Risk Of Pancreatitis In Patients Research Articles

Reducing pancreatitis risk in patients with hypertriglyceridemia.

Reducing pancreatitis risk in patients with hypertriglyceridemia.

PSUN270 Magnified Risk of Pancreatitis by GLP-1: A Case of Necrotizing Pancreatitis in a Patient on Dulaglutide with Baseline Elevated Triglycerides

Abstract Introduction Glucagon-like peptide 1 receptor agonists (GLP-1 RA), used in the treatment of diabetes mellitus, have been associated with pancreatitis in both animal studies and clinical trials. Furthermore, GLP-1 RA are associated with increased levels of serum lipase and amylase, possibly indicating resultant pancreatic inflammation.1 While there is debate on the actual degree of risk of pancreatitis in patients on GLP-1 RA, there may be individuals who are at higher risk due to baseline comorbidities that may have their risk of pancreatitis further potentiated by treatment with GLP-1 RA. We present a case in which a patient with baseline moderately elevated triglycerides on long term GLP-1 RA develops necrotizing pancreatitis after minimal alcohol intake. Case A 46-year-old man with type 2 diabetes mellitus, hyperlipidemia, and depression presented with one day history of severe right upper quadrant abdominal pain, nausea, and non-bloody, non-bilious vomiting. He also endorsed subjective fevers and chills, shortness of breath, chest pain, and constipation. He reported that he had drank one bottle of sparkling wine the day prior but denied drinking regularly. Labs and imaging were consistent with acute necrotizing pancreatitis with elevated lipase (502 U/L), elevated triglycerides (TG) (3,480 mg/dL), and CT abdomen/pelvis showing focal hypoattenuation/edema of the pancreatic head with surrounding fat stranding. Subsequent MRI abdomen showed evolving necrotic pancreatitis with focal area of nonenhancement in the pancreatic head. He denied any history of gallstones, recent trauma, diarrhea, weight loss, or prior pancreatitis. Review of his medications was notable for dulaglutide for management of his diabetes. He also had a history of consistently elevated TG to the mid-300s mg/dL as far back as 3 years ago. Patient was ultimately managed conservatively with intravenous fluids with resolution of symptoms and downtrend of lipase and triglycerides. He was discharged on fenofibrate and icosapent ethyl for further triglyceride control. Discussion While several META analyses have not shown significant association between GLP-1 RA and pancreatitis, there still is a proportion of patients who have developed pancreatitis on GLP-1 RA.2 Our patient had baseline elevated triglycerides, but they were below the typical threshold for treatment. With minimal alcohol consumption, he still developed pancreatitis. We suspect that his risk for pancreatitis was magnified by his GLP-1 RA. We believe that in patients such as ours who have baseline independent risk factors for pancreatitis, GLP-1 RA should be carefully considered before initiation. 1. Trujillo J. Safety and tolerability of once-weekly GLP-1 receptor agonists in type 2 diabetes. J Clin Pharm Ther. 2020;45 Suppl 1(Suppl 1): 43-60. doi: 10.1111/jcpt.13225 2. Monami M, Dicembrini I, Nardini C, Fiordelli I, Mannucci E. Glucagon-like peptide-1 receptor agonists and pancreatitis: a meta-analysis of randomized clinical trials. Diabetes Res Clin Pract. 2014;103(2): 269-275. doi: 10.1016/j.diabres.2014.01.010 Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

Does same session EUS-guided tissue acquisition and ERCP increase the risk of pancreatitis in patients with malignant distal biliary obstruction?

Endoscopic retrograde cholangiopancreatography (ERCP) and endoscopic ultrasonography-guided tissue acquisition (EUS-TA) are increasingly performed in the same session in patients with malignant biliary obstruction. In this retrospective analysis, we investigated adverse events (AE) after same session ERCP and EUS-TA. Patients with malignant distal biliary obstruction who underwent EUS-TA and/or ERCP with self-expandable metal stent (SEMS) placement from January 2015 to April 2020 were included. Primary outcome was post-procedural pancreatitis (PPP). Secondary outcomes were other procedure-related AE. We included 494 patients, of which 118 patients (24%) underwent same session EUS-TA+ERCP, 51 patients (10%) underwent separate session EUS-TA & ERCP, 90 patients (18%) ERCP-only and 235 patients (48%) EUS-TA only. PPP occurred in 22 patients (19%) after same session EUS-TA+ERCP and in 6 patients (12%) after separate EUS-TA & ERCP (p=0.270). When adjusted for other known risk factors (i.e., difficult procedure), the difference in PPP remained non-significant (adjusted odds ratio 1.74 (95%-CI 0.65-4.67, p=0.268). The incidence of other AE was similar, although the overall AE rate was significantly higher after same session EUS-TA+ERCP (36% vs. 20%, p=0.030). Same session EUS-TA+ERCP did not significantly increase the incidence of PPP, although overall AE were significantly higher. These data warrant further prospective studies.

Preeclampsia and the Risk of Pancreatitis: A Nationwide, Population-Based Cohort Study.

Background Preeclampsia is a multiple organ dysfunction during pregnancy, including hepatic, renal, and neurological dysfunction, and is defined as hypertension and proteinuria occurring after 20 weeks of pregnancy. Clinical features seen in preeclampsia are due to relatively poorly perfused placenta and maternal endothelial dysfunction. Some studies have found that preeclampsia may cause acute pancreatitis due to microvascular abnormalities and visceral ischemia. This retrospective cohort study used the Taiwanese National Health Insurance Research Databases (NHIRD) to study the relationship between preeclampsia and the risk of pancreatitis. Methods In total, 606,538 pregnant women were selected from the NHIRD between January 1, 1998 and December 31, 2010. They were divided into a preeclampsia cohort (n = 485,211) and a nonpreeclampsia cohort (n = 121,327). After adjusting for comorbidities that may induce pancreatitis, we analyzed and compared the incidence of pancreatitis in the two cohorts. Results The overall incidence of pancreatitis in the preeclampsia cohort was significantly higher than that in the control cohort (4.29 vs. 2.33 per 10,000 person-years). The adjusted HR of developing pancreatitis increased 1.68-fold (95% CI: 1.19-2.36) in the preeclampsia cohort. In addition, pregnant women with preeclampsia without comorbidities had a significantly high risk of pancreatitis (aHR = 1.83, 95% CI 1.27-2.63). The combined effect of preeclampsia and alcohol-related diseases resulted in the highest risk of pancreatitis (aHR = 43.4, 95% CI: 6.06-311.3). Conclusion Compared with patients without preeclampsia, the risk of pancreatitis in patients with preeclampsia is significantly increased after adjusting for demographics and comorbidities. The risk of pancreatitis is greatly increased when preeclampsia is accompanied by alcohol-related diseases, hepatitis C, gallstones, diabetes, or age of 26–35 years. Early identification and effective control of preeclampsia and the associated comorbidities can reduce the risk of pancreatitis and the associated morbidity and mortality.

Pancreatitis associated with azathioprine and 6-mercaptopurine use in Crohn’s disease: a systematic review

Thiopurines are proven agents in the treatment of Crohn’s disease. While pancreatitis is recognised as an adverse event associated with therapy, the effect size and morbidity of thiopurine-induced pancreatitis is...

Gene expression profiles of recurrent acute pancreatitis risk in patients with sustained chylomicronemia.

A fasting triglyceridemia >10 mmol/L is associated with chylomicronemia (CM) and an increased recurrent acute pancreatitis (RAP) risk. The number of pancreatitis episodes varies significantly between patients with CM. The objective of this study was to investigate gene expression profiles of RAP in patients with CM. A total of 47 CM subjects participated in this study. Prior to the analyses, all patients were divided into three groups covering a wide spectrum of RAP: 0 (n = 21), 1-3 (n = 10) or >4 (n = 16) pancreatitis episodes. Gene expression profiles were compared to those of 15 healthy normolipidemic controls. Differential expression moderated T-tests between studied groups were performed using a linear model of the Bioconductor package Limma. The False discovery rate was controlled using the Benjamini-Hochberg procedure. At a p-value <0.01, a false discovery rate of 5% and a >2-fold change expression significance levels, a set of 41 probes have been found differentially expressed in CM subjects with no pancreatitis, 103 in the CM group with 1 to 3 pancreatitis, and 94 in the group with ≥4 pancreatitis compared to healthy controls. Of the identified annotated probes, 14 are shared by all CM groups; 3 are specific to CM with no pancreatitis; 11 are specific to CM with 1 to 3 pancreatitis, and 17 are specific to CM with ≥4 pancreatitis. Most of the annotated biomarkers are involved in inflammatory, immune, lipoprotein kinetics or signalling biological pathways. These results reveal gene expression signatures of RAP in patients with CM.

Acute pancreatitis risk after kidney transplantation: Propensity score matching analysis of a national cohort

PurposeData for elucidating post-kidney transplantation (KT) acute pancreatitis (AP) risk are limited and no large-scale cohort study has investigated the impact of AP after KT.MethodData from Taiwan National Health Insurance (NHI) Research Database (NHIRD) were calculated through the method of propensity score matching to compare the pancreatitis risk in patients with and without KT.ResultsThe overall pancreatitis incidence rates were 1.71 and 0.61 per 1,000 person-years in the KT and non-KT groups, respectively and corresponding adjusted HR (aHR [95% CI]) for pancreatitis was 2.48 (1.51–4.09) in the KT group. In the multivariable model, AP risk was higher in transplant patients with alcohol-related illnesses (aHR: 3.78, 95% CI: 1.32–10.8), gall stone disease (aHR: 3.53, 95% CI: 1.48–8.44), or past history of pancreatitis (aHR: 10.3, 95% CI: 5.08–20.8). Of note, recurrent AP risk was significantly higher in the KT group (aHR: 8.19, 95% CI: 2.89–23.2). Patients with post-KT AP demonstrated shorter patient and allograft survival than did those without (both P < 0.001, respectively).ConclusionIn conclusion, KT recipients are very likely to be associated with AP. Moreover, their inferior outcomes are strongly associated with post-KT AP.

External Validation of a Predictive Model for Acute Pancreatitis Risk in Patients with Severe Hypertriglyceridemia

Objective: We previously developed a predictive model to assess the risk of developing acute pancreatitis (AP) in patients with severe hypertriglyceridemia (HTG). In this study, we aimed to externally validate this model. Methods: The validation cohort included cross-sectional data between 2013 and 2017. Adult patients (≥18 years old) with triglyceride levels ≥1,000 mg/dL were identified. Based on our previous 4-factor predictive model (age, triglyceride [TG], excessive alcohol use, and gallstone disease), we estimated the probability of developing AP. Model performance was assessed using area under receiver operating characteristic curve (AUROC). Results: In comparison to the original cohort, patients in the validation cohort had more prevalent acute pancreatitis (16.2% versus 9.2%; P<.001) and gallstone disease (7.5% versus 2.1%; P<.001). Other characteristics were comparable and not statistically significant. The AUROCs were almost identical: 0.8337 versus 0.8336 in the validation and the original cohorts, respectively. In univariable analyses, the highest increase in odds of AP was associated with HTG, followed by gallstones, excessive alcohol use, and younger age. Conclusion: This study externally validates the 4-factor predictive model to estimate the risk of AP in adult patients with severe HTG (TG ≥1,000 mg/dL). Younger age was confirmed to place patients at high risk of AP. The clinical risk categories suggested in this study may be useful to guide treatment options. Abbreviations: AP = acute pancreatitis; ASCVD = atherosclerotic cardiovascular disease; AUROC = area under the receiver operating characteristic curve; FRAX = fracture risk assessment tool; HTG = hypertriglyceridemia; OR = odds ratio; TG = triglyceride level.

1635-P: Risk of Pancreatitis among Patients with Type 2 Diabetes Receiving DPP-4 Inhibitors: Nationwide Case-Control Study

Dipeptidyl peptidase-4 inhibitors (DPP-4i) are widely used antidiabetic incretin-based drugs. There remain concerns about the pancreatic safety of DPP-4i due to its pleiotropic effects on the exocrine pancreas. We studied whether DPP-4i are associated with acute and chronic pancreatitis using nationwide population-based cohort study. This study included patients with newly diagnosed type 2 diabetes being treated with antidiabetic drugs (n = 33,208) from 2007 to 2013, from the sample cohort (n = 514,866) of the ***** National Health Insurance Service-Health Screening Cohort database. A Cox proportional hazards model with time-dependent covariates was used to calculate the risk. Lag time of 6 months was applied to reflect a cumulative effect of DPP-4i. Subgroup analyses were also performed according to various confounding factors. Of the 33,208 subjects, 10,210 new DPP-4i users and 22,998 new users of antidiabetic drugs other than DPP-4i were included. DPP-4i significantly increased the risk for pancreatitis (adjusted hazard ratio (aHR) 1.26, 95% CI 1.06-1.50) even after adjusting for age, sex, BMI, smoking and alcohol status, Charlson comorbidity index, and residential region. With a drug-use lag exposure of 6 months, aHR for pancreatitis was still statistically significant as similar (aHR 1.23, 95% CI 1.01-1.51) In subgroup analyses, the risk of pancreatitis was apparent only in subjects with a higher comorbidity score, suggesting a clinical factor which increases the risk of pancreatitis by DPP-4i use. In an analysis of data from a large nation-wide cohort database, we found that DPP-4i are associated with the increased risk of pancreatitis in patients with newly diagnosed type 2 diabetes. Disclosure M. Lee: None. J. Sun: None. M. Han: None. J. Kim: None. Y. Kim: None. I. Lee: None. S. Lee: None. J. Bae: None. Y. Cho: None. J. Lee: None. C. Kim: None. C. Nam: None. E. Kang: None.

Pre-endoscopic retrograde cholangiopancreatography (ERCP) administration of rectal indomethacin in unselected patients to reduce post-ERCP pancreatitis: A systematic review and meta-analysis.

Previous studies have reported that peri-procedural administration of rectal indomethacin reduces the risk of pancreatitis in patients undergoing endoscopic retrograde cholangiopancreatography (ERCP). Based on these studies, gastrointestinal (GI) societies recommend prophylactic rectal indomethacin for all patients undergoing ERCP. However, recent studies have reported contradictory results. The aim of this study was to perform a systematic review and meta-analysis to estimate the pooled relative risk (RR) of post-ERCP pancreatitis (PEP) in unselected patients who received rectal indomethacin before the ERCP (pre-ERCP) compared to patients who received pre-ERCP rectal placebo. We conducted a comprehensive search of multiple electronic databases and conference proceedings (from inception through September 1, 2017) to identify randomized control trials (RCTs) investigating the role of pre-ERCP rectal indomethacin in reducing the risk of PEP in unselected patients undergoing ERCP. The databases included Ovid, Medline, In-Process, and Other Non-Indexed Citations, Ovid MEDLINE, Ovid EMBASE, Ovid Cochrane Central Register of Controlled Trials, Ovid Cochrane Database of Systematic Reviews, Scopus, and Web of Science. We calculated a pooled estimate of the RR of PEP in patients who received pre-ERCP rectal indomethacin compared to patients who received pre-ERCP rectal placebo. The meta-analysis was performed using the random effects model. Six RCTs with a total of 2229 patients were included in the final meta-analysis. There were 1143 patients in the rectal indomethacin group and 1086 patients in the rectal placebo group. There were 71 events of PEP in the rectal indomethacin group and 114 events of PEP in the rectal placebo group. Pre-ERCP administration of rectal indomethacin significantly reduced the risk of PEP compared to pre-ERCP rectal placebo (RR 0.60, 95% CI, 0.45-0.80; p<0.0001). There was no heterogeneity between the studies (I2= 0). The results of this meta-analysis support the routine pre-ERCP administration of rectal indomethacin in unselected patients to prevent PEP.

Dipeptidyl Peptidase-4 Inhibitors and the Risk of Pancreatitis in Patients with Type 2 Diabetes Mellitus: A Population-Based Cohort Study.

Background Information on the risk of acute pancreatitis in patients receiving dipeptidyl-peptidase IV inhibitors (DPP-4i) is limited and controversial. One study suggested that the differences in findings between these meta-analyses were attributed to whether they included large randomized control trials with cardiovascular outcomes or not. The aim of our study was to determine whether the use of DPP-4i increases the risk of acute pancreatitis compared with sulfonylurea (SU) and whether the risk is higher in patients with underlying cardiovascular disease (CVD). Methods A population-based cohort study was performed using Korean National Health Insurance Service-National Sample Cohort data. We included 33,395 new users of SU and DPP-4i from 1 January 2008 to 31 December 2015. SU-treated patients and DPP-4i-treated patients were matched by 1 : 1 propensity score matching. We used Kaplan–Meier curves and Cox proportional hazards regression analysis to calculate the risk of acute pancreatitis. Results The hazard ratio (HR) of hospitalization for acute pancreatitis was 0.642 (95% confidence interval (CI): 0.535–0.771) in DPP-4i-treated patients compared with SU-treated patients. The HR of DPP-4i use was also lower than that of SU use in patients without underlying CVD (HR: 0.591; 95% CI: 0.476–0.735) but not in patients with underlying CVD (HR: 0.727; 95% CI: 0.527–1.003). Conclusion Our findings suggest that DPP-4i is less likely to cause drug-induced pancreatitis than SU. This finding was not evident in patients with CVD, but DPP-4i was not more likely to induce pancreatitis in these patients than SU was.

Eluxadoline in the treatment of diarrhea-predominant irritable bowel syndrome.

Eluxadoline is a novel drug approved for the management of diarrhea predominant irritable bowel syndrome (IBS-D). It has unique pharmacology and works on three different opioid receptors. Several Phase II and III clinical trials have demonstrated eluxadoline’s efficacy in reducing symptoms related to IBS-D. Clinical trial results and postmarketing reports show a risk of pancreatitis in patients without a gallbladder or those abusing alcohol. This review article will include information on clinical trial results related to IBS-D management as well as eluxadoline’s limitations.

Multiple Gene Interaction Increases the Risk of Recurrent Acute Pancreatitis in Patients with Pancreas Divisum

Multiple Gene Interaction Increases the Risk of Recurrent Acute Pancreatitis in Patients with Pancreas Divisum

Role for Pre-ERCP Administration of Rectal Indomethacin in Unselected Patients to Prevent Post ERCP Pancreatitis: A Systematic Review and Meta-analysis

Introduction: Previous studies have reported that peri-procedural administration of rectal indomethacin reduces the risk of pancreatitis in patients undergoing endoscopic retrograde cholangiopancreatography (ERCP). Based on these studies, the European and Japanese GI societies recommend prophylactic rectal indomethacin for all patients undergoing ERCP. However, recent studies have reported contradictory results. The aim of this study was to perform a systematic review and meta-analysis to estimate the pooled relative risk (RR) of post-ERCP pancreatitis (PEP) in unselected patients who received rectal indomethacin before the ERCP (pre-ERCP) compared to patients who received pre-ERCP rectal placebo. Methods: We conducted a comprehensive search of multiple electronic databases and conference proceedings (from inception through May 1st, 2016) to identify randomized control trials (RCT) investigating the role of pre-ERCP rectal indomethacin in reducing the risk of PEP in unselected patients undergoing ERCP. The databases included Ovid Medline In-Process & Other Non-Indexed Citations, Ovid MEDLINE, Ovid EMBASE, Ovid Cochrane Central Register of Controlled Trials, Ovid Cochrane Database of Systematic Reviews, Scopus, and Web of Science. We calculated a pooled estimate of the relative risk (RR) of PEP in patients who received pre-ERCP rectal indomethacin compared to patients who received pre-ERCP rectal placebo. The meta-analysis was performed using random effects model. Results: Five RCTs with a total of 1934 patients were included in the final meta-analysis. There were 996 patients in rectal indomethacin group and 938 patients in rectal placebo group. There were 58 events of PEP in the rectal indomethacin group and 71 events of PEP in rectal placebo group. Pre-ERCP administration of rectal indomethacin reduced the risk of PEP compared to pre-ERCP rectal placebo but the difference was not statistically significant (RR, 0.74, 95% CI, 0.47-1.16; p=0.19) (Figure 1). The heterogeneity between studies was low (I2=41).Figure 1Conclusion: The results of this meta-analysis do not support the routine pre-ERCP administration of rectal indomethacin in unselected patients to prevent PEP. Previous meta-analyses which supported use of NSAIDs had broad inclusion criteria which allowed them to include different NSAID medications, routes of administration, timing of NSAID administration and selected patients at high risk for PEP.

High risk of acute pancreatitis after endoscopic ultrasound-guided fine needle aspiration of side branch intraductal papillary mucinous neoplasms.

Background and Objectives:Data on the risk of acute pancreatitis following endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) of pancreatic cystic lesions are limited. The aim of our study was to evaluate the frequency of acute pancreatitis after EUS-FNA of pancreatic cysts and solid lesions, and determine whether there was a difference in pancreatitis risk in patients with side branch intraductal papillary mucinous neoplasms (SB-IPMN).Patients and Methods:A retrospective review of patients who underwent EUS-FNA of pancreatic cysts and solid lesions was performed. The primary outcome measure was development of acute pancreatitis after EUS-FNA. Factors associated with acute pancreatitis were examined by statistical analysis to determine independent predictors of acute pancreatitis. Statistical significance was determined at a P ≤ 0.05.Results:We identified 186 patients with pancreatic cystic lesions and 557 with solid lesions in which EUS-FNA was performed. The median size of the cysts was 19 mm (range: 10-66 mm). There were 37 IPMNs, 33 mucinous cystic neoplasms, 58 serous cysts and 46 pseudocysts and 12 solid-cystic ductal carcinomas. The majority of patients (75%) with solid lesions were diagnosed with adenocarcinoma. Patients with pancreatic cysts had a statistically greater frequency of developing pancreatitis after EUS-FNA when compared to those with solid lesions (2.6% vs. 0.36% respectively; P = 0.13). In patients with cysts, there were no statistically significant differences between the two groups (with and without pancreatitis) with regard to a cyst location, size of the cyst, and number of needle passes or trainee involvement. Patients with SB-IPMN had a statistically higher frequency of pancreatitis after EUS-FNA compared to those with other cyst types (8% vs. 1.3% respectively; odds ratio = 6.4, 95% confidence intervals = 1.0-40.3, P = 0.05).Discussion:Patients with SB-IPMN are at a higher risk of developing acute pancreatitis after a EUS-FNA. Alternative means of diagnosis such as magnetic resonance cholangiopancreatogram might be necessary to avoid risk of EUS-FNA.

Incretin treatment and risk of pancreatitis in patients with type 2 diabetes mellitus: systematic review and meta-analysis of randomised and non-randomised studies

Objective To investigate the risk of pancreatitis associated with the use of incretin-based treatments in patients with type 2 diabetes mellitus.Design Systematic review and meta-analysis.Data sources Medline, Embase, the Cochrane...

Su1690 Low Risk of Post-ERCP Pancreatitis in Patients Undergoing Pancreatography to Evaluate Ductal Integrity

Su1690 Low Risk of Post-ERCP Pancreatitis in Patients Undergoing Pancreatography to Evaluate Ductal Integrity

Risk of pancreatitis in patients treated with incretin-based therapies.

Incretin-based therapies have been suggested to increase the risk of pancreatitis, but the results of the available studies are controversial. Because results from prospective trials are limited by low statistical power, and because retrospective studies are often subject to bias, a pooled analysis of phase III clinical trials and two endpoint trials was performed. Event numbers for acute pancreatitis and patient-years of exposure (PYOs) were obtained from representatives of the pharmaceutical companies, or by literature research. Data were pooled for glucagon-like peptide 1 (GLP-1) receptor agonists and dipeptidyl-peptidase 4 (DPP-4) inhibitors in comparison with their respective controls and expressed as exposure-adjusted incidence rates. A total of 38 cases of pancreatitis were reported in clinical trials with GLP-1 receptor agonists, comprising 17,775 PYOs. With the comparator treatment, nine events occurred in 5,863 PYOs. The pooled event rates were 2.1 and 1.5 per 1,000 PYOs, respectively, resulting in an OR of 1.39 (95% CI 0.67, 2.88). With DPP-4 inhibitors, 57 events were reported in 45,132 PYOs compared with 46 events in 38,883 PYOs with the comparator treatment. Pooled event rates were 1.3 and 1.2 per 1,000 PYOs, respectively, resulting in an OR of 1.07 (CI 0.72, 1.58). This analysis suggests a trend towards a slightly elevated risk of pancreatitis with GLP-1 receptor agonists. With DPP-4 inhibitors, no consistent trend was found. However, the incidence numbers of cases of pancreatitis were still very small, and the statistical power was limited. Future endpoint trials may help to provide a better estimate of the true risk of pancreatitis with incretin-based therapies.

Necrotizing Pancreatitis in a Patient with Gardnerʼs Variant Familial Adenomatous Polyposis

Purpose: To evaluate the etiology of necrotizing pancreatitis in a patient with Gardner's variant familial adenomatous polyposis (FAP). Review of patient records and literature review with OVID and PubMED. Patient was a 62-year-old male with Gardner's syndrome status-post colectomy and subsequent secondary proctectomy with ileostomy secondary to anastomatic tumor. Patient had high-grade dysplasia of papilla on prior EGD and was undergoing scheduled EGD as part of surveillance. After the endoscopy, the patient was discharged but within 10 minutes of discharge complained of severe pain and a stat CT showed no perforation but some stranding of pancreas. He was hemodynamically stable but labs were significant for WBC 21.04 (16.4 neutrophils, 0.13 bands), amylase 2,312, and lipase 4,477. Other labs were normal. Patient was admitted with pancreatitis and resuscitated aggressively. He was started on empiric antibiotic therapy and re-imaging revealed necrotizing pancreatitis. He continued to deteriorate with development of ARDS and sepsis. Patient was taken for ex-lap 29 days after the EGD with removal of 1.8 L of necrotic fluid. He succumbed to the complications and died 31 days after EGD. Review of literature revealed one other case of iatrogenic necrotizing pancreatitis in a patient with FAP.1 In a case similar to this, patient developed necrotizing pancreatitis after surveillance EGD. Even though the exact incidence of pancreatitis after biopsy is unknown, there appears to be an increased risk of pancreatitis in patients with FAP, even without endoscopic intervention. Classically, this has been attributed to development of obstructive ampullary adenomas (though the incidence of this is also rare). One retrospective review studied eight patients with Gardner's variant FAP who developed pancreatitis.2 Five of eight patients had obstructing focal or diffuse adenomatous disease involving the ampulla and the others had no identifiable cause. Finally, one case series suggests that patients with FAP are at increased risk of pancreatitis regardless of obstruction of ampulla.3 This series reviewed seven patients with FAP who experienced one or more episodes of pancreatitis. None of these patients had obstruction of the ampulla. Two of the seven patients developed pancreatitis after endoscopic treatment of ampullary adenoma, while the etiology of pancreatitis in the other five could not be determined. This suggests that pancreatitis may be a extra-colonic manifestation of FAP through an unknown mechanism. However, despite the risks of iatrogenic pancreatitis (with biopsy or with ampullary lesion) the risk of malignancy supports continued surveillance both ethically and clinically. This is the second case FAP in the literature to have fatal outcome after biopsy of papilla.

Needle Knife Sphincterotomy Does Not Increase the Risk of Pancreatitis in Patients With Difficult Biliary Cannulation

Biliary cannulation is unsuccessful during 5%-10% of endoscopic retrograde cholangiopancreatography (ERCP) procedures. Needle knife sphincterotomy (NKS) can improve success of cannulation but is often used as a last resort and is associated with post-ERCP pancreatitis (PEP). We evaluated the safety and efficacy of performing NKS during early stages of difficult cannulation and the relationship between difficult cannulation and the risk of PEP. We performed a prospective trial of consecutive patients with an intact papilla who were undergoing ERCP at tertiary referral center; 73 patients were defined as having difficult biliary cannulation according to predefined cannulation parameters. These patients were randomly assigned to groups that received either NKS or continued standard cannulation. Main outcome measures were PEP and successful biliary cannulation. Of 464 patients with an intact papilla undergoing ERCP, 73 met the criteria for difficult cannulation. Cannulation success in difficult cannulation cases was 86%, with a PEP rate of 19%. There was no difference in eventual cannulation success between the groups. However, 65% of the patients assigned to the standard cannulation group required crossover to NKS. There was no significant difference in development of PEP among patients in the early NKS group (20.5%) vs standard cannulation (17.6%). Pancreatic duct stents were inserted in 23 of the patients in the early NKS arm and in 15 in the standard cannulation arm. The number of cannulation attempts (more than 7) increased the risk of PEP (P < .01). On the basis of multivariate analysis, independent risk factors for PEP were failure of early cannulation and failure of biliary cannulation. Early application of NKS during difficult cannulation does not increase the risk of PEP. The risk of PEP increases greatly after 7-8 attempts at or failure of cannulation. Further studies are required to assess whether early implementation of NKS during difficult cannulation reduces the development of PEP. Australia and New Zealand Clinical Trials registry: ANZTRN 12,612,000,060,842.