Indomethacin may reduce the incidence and severity of acute pancreatitis after ERCP

OBJECTIVES: Acute pancreatitis is the most common complication of endoscopic retrograde cholangiopancreatography (ERCP). Many medications have been used to prevent this complication. We aimed to evaluate the efficacy of rectally administered indomethacin for the prevention of post-ERCP pancreatitis. METHODS: During 18 months, all eligible patients who underwent ERCP were enrolled in this study. In a double-blind randomized trial, patients received a suppository containing indomethacin, 100 mg, or an inert placebo immediately before ERCP. Serum amylase levels and clinically pertinent evaluations were measured in all patients after ERCP. RESULTS: A total of 490 patients entered the trial, of which half received indomethacin. Twenty-two patients developed pancreatitis; seven cases in the indomethacin group and 15 in the placebo group (P=0.06). Pancreatic duct injection (OR=3.0, 95% CI: 1.3-7.4), pancreatic duct cannulation more than once (OR=4.2, 95% CI: 1.7-10.0), and age less than 60 yr (OR=2.7, 95% CI: 1.0-7.1) were shown to be significant risk factors for developing post-ERCP pancreatitis. In patients who underwent pancreatography with or without cholangiography, the risk of pancreatitis was significantly lower in the indomethacin group compared with the control group (P=0.01, RRR=88%, ARR=0.16, NNT=6). Moderate to severe pancreatitis was significantly higher in the placebo group (P= 0.03). CONCLUSIONS: This trial shows that rectal indomethacin given immediately before ERCP can reduce the incidence and severity of post-ERCP pancreatitis.     

Prophylactic Corticosteroids Do Not Prevent Post-ERCP Pancreatitis: A Meta-Analysis of Randomized Controlled Trials

Background: Data regarding the use of corticosteroids for the prevention of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis are conflicting. The aim of this meta-analysis was to compare corticosteroids with placebo for prevention of post-ERCP pancreatitis. Methods: Multiple databases including MEDLINE, EMBASE, Cochrane controlled trials register, the Cochrane Library, Science Citation Index, Google Scholar and Google updated to June 2007 were searched to retrieve the relevant randomized controlled trials. Primary outcome measure was post-ERCP pancreatitis. Results: Six randomized controlled trials involving 2,448 patients were identified. The analysis showed that corticosteroids did not prevent post-ERCP pancreatitis (OR 1.13:95% CI [0.88,1.46]). Subsequent sensitivity and subgroup analyses according to different criteria all confirmed these results. Conclusions: Based on available evidence, prophylactic corticosteroids do not reduce the incidence of post-ERCP pancreatitis.     

Hope or hype--cytokine therapy in ERCP-induced pancreatitis.

In a single-center study from Belgium, Deviere et al. reported the use of the anti-inflammatory cytokine interleukin (IL) 10 as prophylaxis against ERCP-induced pancreatitis. One hundred forty-four patients undergoing ERCP were randomized to receive either a placebo (group 0) or a single i.v. injection of 4 μg/kg (group 1) or 20 μg/kg (group 2) of IL-10 in a double-blinded manner. Seven patients were excluded on an intention to treat or per protocol basis. The primary endpoint of the study was the effect of IL-10 on serum hydrolases (amylase and lipase) measured at 4, 24, and 48 h after ERCP. Hyperhydrolasemia was defined as an increase in amylase and/or lipase levels more than three times normal values. The secondary endpoint was to evaluate changes in plasma cytokines (IL-6, IL-8, and tumor necrosis [TNF] serum levels) and the incidence of clinical acute pancreatitis. This was defined as hyperhydrolasemia associated with new or worsened abdominal pain persisting for more than 4 h after ERCP. The three groups were comparable for number of patients (groups 0, 1, and 2 consisted of 45, 48, and 44 patients, respectively) as well as for age, sex, underlying disease, indication for treatment, and baseline plasma levels of C-reactive protein, cytokines, and hydrolases. The authors found no significant difference in serum C-reactive protein, cytokine, and hydrolase plasma levels between the groups after ERCP. Overall, 43 of the 137 study patients developed hyperhydrolasemia. These were distributed as follows: 18 (40%) in group 0, 14 (29%) in group 1, and 11 (25%) in group 2 (p = 0.297, nonsignificant). Overall, 19 patients (of the entire study population) developed acute clinical pancreatitis and were distributed as follows: 11 (24.4%) in group 0, five (10.4%) in group 1, and three (6.8%) in group 2 (p = 0.038). Two severe cases were observed in the placebo group.Logistic regression identified three independent risk factors for post-ERCP pancreatitis: IL-10 administration (odds ratio [OR] = 0.46, 95% CI = 0.22–0.96, p = 0.039), pancreatic sphincterotomy (OR = 5.04, 95% CI = 1.53–16.61, p = 0.008), and acinarization (OR = 8.19, 95% CI = 1.83–36.57, p = 0.006). The authors conclude that a single i.v. dose of IL-10 30 min before the procedure independently reduces the frequency of post-ERCP pancreatitis.     

Pharmacologic treatment can prevent pancreatic injury after ERCP: a meta-analysis

BACKGROUND: The identification of therapeutic agents that can prevent the pancreatic injury after endoscopic retrograde cholangiopancreatography (ERCP) is of considerable importance. METHODS: We performed a meta-analysis including 28 clinical trials on the use of somatostatin (12 studies), octreotide (10 studies), and gabexate mesilate (6 studies) after ERCP. Outcome measures evaluated were the incidence of acute pancreatitis, hyperamylasemia, and pancreatic pain. Three analyses were run separately: for all available studies, for randomized trials only, and for only those studies published as complete reports. RESULTS: When all available studies were analyzed, somatostatin and gabexate mesilate were significantly associated with improvements in all three outcomes. Odds ratios (OR) for gabexate mesilate were 0.27 (95% CI [0.13, 0. 57], p = 0.001) for acute pancreatitis, 0.66 (95% CI [0.48, -0.89], p = 0.007) for hyperamylasemia, and 0.33 (95% CI [0.18, 0.58], p = 0. 0005) for post-procedural pain. Somatostatin reduced acute pancreatitis (OR 0.38: 95% CI [0.22, 0.65], p < 0.001), pain (OR 0. 24: 95% CI [0.14, 0.42], p < 0.001), and hyperamylasemia (OR 0.65: 95% CI [0.48, 0.90], p = 0.008). Octreotide was associated only with a reduced risk of post-ERCP hyperamylasemia (OR 0.51: 95% CI [0.31, 0.83], p = 0.007) but had no effect on acute pancreatitis and pain. The statistical significance of data did not change after analyzing randomized trials only or studies published as complete reports. For each considered outcome, the publication bias assessment and the number of patients that need to be treated to prevent one adverse effect were, respectively, higher and lower for somatostatin than for gabexate mesilate. CONCLUSIONS: The pancreatic injury after ERCP can be prevented with the administration of either somatostatin or gabexate mesilate, but the former agent is more cost-effective. Additional studies comparing the efficacy of short-term infusion of somatostatin versus gabexate mesilate in patients at high risk for post-ERCP complications seem warranted.     

Post-ERCP pancreatitis

Pancreatitis remains the most common severe complication of endoscopic retrograde cholangiopancreatography (ERCP). Detailed information about the findings of previous studies concerning post-ERCP pancreatitis has not been utilized sufficiently. The purpose of the present article was to present guidelines for the diagnostic criteria of post-ERCP pancreatitis, and its incidence, risk factors, and prophylactic procedures that are supported by evidence. To achieve this purpose, a critical examination was made of the articles on post-ERCP pancreatitis, based on the data obtained by research studies published up to 2009. At present, there are no standardized diagnostic criteria for post-ERCP pancreatitis. It is appropriate that post-ERCP pancreatitis is defined as acute pancreatitis that has developed following ERCP, and its diagnosis and severity assessment should be made according to the diagnostic criteria and severity assessment of the Japanese Ministry of Health, Labour and Welfare. The incidence of acute pancreatitis associated with diagnostic and therapeutic ERCP is 0.4–1.5 and 1.6–5.4%, respectively. Endoscopic papillary balloon dilation is associated with a high risk of acute pancreatitis compared with endoscopic sphincterotomy. It was made clear that important risk factors include dysfunction of the Oddi sphincter, being of the female sex, past history of post-ERCP pancreatitis, and performance of pancreaticography. Temporary prophylactic placement of pancreatic stents in the high-risk group is useful for the prevention of post-ERCP pancreatitis [odds ratio (OR) 3.2, 95% confidence interval (CI) 1.6–6.4, number needed to treat (NNT) 10]. Use of nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with a reduction in the development of post-ERCP pancreatitis (OR 0.46, 95% CI 0.32–0.65). Single rectal administration of NSAIDs is useful for the prevention of post-ERCP pancreatitis [relative risk (RR) 0.36, 95% CI 0.22–0.60, NNT 15] and decreases the development of pancreatitis in both the low-risk group (RR 0.29, 95% CI 0.12–0.71) and the high-risk group (RR 0.40, 95% CI 0.23–0.72) of post-ERCP pancreatitis. As for somatostatin, a bolus injection may be most useful compared with short- or long-term infusion (OR 0.271, 95% CI 0.138–0.536, risk difference 8.2%, 95% CI 4.4–12.0%). The usefulness of gabexate mesilate was not apparent in any of the following conditions: acute pancreatitis (control 5.7 vs. 4.8% for gabexate mesilate), hyperamylasemia (40.6 vs. 36.9%), and abdominal pain (1.7 vs. 8.9%). Formulation of diagnostic criteria for post-ERCP pancreatitis is needed. Temporary prophylactic placement of pancreatic stents in the high-risk group offers the most promise as a means of preventing post-ERCP pancreatitis. As for pharmacological attempts, there are high expectations concerning NSAIDs because they are excellent in terms of cost-effectiveness, ease of use, and safety. There was no evidence of effective prophylaxis with the use of protease inhibitors, especially gabexate mesilate.     

Increased severity of complications after therapeutic ERCP in geriatric patients with chronic pancreatitis: An observational study

Studies of therapeutic endoscopic retrograde cholangiopancreatography (ERCP) in geriatric patients have mainly examined patients with biliary diseases, rather than chronic pancreatitis (CP). This study aimed to evaluate the safety and success rate of therapeutic ERCP in geriatric patients with CP.The medical records of patients with CP aged over 65 years (group A) were retrospectively collected in a tertiary hospital from January 2013 to December 2018. Sex-matched CP patients under 65 years (group B) were randomly selected into the control group (matching ratio = 1:2). The success rate and the complication rate of therapeutic ERCP in 2 groups were compared. The risk factors for post-ERCP pancreatitis were investigated by univariate and multivariate analyses.A total of 268 ERCPs were performed in 179 patients of group A and 612 ERCPs in 358 patients of group B. The success rate of ERCP in group A was similar to that of group B (92.16% vs 92.32%; P = .936). The overall incidence of post-ERCP complications was 7.09% (19/268) and 5.72% (35/612) in group A and B, respectively (P = .436). However, geriatric patients had a significantly increased occurrence of moderate to severe complications (2.61% vs 0.16%; P = .002). Female gender (odds ratio [OR] = 3.40; P = .046), pancreas divisum (OR = 7.15; P = .049), dorsal pancreatogram (OR = 7.40; P = .010), and lithotripsy (OR = 0.15; P = .016) were significantly associated with risk of post-ERCP pancreatitis in geriatric patients.Therapeutic ERCP is safe and feasible in elderly patients with CP. However, occurrence of moderate to severe complications after ERCP increased in geriatric patients.     

Does prophylactic pancreatic stent placement reduce the risk of post-ERCP acute pancreatitis? A meta-analysis of controlled trials

BACKGROUND: Impaired drainage of the pancreatic duct is one of the possible triggers for post-ERCP acute pancreatitis. The aim of this meta-analysis was to determine whether temporary stent placement across the main pancreatic-duct orifice lowers the frequency of post-ERCP acute pancreatitis in patients at high risk for this complication. METHODS: Two reviewers systematically identified prospective studies that (1) compared the risk of post-ERCP acute pancreatitis in patients with pancreatic stent placement vs. no stent placement and (2) included patients at high risk of developing this complication. Studies were assessed for methodologic quality and variations in execution and design. Frequency and severity of post-ERCP acute pancreatitis were the primary outcomes evaluated. RESULTS: Five trials involving 481 patients were selected. Of the 481, 55 (11.4%) patients developed pancreatitis after ERCP. Patients in the no stent group had 3-fold higher odds of developing pancreatitis compared with the stent group (15.5% vs. 5.8%; OR 3.2: 95% CI[1.6, 6.4]). Number needed to treat analysis showed that one in every 10 patients (95% CI[6,18]) could be expected to benefit from pancreatic-duct stent placement. CONCLUSIONS: Prophylactic temporary stent placement across the main pancreatic-duct orifice reduces the risk of post-ERCP acute pancreatitis in patients at risk for developing this complication.     

Complications of endoscopic sphincterotomy: can heparin prevent acute pancreatitis after ERCP?

BACKGROUND: An exploratory analysis of a prospective study of risk factors for acute pancreatitis after ERCP combined with endoscopic sphincterotomy showed that the frequency of acute pancreatitis was lower in patients who received heparin compared with patients not treated with heparin. The study was continued to further analyze the effect of heparin on the frequency of acute pancreatitis. METHODS: Potential risk factors for acute pancreatitis and outcomes were evaluated prospectively for all ERCP procedures with endoscopic sphincterotomy performed between September 1994 and December 1998. The results were analyzed by univariate and multivariate methods to determine risk factors for complications. Heparin was administered to 32.9% of the patients (heparin group [HEP group], n = 268) for various clinical reasons (low-molecular-weight heparin, n = 208, unfractionated heparin n = 60). A group of 547 patients who did not receive heparin served as control patients (CON group). RESULTS: Eight hundred fifteen patients underwent ERCP with endoscopic sphincterotomy; acute pancreatitis occurred in 6.4% (n = 52). The frequency of acute pancreatitis was significantly lower in the HEP group versus the CON group in the final multivariate model, which included significant risk factors for acute pancreatitis (HEP group: 3.4%, 9/268 vs. CON group: 7.9%, 43/547; p = 0.005). HEP did not increase the risk of hemorrhage (HEP group: 1.1%, 3/268, 2 severe, none fatal vs. CON group: 2.0%, 11/547, 3 severe, 2 fatal). HEP (p = 0.005; OR 0.3: 95% CI [0.16, 0.73]) and the number of risk factors present (p = 0.0001; OR 2.5: 95% CI [1.80, 3.50]) influenced the frequency of acute pancreatitis independently. CONCLUSIONS: Heparin was significantly associated with an extremely low frequency of post-ERCP pancreatitis without increasing the risk of hemorrhage after endoscopic sphincterotomy. Because this effect could not be attributed to other known or suspected confounders, our conclusion was that heparin administration before ERCP reduces the risk of pancreatitis.     

Placement of prophylactic pancreatic stents to prevent post-endoscopic retrograde cholangiopancreatography pancreatitis in high-risk patients: A meta-analysis

AIM:To assess the effectiveness of pancreatic stents for preventing pancreatitis in high-risk patients after endoscopic retrograde cholangiopancreatography(ERCP).METHODS:PubMed,Embase,Science Citation Index,and Cochrane Controlled Trials Register were searched to identify relevant trials published in English.Inclu-sion and exclusion criteria were used to screen for suitable studies.Two reviewers independently judged the study eligibility while screening the citations.The methodological quality of the included trials was assessed using the Jadad scoring system.All results were expressed as OR and 95%CI.Data were analyzed using Stata12.0 software.RESULTS:Ten eligible randomized controlled trials were selected,including 1176 patients.A fixed-effects model in meta-analysis supported that pancreatic duct stents significantly decreased the incidence of postERCP pancreatitis(PEP)in high-risk patients(OR=0.25;95%CI:0.17-0.38;P<0.001).Pancreatic stents also alleviated the severity of PEP(mild pancreatitis after ERCP:OR=0.33;95%CI:0.21-0.54;P<0.001;moderate pancreatitis after ERCP:OR=0.30;95%CI:0.13-0.67;P=0.004).The result of severe pancreatitis after ERCP was handled more rigorously(OR=0.24;95%CI:0.05-1.16;P=0.077).Serum amylase levels were not different between patients with pancreatic stents and control patients(OR=1.08;95%CI:0.82-1.41;P=0.586).CONCLUSION:Placement of prophylactic pancreatic stents may lower the incidence of post-ERCP pancreatitis in high-risk patients and alleviate the severity of this condition.     

Sphincter of Oddi manometry does not predispose to post-ERCP acute pancreatitis

BACKGROUND: Sphincter of Oddi manometry is helpful in selecting patients with sphincter of Oddi dysfunction who will respond to sphincterotomy. However, studies have shown that sphincter of Oddi manometry is associated with a high risk of post-procedure pancreatitis. The primary objective of this study was to evaluate the safety of sphincter of Oddi manometry in patients with sphincter of 2Oddi dysfunction. The secondary objective was to determine the risk factors for post-ERCP pancreatitis in patients with sphincter of Oddi dysfunction. METHODS: Data were collected retrospectively for 268 patients who had elective ERCP performed at 3 tertiary care medical centers between 1996 and 2000. Consecutive patients with suspected sphincter of Oddi dysfunction formed the case group; the control group consisted of patients with bile duct stone. The case group was further subclassified into group A, patients who underwent sphincter of Oddi manometry followed by immediate ERCP, and group B, patients who had ERCP without manometry. The rate of post-ERCP acute pancreatitis was compared between case and control groups. RESULTS: Twenty-seven percent of patients in the case group with suspected sphincter of Oddi dysfunction developed acute pancreatitis compared with 3.2% of patients in the control group with bile duct stone (p<0.001). There was no significant difference in the rate of acute pancreatitis in patients with sphincter of Oddi dysfunction who underwent sphincter of Oddi manometry and ERCP compared with patients with sphincter of Oddi dysfunction who had ERCP without sphincter of Oddi manometry (odds ratio 0.72: 95% CI[0.08, 9.2]). Multivariable logistic regression analysis showed that biliary sphincterotomy (p=0.006) and pancreatography (p=0.03) were independent predictors of acute pancreatitis. CONCLUSIONS: Patients with suspected sphincter of Oddi dysfunction are at higher risk of post-ERCP acute pancreatitis. Sphincter of Oddi manometry by itself does not appear to predispose to this complication.     

A Prospective Cohort Study of Smoking in Acute Pancreatitis

Background/Aims: Little is known about risk factors for acute pancreatitis other than gallstones and alcohol consumption. The aim of this study was to investigate if smoking or body mass index (BMI) are associated with acute pancreatitis and to determine relative risks (RR) for acute pancreatitis related to smoking, BMI, and alcohol consumption. Methods: From 1974 to 1992, selected birth-year cohorts of residents in Malmö, Sweden (born 1921–1949) were invited to a health-screening investigation including physical examination, blood sampling and a questionnaire. In total, 33,346 individuals participated. Cases of acute pancreatitis were identified from diagnosis registries (n = 179). Incidence rates were calculated in different risk factor categories. A Cox's analysis revealed RR. Results: Current versus never smoking at baseline was associated with acute pancreatitis (RR 2.14, 95% confidence interval (CI) 1.48–3.09) after adjustment for age, sex, BMI and alcohol consumption. This association was stronger in heavy smokers (20–30 cigarettes/day) (RR 3.19, 95% CI 2.03–5.00). Smoking was associated with a RR of 3.57 (95% CI 0.98–13.0) for acute pancreatitis in subjects who reported no alcohol consumption. An increased risk for acute pancreatitis was also found for high versus low risk, self-reported alcohol consumption (RR 2.55,95% CI 1.59–4.08) and for γ-GT levels in the highest versus the lowest quartile (RR 2.14,95%CI 1.32–3.49). There was alsoa weakcorrelation between BMI and acute pancreatitis. Conclusions: Smoking is associated with the incidence of acute pancreatitis in a dose-response manner.     

Risk of pancreatitis after endoscopic retrograde cholangiopancreatography and endoscopic biliary drainage

Background:

Pancreatitis is the most common and serious complication to occur after endoscopic retrograde cholangiopancreatography (ERCP). It is often associated with additional diagnostic modalities and/or treatment of obstructive jaundice. The aim of this study was to determine the risk of post-ERCP pancreatitis associated with pancreaticobiliary examination and endoscopic biliary drainage (EBD).

Methods:

A total of 740 consecutive ERCP procedures performed in 477 patients were analysed for the occurrence of pancreatitis. These included 470 EBD procedures and 167 procedures to further evaluate the pancreaticobiliary tract using brush cytology and/or biopsy, intraductal ultrasound and/or peroral cholangioscopy or peroral pancreatoscopy. The occurrence of post-ERCP pancreatitis was analysed retrospectively.

Results:

The overall incidence of post-ERCP pancreatitis was 3.9% (29 of 740 procedures). The risk factors for post-ERCP pancreatitis were: being female (6.5%; odds ratio [OR] 2.5, P= 0.02); first EBD procedure without endoscopic sphincterotomy (ES) (6.9%; OR 3.0, P= 0.003), and performing additional diagnostic procedures on the pancreatobiliary duct (9.6%; OR 4.6, P < 0.0001). Pancreatitis after subsequent draining procedures was rare (0.4%; OR for first-time drainage 16.6, P= 0.0003). Furthermore, pancreatitis was not recognized in 59 patients who underwent ES. Seven patients with post-EBD pancreatitis were treated with additional ES.

Conclusions:

Invasive diagnostic examinations of the pancreaticobiliary duct and first-time perampullary biliary drainage without ES were high-risk factors for post-ERCP pancreatitis. Endoscopic sphincterotomy may be of use to prevent post-EBD pancreatitis.     

Are drugs a risk factor of post-ERCP pancreatitis?

Background

Pancreatitis is the most severe complication of ERCP. The aim of this study was to assess whether the use of potentially pancreatotoxic drugs is a risk factor for post-ERCP pancreatitis.

Methods

Risk factors for post-ERCP pancreatitis and all drugs taken during the month before ERCP were recorded retrospectively in a database. Patients with other causes of acute pancreatitis or chronic pancreatitis were excluded from the analysis. Post-ERCP pancreatitis was defined as abdominal pain and/or vomiting associated with amylase/lipase plasma levels equal to or greater than twice the upper normal value.

Results

A total of 173 patients (95 men, 78 women; mean age, 68 [16] years) were included. Post-ERCP pancreatitis occurred in 31 patients (18%). Several risk factors were identified in a multivariate analysis: difficulty in cannulation (p<0.001), endoscopic sphincterotomy (p<0.005), and female gender (p = 0.02). Having taken potent pancreatotoxic drugs increased the occurrence of post-ERCP pancreatitis: odds ratio 3.7: 95% confidence intervals [1.1,12.4], p = 0.04.

Conclusions

Use of pancreatotoxic drugs before or during ERCP significantly increased the risk of post-ERCP pancreatitis. Thus, discontinuation of the use of such drugs before ERCP seems justified whenever possible.     

Nifedipine for prevention of post-ERCP pancreatitis: a prospective,double-blind randomized study

BACKGROUND: Pancreatitis is the most common complication of ERCP. Calcium channel inhibitors have been shown to prevent the development of experimental pancreatitis. The aim of this randomized, placebo-controlled trial was to determine whether the calcium channel blocker nifedipine prevents post-ERCP pancreatitis. METHODS: Patients referred for ERCP were enrolled. Those being treated with a calcium channel inhibitor and those with acute or chronic pancreatitis were excluded. Nifedipine or placebo was administered orally less than 3 hours before and within 6 hours after ERCP. The main outcome measure was the number of cases of post-ERCP pancreatitis; a secondary outcome was the rate of post-ERCP pain (without pancreatitis) that persisted for 12 or more hours. RESULTS: One hundred fifty-five patients (70 women, 85 men; mean [SD] age 65.8 [18.2] years; range, 23-97 years) were enrolled and randomized to receive nifedipine (76 patients) or placebo (79 patients). The two groups were comparable. Procedures performed were retrograde diagnostic cholangiopancreatography alone (n = 33), biliary sphincterotomy (n = 31), stone extraction (n = 39), stent placement (n = 37), sphincteroplasty (n = 5), and other (n = 3). ERCP was unsuccessful in 5 patients. A single case of severe pancreatitis was observed (placebo group). The rate of post-ERCP pancreatitis was not different between groups (nifedipine, 10 patients, 13.2%; placebo, 14 patients, 17.7%; p = 0.4). The frequency of post-ERCP pain was not different between the groups. The only independent predictor of post-ERCP pancreatitis was difficult cannulation in both groups (OR = 3.78: 95% CI [1.25, 11.45]). CONCLUSION: This study failed to demonstrate a significant effect of nifedipine in the prevention of post-ERCP pancreatitis. A multicenter trial with greater statistical power would be needed to demonstrate a benefit for this drug.     

Nasobiliary drainage can reduce the incidence of post-ERCP pancreatitis after papillary large balloon dilation plus endoscopic biliary sphincterotomy: a randomized controlled trial

Background and aims: Post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis can be reduced following endoscopic papillary balloon dilation with the placement of an endoscopic nasobiliary drainage (ENBD) catheter. The aim of this study was to determine whether the placement of an ENBD reduces the risk of post-ERCP pancreatitis following endoscopic papillary large balloon dilation together with endoscopic biliary sphincterotomy.

Methods: A total of 160 patients with bile duct stones were randomly assigned (1:1) to an ENBD group or no-ENBD group. The primary outcome of this study was the incidence of post-ERCP pancreatitis. The secondary outcome was the incidence of post-ERCP hyperamylasemia.

Results: In total, 160 patients were randomized, and 155 were found to be eligible for the analysis. The two groups were similar regarding clinical and demographic factors as well as patient- and procedure-related risk factors for post-ERCP pancreatitis. Post-ERCP pancreatitis developed in 9 patients, that is, 8/77 (10.4%) of the control group and 1/78 (1.28%) of the ENBD group (p?=?.018; per protocol analysis). Intention to treat analysis also revealed that ENBD reduced the rate of post-ERCP pancreatitis (8/80 (10%) in the control group vs. 1/80 (1.25%) the ENBD group (p?=?.034)). Multivariate regression analysis identified not undergoing ENBD as an independent risk factor for post-ERCP pancreatitis (ENBD compared with no-ENBD: OR 0.087, 95% CI 0.011–0.734; p?=?.025).

Conclusion: This study demonstrated that placement of an ENBD was effective and safe for the prevention of post-ERCP pancreatitis in patients undergoing endoscopic papillary large balloon dilation together with endoscopic biliary sphincterotomy.     

Android fat distribution as predictor of severity in acute pancreatitis

Background/Aims: Obesity is considered an independent risk factor for the development of severe acute pancreatitis (AP). The purpose of this study was to define the type of fat distribution related to severity in AP. Methods: Eighty-eight patients with first-time AP underwent measurements of weight, height, waist and hip circumferences, and skinfold thickness on admission. Severity was defined according to Atlanta criteria. Results: AP was severe in 27 (31%) patients. There was a tendency for obese patients to develop severe AP (p = 0.11). Android fat distribution by waist-to-hip ratio and waist circumference above ideal cut-off value (ROC curves analysis) were significantly associated with severity (RR: 5.54, 95% CI 1.39-22.04, and RR: 4.36, 95% CI 1.40–13.57, respectively). After adjusting for potential confounders, both measurements remained predictors of severity in the logistic regression model (OR: 9.23, 95% CI 1.6751.07, and OR: 13.41, 95% CI 2.43–73.97, respectively). Body fat percentage was not associated with incidence of severity. Conclusions: Patients with android fat distribution and higher waist circumference are at greater risk for developing severe AP. Findings could be related to the amount of abdominal fat but also to an overactive systemic inflammatory response that tend to be upregu-lated in android fat distribution.     

Risk factors for post-endoscopic retrograde cholangiopancreatography (ERCP) abdominal pain in patients without post-ERCP pancreatitis

BackgroundAbdominal pain is often observed after endoscopic retrograde cholangiopancreatography (ERCP). Few studies have focused on the risk factors of post-ERCP abdominal pain without post-ERCP pancreatitis (PEP). This study aimed to identify risk factors of post-ERCP abdominal pain without PEP and investigate characteristics of the abdominal pain in non-PEP patients.MethodsData from patients who underwent ERCP from August 2019 to January 2020 were retrospectively collected. Characteristics of the abdominal pain after ERCP were recorded and compared between PEP and non-PEP patients. Multivariate analysis was conducted to identify risk factors of non-PEP abdominal pain.ResultsA total of 1295 ERCP procedures were investigated in this study, among which 100 (7.72%) patients presented post-ERCP abdominal pain without PEP and 63 (4.86%) patients with PEP. Multivariate analysis found 9 risk factors of non-PEP abdominal pain: age ≤ 65 years [odds ratio (OR): 1.971], primary ERCP (OR: 2.442), dilated extrahepatic bile duct (OR: 1.803), no papilla opening (OR: 2.095), pancreatic guidewire passages (OR: 2.258), white blood cells (WBC) ≤ 6.0 × 10⁹/L (OR: 1.689), platelet (PLT) ≤ 250 × 10⁹/L (OR: 2.505), serum γ-glutamyl transferase (γ ? GT) ≤ 35 U/L (OR: 2.190), and albumin ≥ 40 g/L (OR: 1.762). The PEP group had later pain onset, higher pain frequency and longer hospital stay than those of the non-PEP pain group (P < 0.05). There were no significant differences in the pain duration, visual analogue scale score and mortality between the PEP group and non-PEP pain group (P > 0.05).ConclusionsThis study indicated that age ≤ 65 years, primary ERCP, dilated extrahepatic bile duct, no papilla opening, pancreatic guidewire passages, lower WBC, lower PLT, normal γ ? GT and elevated albumin were independent risk factors for post-ERCP abdominal pain without PEP. The pain occurred earlier in non-PEP patients than in PEP patients.     

Monocyte Chemoattractant Protein 1, Active Carboxypeptidase B and CAPAP at Hospital Admission Are Predictive Markers for Severe Acute Pancreatitis

Background: CAPAP, the activation peptide of procarboxypeptidase B, is a predictor of severe acute pancreatitis (AP). Active carboxypeptidase (aCAP) may be a better predictor, as its turnover is slower. Monocyte chemotactic protein-1 (MCP-1) is an early inflammatory marker and increases before complications in severe AP. We conducted a cohort study to evaluate these markers as predictors for severe AP. Method: 140 patients with AP were included, retrospectively grouped as severe or mild by the Atlanta classification. CAPAP, MCP-1 and aCAP were analyzed in admission samples. Receiver operating characteristic curves determined high vs. low levels. Results: The levels of all markers were significantly higher in patients with severe disease. High levels of serum MCP-1 was associated with a high risk of developing severe AP (OR 40.8; 95% CI 8.5–195). High ORs were also seen for urine MCP-1 (OR 7.3; 95% CI 2.2-24.3), serum CAPAP (OR 5.4; 95% CI 1.6–17.7), urine CAPAP (OR 4.8; 95% CI 1.6–14.2), and serum aCAP (OR 3.7; 95% CI 1.2–11.3). Conclusion: Serum MCP-1 at admission was strongly associated with development of severe AP. MCP-1 in urine, CAPAP in serum and urine and aCAP may also be useful for predicting Severe AP.     

Low-molecular-weight heparin does not prevent acute post-ERCP pancreatitis

BACKGROUND: Studies suggest that heparin has anti-inflammatory effects that could prevent acute post-ERCP pancreatitis. The aim of this investigator-initiated, prospective, randomized, double-blind, multicenter study was to determine whether low-molecular-weight heparin can prevent acute post-ERCP pancreatitis. METHODS: Patients at increased risk for acute post-ERCP pancreatitis based on assessment of known risk factors were randomized to receive low-molecular-weight heparin (Certoparin 3000 IU subcutaneously) or placebo (saline solution 0.3 mL subcutaneously) the day before ERCP. The drug was given 2 hours before and 22 hours after ERCP. Documentation and follow-up included patient history, risk factors for acute post-ERCP pancreatitis, procedure-related data, assessment of pain (visual analogue scale, need for pain medication), laboratory findings before and after ERCP (0, 4, and 24 hours), as well as post-ERCP complications. The two-sided Fisher exact test was used for statistical comparison, and a p value < or =0.05 was considered significant. RESULTS: A total of 458 patients were enrolled in the study. Data from 10 patients could not be evaluated, leaving 221 patients in the low-molecular-weight heparin group and 227 in the placebo group (total 448 patients; 135 men, 313 women; mean age 58 [15] years). Low-molecular-weight heparin and placebo groups were comparable with regard to risk factors for acute post-ERCP pancreatitis (gender distribution, age <65 years, history of pancreatitis, pancreas divisum, disorders of sphincter of Oddi) and procedure-related data (difficult cannulation, diagnostic or therapeutic ERCP, needle-knife papillotomy, endoscopic sphincterotomy, biliary or pancreatic procedure, pancreatic contrast injection, success and final diagnosis of ERCP). Acute post-ERCP pancreatitis occurred in 8.5% (38/448), with one death resulting from severe pancreatitis. Low-molecular-weight heparin offered no benefit compared with placebo based on the frequency of acute post-ERCP pancreatitis (low-molecular-weight heparin, 18/221 vs. placebo, 20/227; p=0.87) and the severity of acute post-ERCP pancreatitis (low-molecular-weight heparin, 14 mild, 3 moderate, one severe; placebo, 18 mild, two moderate, 0 severe). The 24-hour serum amylase values and 24-hour pain scores did not differ significantly between the low-molecular-weight heparin group and the placebo group. Bleeding complications occurred in two patients, both in the low-molecular-weight heparin group (one mild, one moderate). CONCLUSIONS: Prophylactic subcutaneous administration of low-molecular-weight heparin does not prevent acute post-ERCP pancreatitis.     

Use of Angiotensin II Receptor Blockers and the Risk of Acute Pancreatitis: A Nested Case-Control Study

Background: There is no specific treatment aqainst acute pancreatitis (AP). A protective effect by angiotensin II receptor blockers (ARB) on AP has been suggested experimentally, but clinical evidence is scarce. Methods: We conducted a population-based case-control study using The Health Improvement Network in the United Kingdom, comprising about 167,000 hypertensive patients in the study period 1996–2005. In multivariate logistic regression analysis, odds ratios were calculated with 95% confidence intervals (CI). Adjustments included sex, age, calendar year, body mass index, tobacco smoking, alcohol, general practitioner visits per year, and various antihypertensive medications with regard to exposure to ARB, and risk of AP. Results: Among 633,281 person-years at risk, 265 new cases of AP were identified. Current users of ARB had a 37% statistically non-significant reduced risk of developing AP as compared to non-users (OR 0.63, 95% CI Q.38–1.02). No clear association was found between use of other antihypertensive drugs and risk of AP. Conclusion: Our study adds some support to previous experimental findings. Use of ARB might be associated with a reduced risk of AP. More research is needed to elucidate the potential role of ARB in the development of AP in the clinical setting.