|Year : 2018 | Volume
| Issue : 1 | Page : 73-80
Association of Helicobacter pylori infection with somatostatin deficiency and its relation to post-endoscopic retrograde cholangiopancreatography pancreatitis
Madiha Abd-Elghany El-Ziny1, Mohamed A Afify1, Abeer M Abo El-Ela1, Sahar S Khattab2, Noura A.G Zeidan2
1 Tropical Medicine Department, Faculty of Medicine, Al-Azhar University, Cairo, Egypt
2 Clinical Pathology Department, Faculty of Medicine for Girls, Al-Azhar University, Cairo, Egypt
|Date of Submission||17-Jul-2018|
|Date of Acceptance||12-Aug-2018|
|Date of Web Publication||20-Nov-2018|
Noura A.G Zeidan
Faculty of Medicine for Girls, Al- Azhar University, Cairo, 71115
Source of Support: None, Conflict of Interest: None
Background Post-endoscopic retrograde cholangiopancreatography pancreatitis (PEP) is the most common complication of endoscopic retrograde cholangiopancreatography (ERCP). It can be diagnosed clinically in patients complaining of severe abdominal pain with rising of serum amylase and lipase more than three-folds of high normal levels within 24 h of the procedure.
Aim The aim of this work was to determine if there is an association between Helicobacter pylori infection and low somatostatin level and its relation to PEP.
Patients and methods A total of 80 patients with obstructive jaundice requiring ERCP were enrolled in this study and were, divided according to H. pylori infection into the following: 37 H. pylori positive patients (group A) and 43 H. pylori negative patients (group B). All patients were subjected to full history taking; clinical examination, serum bilirubin, serum amylase and serum lipase just before and 24 h after ERCP; histological examination of gastric biopsies to detect H. pylori and serum somatostatin level with follow-up for 24 h for any symptom or signs suggestive of PEP.
Results The percentage of PEP was 10.8% in group A and 9.3% in group B, with an overall percentage of 10%. Patients who experienced PEP had a statistically significant lower somatostatin level than patients who did not experience PEP. Significant increase in somatostatin level was registered in H. pylori-infected patients. Certain ERCP-related maneuvers, such as difficult ampullary cannulation, repeated pancreatic duct cannulation and precut sphincterotomy, carry the risk of PEP.
Conclusion No association between H. pylori infection and PEP was seen. Low somatostatin level can be useful in prediction of PEP.
Keywords: endoscopic retrograde cholangiopancreatography, Helicobacter pylori, somatostatin
|How to cite this article:|
El-Ziny MA, Afify MA, Abo El-Ela AM, Khattab SS, Zeidan NA. Association of Helicobacter pylori infection with somatostatin deficiency and its relation to post-endoscopic retrograde cholangiopancreatography pancreatitis. Al-Azhar Assiut Med J 2018;16:73-80
|How to cite this URL:|
El-Ziny MA, Afify MA, Abo El-Ela AM, Khattab SS, Zeidan NA. Association of Helicobacter pylori infection with somatostatin deficiency and its relation to post-endoscopic retrograde cholangiopancreatography pancreatitis. Al-Azhar Assiut Med J [serial online] 2018 [cited 2019 Oct 16];16:73-80. Available from: http://www.azmj.eg.net/text.asp?2018/16/1/73/244155
| Introduction|| |
Endoscopic retrograde cholangiopancreatography (ERCP) is widely used to treat biliary and pancreatic diseases. ERCP is generally considered effective and safe. Post-ERCP complication rates vary widely depending on the complexity of the intervention and the individual patient. These complications involve bleeding, infection, and perforation. Pancreatitis remains the most common severe complication of ERCP. Although asymptomatic elevation of serum amylase is a common occurrence after ERCP, the incidence of clinically significant post-endoscopic retrograde cholangiopancreatography pancreatitis (PEP) ranges from 1 to 15.7% .
The pathophysiology of PEP is not well understood. Several factors may be involved independently or in combination in the development of pancreatitis such as mechanical injury from instrumentation of the pancreatic duct, hydrostatic injury from over-injection, thermal injury produced by electrocautery, and chemical or allergic injury to contrast medium. These factors may obstruct the flow of pancreatic secretions causing intraluminal activation of proteolytic enzymes and cellular autodigestion. It has also been suggested that infection plays a part, owing to the possible introduction of luminal contamination into the ducts .
Helicobacter pylori infection is one of the most common bacterial infections in the world, colonizing approximately half the population. Colonization usually occurs before the age of 10 years, and once established within the gastric mucosa, the bacterium can persist for life, although transient infection occurs in a few individuals .
Somatostatin prevents pancreatitis throughout inhibiting pancreatic exocrine secretion by inhibiting the release of secretin and cholecystokinin and reducing the pressure in the intra-pancreatic ducts by restricting the motility of the sphincter of Oddi .
Moreover, somatostatin dose-dependently inhibits tumor necrosis factor-α induced interleukin-6 secretion, and some of the therapeutic actions of somatostatin on acute pancreatitis may be mediated by the reduction of local interleukin-6 secretion .
| Aim|| |
The aim of this work is to determine if there is a relation between H. pylori infection, its effect on somatostatin level, and PEP.
| Patients and methods|| |
A total of 80 patients with different causes of obstructive jaundice requiring ERCP, recruited from the ERCP units of Al-Hussein University Hospital and El-Galaa Military Hospital, were enrolled in this study.
Patients with any contraindication for ERCP or history of suspected acute or chronic pancreatitis and their precipitating factors, for example, hypertriglyceridemia, diabetes mellitus or intake of drugs known to produce acute pancreatitis, as azathioprine, were excluded from the study.
Before endoscopic retrograde cholangiopancreatography
- All patients were subjected to full history taking and clinical examination with an emphasis on the indications for the ERCP, previous procedures in the pancreatic and biliary ducts, previous acute pancreatitis, drug therapy and history of systemic diseases.
- Laboratory investigations including complete blood count, total and direct bilirubin, serum aminotransferases (alanine aminotransferase and aspartate transaminase), prothrombin time, international normalized ratio, and baseline values of serum amylase and lipase.
- Gastric biopsies were taken during ERCP by the same endoscope (duodenoscope) for diagnosis of H. pylori using histopathological examination.
- Serum somatostatin level measurement using human somatostatin ELISA kit (catalog no.: SG-10685; SinoGeneClon Biotech Co. Ltd., Hangzhou, China). Detection range was 0.6–22 µg/l.
- Abdominal ultrasound using Toshiba ‘Just vision’ model SSA-325A (Hong Kong, China), real time scanner instrument with a 3.5 MHz convex transducer (after an overnight fasting), commenting on gall bladder, common bile duct (CBD), intrahepatic and extrahepatic biliary radicals and pancreas.
Endoscopic retrograde cholangiopancreatography procedure
Patients underwent ERCP after a 12 h fast under general anesthesia. All procedure details were recorded (e.g. time of cannulation, number of trials for cannulation, use of precut papillotomy, and amount of dye injected).
After the procedure
- All patients were monitored in the ward for 24 h for any symptom or sign suggestive of acute pancreatitis.
- Serum amylase and lipase were measured 24 h after the procedure.
Patients were divided according to H. pylori infection into two groups:
- Group A: included 37 H. pylori positive patients.
- Group B: included 43 H. pylori negative patients.
Clinical and biochemical evidence of PEP were evaluated in both groups.
Diagnosis of acute pancreatitis requires two of three features: (i) abdominal pain consistent with acute pancreatitis, (ii) serum lipase or amylase greater than three times the upper limit of normal and (iii) characteristic findings of acute pancreatitis on contrast-enhanced computed tomography scan, MRI, or transabdominal ultrasound.
Informed consent was obtained from all participants before enrollment in the study and the study was approved by Ethical Committee of Faculty of Medicine, Al-Azhar University. It is in accordance with Helsinki Declaration of 1975, as revised in 2000.
Analysis of data was done using statistical package for the social sciences (IBM SPSS) version 20 (IBM SPSS Inc., Chicago, US). The following tests were used: χ2-test was used in the comparison between two groups with qualitative data, and Fisher exact test was used instead of the χ2-test when the expected count in any cell was found less than five. Independent t-test was used in the comparison between two groups with quantitative data and parametric distribution. Mann–Whitney test was used in the comparison between two groups with quantitative data and nonparametric distribution. A probability value of 0.05 or less was considered to be statistically significant. Diagnostic performance of somatostatin level as a marker of PEP was done using receiver operator characteristic curve analysis with estimation of the proper cutoff level and assessment of its sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV).
| Results|| |
The indications of endoscopy in H. pylori infected patients (group A) were CBD stone in 13 (35.1%) patients, cancer head of pancreas in 10 (27%) patients, cholangiocarcinoma in 10 (27%) patients, sphincter of Oddi dysfunction in two (5.4%) patients, stent removal in one (2.7%) patient, and sclerosing cholangitis in one (2.7%) patient, whereas in H. pylori noninfected patients (group B) were CBD stone in 28 (65.1%) patients, cancer head of pancreas in three (7%) patients, cholangiocarcinoma in six (14%) patients, sphincter of Oddi dysfunction in one (2.3%) patient, stent removal in four (9.3%) patients, and infectious cholangitis in one (2.3%) patient.
There were no significant differences in precut papillotomy, sphincterotomy, cannulation time and number of trials, pancreatic duct cannulation, and CBD stent application between both the studied groups. There was a significant increase in CBD stone and its removal in group B compared with group A and a significant increase in balloon dilator in group A compared with group B ([Table 1]).
|Table 1 Comparison of endoscopic retrograde cholangiopancreatography findings and different procedures related to endoscopic retrograde cholangiopancreatography between the studied groups|
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The percentage of PEP was 10.8% (four patients in group A) and 9.3% (four patients in group B) with an overall percentage of 10% of the studied group.
Patients were divided according to occurrence of PEP into the following: eight patients with positive PEP and 72 patients with negative PEP.
No significant difference between both positive and negative PEP patients was seen regarding age and sex. According to ERCP-related maneuvers, cannulation time and number of trials, pancreatic duct cannulation and precut papillotomy were associated with a higher risk of PEP ([Table 2]).
|Table 2 Comparison of endoscopic retrograde cholangiopancreatography findings and different procedures related to endoscopic retrograde cholangiopancreatography between positive post-endoscopic retrograde cholangiopancreatography pancreatitis and negative post-endoscopic retrograde cholangiopancreatography pancreatitis|
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Assessing the value of somatostatin levels in the prediction of PEP, we found that the best cutoff value of somatostatin level is up to 0.02 mcg/l, with sensitivity of 50%, specificity of 100%, PPV of 100%, and NPV of 94.7% ([Table 3] and [Table 4).
|Table 3 Comparison of serum somatostatin, amylase and lipase levels between the studied groups|
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|Table 4 Comparison of serum somatostatin, amylase and lipase levels between both positive and negative cases for post-endoscopic retrograde cholangiopancreatography pancreatitis|
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| Discussion|| |
The present study was planned to assess if there is an association between H. pylori infection and low somatostatin level, and its relation to PEP.
In our study, we recorded eight cases with PEP, four cases in each group with no significant difference. The percentage of PEP was 10.8% (four patients in group A) and 9.3% (four patients in group B) with an overall percentage of 10% of the studied groups and this goes in agreement with Zouhairi et al.  who reported that the incidence of PEP in large prospective studies ranges from 1.6 to 15.1%. In addition, Abdel-Mageed et al.  reported that the incidence of PEP was 11.2%.
Our study revealed statistically significant increase in somatostatin level in group A (H. pylori positive) compared with group B (H. pylori negative). This was in agreement with Abdel-Mageed et al.  who found increased serum somatostatin level in H. pylori positive patients in comparison with H. pylori negative patients but with no significant difference.
Also, Isomoto et al.  reported no significant differences in plasma somatostatin level with reference to H. pylori status (11.3±5.7 vs. 9.7±6.2).
Zaki et al.  found that acute administration of H. pylori is capable of inhibiting acid secretion directly as well as indirectly by activating intramural calcitonin gene related peptide sensory neurons that are coupled to stimulate somatostatin secretion. Activation of calcitonin gene related peptide neurons offers an explanation as to how initial patchy superficial colonization of the stomach by H. pylori can induce acute hypochlorhydria in humans.
Czaja et al.  reported no changes in either G cell or D cell density in the gastric mucosa in children regardless of the presence of gastritis or H. pylori infection.
However, Liu et al. , Jeffery et al.  and Bulajic et al.  found that H. pylori infection provokes changes in the number of endocrine cells important for regulating acid secretion. The percentage of G cells as a percentage of mucosal endocrine cells was increased and that of D cells was decreased, and this results in reduced mucosal somatostatin level. Moreover, they found that the alterations correlate best with the severity of inflammation and not with H. pylori density. None of these studies measure serum somatostatin level.
Although there have been some studies on animal models suggesting a possible role for H. pylori infection in acute pancreatitis , no author has yet found a significant association between H. pylori infection and acute pancreatitis in humans .
Our study revealed statistically significant lower somatostatin levels in patients who experienced PEP than patients who did not experience PEP and this goes in agreement with Abdel-Mageed et al.  who reported that patients who experienced PEP had a statistically significant lower somatostatin level than patients who did not experience PEP.
Extensive clinical studies were done which include assessment of therapies such as antisecretory agents like protease inhibitors , somatostatin ,, nitrates  and anti-inflammatory agents  but none of these studies had dealt with serum somatostatin level measurement and ever relate it to PEP.
Assessing the value of somatostatin levels in prediction of PEP, we found that the best cutoff value of somatostatin level is up to 0.02 mcg/l, with sensitivity of 50%, specificity of 100%, PPV of 100%, and NPV of 94.7%. Abdel-Mageed et al.  found that the cutoff value of somatostatin in prediction of PEP is somatostatin level up to 6.25 ng/l, with sensitivity of 100%, specificity of 33.8%, PPV of 16.1%, and NPV of 100%.
On dividing the patients according to occurrence of PEP, the results showed no statistically significant differences between both groups as regarding age and sex. Our results are in agreement with Nader et al.  and Abdel-Mageed et al. , but are not with Cotton et al.  and Anderson et al.  who found that younger age, and female sex were an independent risk factor for PEP. This may be attributed to the aging effect on pancreatic exocrine function, smaller CBD diameter and the higher incidence of sphincter of Oddi dysfunction in younger female .
Regarding ERCP-related maneuvers, difficult cannulation (characterized by a greater number of attempts or longer time needed to successfully cannulate the bile duct or frequent pancreatic duct cannulation) was associated with a higher risk of PEP. The repeated trials for CBD cannulation reflect the difficulty of the procedure and subsequent further trauma. Cheng et al.  reported that cannulation trauma to the papilla induces edema, narrowing the papillary orifice, thus making an obstacle to the flow of pancreatic juice.
These results were in agreement with Toshio et al.  who reported that the number of times the papilla was manipulated was significantly higher in the group with hyperamylasemia than the group without it.
The results of Vandervoort et al.  are consistent with the results of the present study where they found that the risk of PEP increased gradually from 3.3% with less than five cannulation attempts to 14.9% when more than 20 attempts were made.
Omar et al.  stating that pancreatic duct cannulation is significantly associated with the risk for PEP. It is most probably owing to manipulation of pancreatic duct and pancreatic sphincter, leading to subsequent spasm of pancreatic duct and obstruction of the flow of pancreatic enzymes. In addition, injury to the pancreatic duct and pancreatic parenchyma may cause premature activation of pancreatic enzymes leading to autodigestion of the pancreas.
Regarding precut papillotomy, it was done in 3/8 (37.5%) patients among PEP positive patients and in 7/72 (9.7%) patients among PEP negative patients, and this difference was statistically significant.
Regarding sphincterotomy, it was done in 4/8 (50%) patients among PEP positive patients and in 53/72 (73.6%) patients among PEP negative patients, and this difference was statistically insignificant.
Our results were in agreement with Omar et al.  and Dumonceau et al.  who found that precut papillotomy was an independent risk factor for PEP as it causes papillary edema which retains pancreatic secretion resulting in PEP. However, our results are not with Freeman et al.  and Nader et al.  who found that papilla sphincterotomy was an independent risk factor for PEP.
Some authors indicate that precut sphincterotomy is usually preceded by difficult cannulation through the conventional approach and that the later, not the precut sphincterotomy itself, is responsible for the development of PEP. This is supported by the finding that precut sphincterotomy was not reported as a risk factor for PEP from endoscopists who adopted precut sphincterotomy as a preferred technique from the start not just a salvage procedure after difficult cannulation through conventional cannulation methods . Early precut leads to more successful cannulation rate without more hazard of morbidity after ERCP .
Our data showed that CBD diameter was insignificant risk factor for PEP. This result is in agreement with most studies that have found no independent influence of duct size on the risk for PEP ,,. In contrast, many early studies suggested small CBD diameter as a risk factor for pancreatitis .
Moreover, we reported that CBD stone was an insignificant risk factor for PEP. This result is in disagreement with Matsubayashi et al.  who reported that the higher incidence of pancreatitis in patients with benign obstructive jaundice in comparison with patients with malignant obstructive jaundice may be attributed to gallstones (the commonest indication in patients with benign obstructive jaundice), which increases the risk for pancreatitis. Proposed mechanisms include reflux of noxious bile into the pancreatic duct from transient obstruction of the ampulla during gallstone passage and pancreatic ductal hypertension from either a stone impacted at the ampulla or ampullary trauma caused by stone passage .
In our study, balloon dilatation of the CBD orifice was insignificant risk factor for PEP. This result was consistent with several studies that have demonstrated that balloon dilatation of the distal CBD and ampulla can be a well-tolerated and effective technique for the removal of biliary stones without increasing the rate of PEP . In contrast, other studies showed that balloon dilatation has been associated with a markedly increased risk for PEP .
The comparison of serum amylase and lipase levels between the studied groups revealed increase in both post-ERCP serum amylase and lipase levels in group B (H. pylori negative) (97 and 130, respectively) compared to group A (H. pylori positive) (80 and 92, respectively), with significant difference as regarding post-ERCP lipase.This was in agreement with Abdel-Mageed et al.  who found increase in both post-ERCP serum amylase and lipase levels in H. pylori uninfected patients compared with H. pylori infected patients, with no significant difference.
On the contrary, our study also revealed highly significant increase in both post-ERCP serum amylase and lipase levels (766.5 and 2598.5, respectively) in patients who experienced PEP than patients who did not experience PEP (74 and 101.5, respectively).
Early recognition of pancreatic damage after the procedure is indispensable. Although clinical symptoms are reliable indicators of pancreatic inflammation, in a reported study, ∼30% of the patients who developed PEP showed no clinical signs at 2 h after the procedure . Utility of the measurement of serum amylase and lipase has been reported for early diagnosis of pancreatitis .
| Conclusion|| |
- A significant increase in somatostatin level was registered in H. pylori-infected patients.
- A significant decrease in somatostatin level was registered in patients who experienced PEP than patients who did not experience PEP.
- Serum amylase and lipase were of most importance in diagnosis of PEP, as they were elevated early in the course of the disease, permitting early interference to decrease mortality and morbidity associated with this condition.
- H. pylori screening and treatment is not mandatory before ERCP as H. pylori infection was found to be not associated with PEP.
- Low somatostatin level may have a role in prediction of PEP but further multicentric studies on large number of cases are recommended for further confirmation ,.
The authors acknowledge Dr Mona Ramadan, Professor and Head of Tropical Medicine, Faculty of Medicine (Girls), Al-Azhar University, for her great support and valuable unlimited help throughout the work.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Cotton PB, Garrow DA, Gallagher J, Romagnuolo J. Risk factors for complications after ERCP: a multivariate analysis of 11497 procedures over 12 years. Gastrointest Endosc 2009; 70:80–88.
Toshio T, Tadahiro O, Osamu Y. Risk management in endoscopic treatment of endoscopic sphincterotomy and endoscopic papillary balloon dilation. Dig Endosc 2007; 19:S49–S51.
Jeffery PL, McGuckin MA, Linden SK. Endocrine impact of Helicobacter pylori
: focus on ghrelin and ghrelin o-acyltransferase. World J Gastroenterol 2011; 17:1249–1260.
Chan HH, Lai KH, Lin CK, Tsai WL, Lo GH, Hsu P et al.
Effect of somatostatin in the prevention of pancreatic complications after endoscopic retrograde cholangiopancreato-graphy. J Chin Med Assoc 2008; 71:605–609.
Katsinelos P, Fasoulas K, Paroutoglou G, Chatzimavroudis G, Beltsis A, Terzoudis S et al.
Combination of diclofenac plus somatostatin in the prevention of post-ERCP pancreatitis: a randomized, double-blind, placebo-controlled trial. Endoscopy 2012; 44:53–59.
Zouhairi ME, Swartz D, Shah T. Post-ERCP pancreatitis: mechanisms, risk factors, and prevention. Pancreatic Dis Ther 2013; 3:116.
Abdel-Mageed KH, Keddeas MW, Ali-Eldin ZA, Abdel-Bary SA, Mohammed ES, Samaan AI. Relation of Helicobacter pylori
to post endoscopic retrograde cholangiopancreatography pancreatitis. Int J Recent Sci Res 2016; 7:8718–8722.
Isomoto H, Ueno H, Nishi Y, Wen CY, Nakazato M, Kohno S. Impact of Helicobacter pylori
infection on ghrelin and various neuroendocrine hormones in plasma. World J Gastroenterol 2005; 11:1644–1648.
Zaki M, Coudron PE, McCuen RW, Harrington L, Chu S, Schubert ML. H. pylori
acutely inhibits gastric secretion by activating CGRP sensory neurons coupled to stimulation of somatostatin and inhibition of histamine secretion. Am J Physiol Gastrointest Liver Physiol 2013; 304:G715–G722.
Czaja M, Szarszewski A, Kamińska B, Bogotko-Szarszewska M, Luczak G, Kozielska E et al.
Serum gastrin concentration and changes in G and D cell densities in gastric antrum in children with chronic gastritis. Int J Clin Pract 2008; 62:1044–1049.
Liu Y, Vosmaer GD, Tytgat GN, Xiao SD, Ten Kate FJ. Gastrin (G) cells and somatostatin (D) cells in patients with dyspeptic symptoms: Helicobacter pylori
associated and non-associated gastritis. J Clin Pathol 2005; 58:927–931.
Bulajic M, Panic N, Löhr JM. Helicobacter pylori
and pancreatic diseases. World J Gastrointest Pathophysiol 2014; 5:380–383.
Warzecha Z, Dembiński A, Ceranowicz P, Dembiński M, Sendur R, Pawlik WW et al.
Deleterious effect of Helicobacter pylori
infection on the course of acute pancreatitis in rats. Pancreatology 2002; 2:386–395.
Seta T, Noguchi Y. Protease inhibitors for preventing complications associated with ERCP: an updated meta-analysis. Gastrointest Endosc 2011; 73:700–706.
Concepción-Martín M, Gómez-Oliva C, Juanes A, Díez X, Prieto-Alhambra D, Torras X et al.
Somatostatin for prevention of post-ERCP pancreatitis: a randomized, double-blind trial. Endoscopy 2014; 46:851–856.
Zhao WY, Zhuang C, Xu J, Wang M, Zhang Z, Tu L et al.
Somatostatin receptors in gastrointestinal stromal tumors: new prognostic biomarker and potential therapeutic strategy. Am J Transl Res 2014; 6:831–840.
Ding J, Jin X, Pan Y, Liu S, Li Y. Glyceryl trinitrate for prevention of post-ERCP pancreatitis and improls. PLoS One 2013; 8:e75645.
Sotoudehmanesh R, Eloubeidi MA, Khatibian M. A randomized trial of rectal indomethacin and sublingual nitrates to prevent post-ERCP pancreatitis. Am J Gastroenterol 2014; 109:903–909.
Nader FM, Magdey AK, Mossalam HY, Rashad FE. Risk factors of post-ERCP pancreatitis. AAMJ 2007; 5:36–44.
Anderson MA, Fisher L, Jain R, Evans JA, Appalaneni V, Ben-Menachem T et al.
Complications of ERCP. Gastrointest Endosc 2012; 75:467–473.
El Nakeeb A, El Hanafy E, Salah T, Atef E, Hamed H, Sultan AM et al.
Post-endoscopic retrograde cholangiopancreatography pancreatitis: risk factors and predictors of severity. World J Gastrointest Endosc 2016; 8:709–715.
Cheng CL, Sherman S, Watkins JL, Barnett J, Freeman M, Geenen J et al.
Risk factors for post-ERCP pancreatitis: a prospective multicenter study. Am J Gastroenterol 2006; 101:139–147.
Vandervoort J, Soetikno RM, Tham TC Risk factors for complications after performance of ERCP. Gastrointest Endosc 2002; 56:652–656.
Omar MA, Ahmed AE, Said OA, El-Amin H. Risk factors for post-ERCP pancreatitis: a prospective multicenter study in upper Egypt. Egypt J Surg 2015; 34:1–10. [Full text]
Dumonceau JM, Andriulli A, Deviere J, Mariani A, Rigaux J, Baron TH et al.
European Society of Gastrointestinal Endoscopy (ESGE) Guideline: prophylaxis of post-ERCP pancreatitis. Endoscopy 2010; 42:503–515.
Freeman ML, Overby C, Qi D. Pancreatic stent insertion: consequences of failure and results of a modified technique to maximize success. Gastrointest Endosc 2004; 59:8–14.
Freeman ML, Guda NM. ERCP cannulation: a review of reported techniques. Gastrointest Endosc 2005; 61:112–125.
Zhang QS, Han B, Xu JH, Gao P, Shen YC. Needle-knife papillotomy and fistulotomy improved the treatment outcome of patients with difficult biliary cannulation. Surg Endosc 2016; 30:5506–5512.
Testoni PA, Mariani A, Giussani A, Vailati C, Masci E, Macarri G et al.
Risk factors for postERCP pancreatitis in high- and low volume centers and among expert and non-expert operators: a prospective multicenter study. Am J Gastroenterol 2010; 105:1753–1761.
Wang P, Li ZS, Liu F, Ren X, Lu NH, Fan ZN et al.
risk factors for ERCP-related complications: a prospective multi-center study. Am J Gastroenterol 2009; 104:31–40.
Dickinson RJ, Davies S. Post-ERCP pancreatitis and hyperamylasemia: the role of operative and patient factors. Eur J Gastroenterol Hepatol 1998; 10:423–428.
Matsubayashi H, Fukutomi A, Kanemoto H, Maeda A, Matsunaga K, Uesaka K et al.
Risk of pancreatitis after endoscopic retrograde cholangio-pancreatography and endoscopic biliary drainage. HPB (Oxford) 2009; 11:222–228.
Cappell MS. Acute pancreatitis: etiology, clinical presentation, diagnosis, and therapy. Med Clin North Am 2008; 92:889–923.
Maydeo A, Bhandari S. Balloon sphincteroplasty for removing difficult bile duct stones, Endoscopy 2007; 39:958–961.
Baron TH, Harewood GC. Endoscopic balloon dilation of the biliary sphincter compared to endoscopic biliary sphincterotomy for removal of common bile duct stones during ERCP: a meta-analysis of randomized, controlled trials. Am J Gastroenterol 2004; 99:1455–1460.
Ito K, Fujita N, Noda Y, Kobayashi G, Horaguchi J, Takasawa O et al.
Relationship between post-ERCP pancreatitis and the change of serum amylase level after the procedure. World J Gastroenterol 2007; 13:3855–3860.
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.
Cheon YK. Can postendoscopic retrograde cholangiopancreatography pancreatitis be prevented by a pharmacological approach? Korean J Intern Med 2013; 28:141–148.
Thaker AM, Mosko JD, Berzin TM. Postendoscopic retrograde cholangiopancreatography pancreatitis. Gastroenterol Rep (Oxf) 2015; 3:32–40.
[Table 1], [Table 2], [Table 3], [Table 4]