-controlled, randomized clinical trial. Gastrointest Endosc. 2002;56:488-495.  [PubMed]  [DOI]  [Cited in This Article: ]
149.  Cavallini G, Tittobello A, Frulloni L, Masci E, Mariana A, Di Francesco V. Gabexate for the prevention of pancreatic damage related to endoscopic retrograde cholangiopancreatography. Gabexate in digestive endoscopy--Italian Group. N Engl J Med. 1996;335:919-923.  [PubMed]  [DOI]  [Cited in This Article: ]
150.  Choi CW, Kang DH, Kim GH, Eum JS, Lee SM, Song GA, Kim DU, Kim ID, Cho M. Nafamostat mesylate in the prevention of post-ERCP pancreatitis and risk factors for post-ERCP pancreatitis. Gastrointest Endosc. 2009;69:e11-e18.  [PubMed]  [DOI]  [Cited in This Article: ]
151.  Yoo JW, Ryu JK, Lee SH, Woo SM, Park JK, Yoon WJ, Lee JK, Lee KH, Hwang JH, Kim YT. Preventive effects of ulinastatin on post-endoscopic retrograde cholangiopancreatography pancreatitis in high-risk patients: a prospective, randomized, placebo-controlled trial. Pancreas. 2008;37:366-370.  [PubMed]  [DOI]  [Cited in This Article: ]
152.  Tsujino T, Komatsu Y, Isayama H, Hirano K, Sasahira N, Yamamoto N, Toda N, Ito Y, Nakai Y, Tada M. Ulinastatin for pancreatitis after endoscopic retrograde cholangiopancreatography: a randomized, controlled trial. Clin Gastroenterol Hepatol. 2005;3:376-383.  [PubMed]  [DOI]  [Cited in This Article: ]
153.  Kapetanos D, Kokozidis G, Christodoulou D, Mistakidis K, Sigounas D, Dimakopoulos K, Kitis G, Tsianos EV. A randomized controlled trial of pentoxifylline for the prevention of post-ERCP pancreatitis. Gastrointest Endosc. 2007;66:513-518.  [PubMed]  [DOI]  [Cited in This Article: ]
154.  Sherman S, Alazmi WM, Lehman GA, Geenen JE, Chuttani R, Kozarek RA, Welch WD, Souza S, Pribble J. Evaluation of recombinant platelet-activating factor acetylhydrolase for reducing the incidence and severity of post-ERCP acute pancreatitis. Gastrointest Endosc. 2009;69:462-672.  [PubMed]  [DOI]  [Cited in This Article: ]
155.  van Westerloo DJ, Rauws EA, Hommes D, de Vos AF, van der Poll T, Powers BL, Fockens P, Dijkgraaf MG, Bruno MJ. Pre-ERCP infusion of semapimod, a mitogen-activated protein kinases inhibitor, lowers post-ERCP hyperamylasemia but not pancreatitis incidence. Gastrointest Endosc. 2008;68:246-254.  [PubMed]  [DOI]  [Cited in This Article: ]
156.  Lee KT, Lee DH, Yoo BM. The prophylactic effect of somatostatin on post-therapeutic endoscopic retrograde cholangiopancreatography pancreatitis: a randomized, multicenter controlled trial. Pancreas. 2008;37:445-448.  [PubMed]  [DOI]  [Cited in This Article: ]
157.  Arvanitidis D, Anagnostopoulos GK, Giannopoulos D, Pantes A, Agaritsi R, Margantinis G, Tsiakos S, Sakorafas G, Kostopoulos P. Can somatostatin prevent post-ERCP pancreatitis? Results of a randomized controlled trial. J Gastroenterol Hepatol. 2004;19:278-282.  [PubMed]  [DOI]  [Cited in This Article: ]
158.  Poon RT, Yeung C, Liu CL, Lam CM, Yuen WK, Lo CM, Tang A, Fan ST. Intravenous bolus somatostatin after diagnostic cholangiopancreatography reduces the incidence of pancreatitis associated with therapeutic endoscopic retrograde cholangiopancreatography procedures: a randomised controlled trial. Gut. 2003;52:1768-1773.  [PubMed]  [DOI]  [Cited in This Article: ]
159.  Poon RT, Yeung C, Lo CM, Yuen WK, Liu CL, Fan ST. Prophylactic effect of somatostatin on post-ERCP pancreatitis: a randomized controlled trial. Gastrointest Endosc. 1999;49:593-598.  [PubMed]  [DOI]  [Cited in This Article: ]
160.  Bordas JM, Toledo-Pimentel V, Llach J, Elena M, Mondelo F, Ginès A, Terés J. Effects of bolus somatostatin in preventing pancreatitis after endoscopic pancreatography: results of a randomized study. Gastrointest Endosc. 1998;47:230-234.  [PubMed]  [DOI]  [Cited in This Article: ]
161.  Schwartz JJ, Lew RJ, Ahmad NA, Shah JN, Ginsberg GG, Kochman ML, Brensinger CM, Long WB. The effect of lidocaine sprayed on the major duodenal papilla on the frequency of post-ERCP pancreatitis. Gastrointest Endosc. 2004;59:179-184.  [PubMed]  [DOI]  [Cited in This Article: ]