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CONTEXT: Acute pancreatitis is the most common complication in ERCP, and some risk factors were associated with the development of hyperamylasemia and post-ERCP pancreatitis. OBJECTIVES: identifying new factors associated with the development of hyperamylasemia or post-ERCP pancreatitis in patients attended at our center. MATERIAL AND METHODS: A (retrospective) cohort study was carried out in 170 patients on which a diagnostic-therapeutic ERCP was done due to biliopancreatic disease. 67 patients developed hyperamylasemia (39.4%) and 6 post-ERCP pancreatitis (3.5%). The following diagnostic criteria were applied: Hyperamylasemia: increase in the serum amylase level above the normal value (90 I/U). Acute post-ERCP pancreatitis: clinical: continuous abdominal pain for over 24 hours and biochemical: elevation of amylase3 times above normal value (90 U/I). RESULTS: The number of cannulations more than 4 (19 patients), (p=0.006; RR= 3.00) was associated significantly with the development of hyperamylasemia and the placing of biliary stent (14 patients), (p=0.00; RR= 0.39) was a protective factor. The factors associated with the development of post-ERCP pancreatitis were related with the patient (peridiverticular location of the papilla (p=0.00; RR= 2.00) and the sphincter of Oddi dysfunction (p=0.000; RR=1.20). CONCLUSION: Technical factors were associated with the development of hyperamylasemia, however, the factors associated with the development of post-ERCP pancreatitis in our universe of study were related mainly with the patient.

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Contexto: La pancreatitis aguda es la complicación más frecuente de la PCRE y algunos factores de riesgo son asociados con el desarrollo de hiperamilasemia y pancreatitis post PCRE. Objetivos: Identificar factores nuevos asociados con hiperamilasemia y pancreatitis post PCRE en pacientes que acudieron a nuestro centro. Material y métodos: Un estudio retrospectivo de cohorte se llevó a cabo en 170 pacientes en quienes se realizó una CPRE diagnóstico-terapéutica por enfermedad biliopancreática. 67 pacientes desarrollaron hiperamilasemia (39,4%) y 6 pancreatitis post PCRE (3,5%). Se aplicaron los siguientes criterios diagnósticos: Hiperamilasemia: elevación de la amilasa sérica por encima del valor normal (90IU).Pancreatitis aguda post PCRE: dolor abdominal continuo por más de 24 horas y elevación de la amilasa tres veces por encima del valor normal. Resultados: El número de canulaciones, más de 4 (19 pacientes), (p=0,006; RR= 3,00) se asoció significativamente con el desarrollo de la hiperamilasemia y la puesta de stents biliares (14 pacientes) se asoció como un factor protector (p=0,00; RR= 0,39). Los factores asociados con el desarrollo de la pancreatitis post PCRE se relacionaron con el paciente (localización peridiverticular de la papila (p=0,00; RR= 2,00) y disfunción del Esfinter de Oddi (p=0,000; RR=1,20). Conclusiones: Factores técnicos fueron asociados con el desarrollo de la hiperamilasemia, sin embargo, los relacionados con el desarrollo de la pancreatitis post PCRE fueron mayoritariamente relacionados al paciente.

Context: Acute pancreatitis is the most common complication in ERCP, and some risk factors were associated with the development of hyperamylasemia and post-ERCP pancreatitis. Objectives: identifying new factors associated with the development of hyperamylasemia or post-ERCP pancreatitis in patients attended at our center. Material and methods: A (retrospective) cohort study was carried out in 170 patients on which a diagnostic-therapeutic ERCP was done due to biliopancreatic disease. 67 patients developed hyperamylasemia (39.4%) and 6 post-ERCP pancreatitis (3.5%). The following diagnostic criteria were applied: Hyperamylasemia: increase in the serum amylase level above the normal value (90I/U). Acute post-ERCP pancreatitis: clinical: continuous abdominal pain for over 24 hours and biochemical: elevation of amylase 3 times above normal value (90U/I). Results: The number of cannulations more than 4 (19 patients), (p=0.006; RR= 3.00) was associated significantly with the development of hyperamylasemia and the placing of biliary stent (14 patients), (p=0.00; RR= 0.39) was a protective factor. The factors associated with the development of post-ERCP pancreatitis were related with the patient (peridiverticular location of the papilla (p=0.00; RR= 2.00) and the sphincter of Oddi dysfunction (p=0.000; RR=1.20). Conclusion: Technical factors were associated with the development of hyperamylasemia, however, the factors associated with the development of post-ERCP pancreatitis in our universe of study were related mainly with the patient.

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BACKGROUND AND STUDY AIMS: There have been reports, mainly retrospective, of pancreatitis and hyperamylasemia after anterograde double-balloon enteroscopy (DBE). Our aim was to report the incidence of pancreatitis and hyperamylasemia after DBE and investigate possible risk factors associated with its occurrence. PATIENTS AND METHODS: In this single-center prospective cohort study, serum samples were taken for amylase and lipase before and 3 hours after anterograde DBE in consecutive patients. Multiple variables were recorded, including total procedure time, insertion depth, and number of passes. Patients were evaluated to 24 hours later for signs of pancreatitis. The main outcome measures were the occurrence of hyperamylasemia and pancreatitis. RESULTS: 92 patients were included in the analysis (58 women, 34 men; mean age 54 years, range 18-89). The mean total procedure time was 62 minutes (range 30-120). The mean post-procedure amylase and lipase levels were significantly higher in comparison with the baseline levels (165 U/L vs. 69 U/L and 144 U/L vs. 28 U/L respectively, P<.05); 36 patients (39%) showed hyperamylasemia after the procedure and three patients developed acute mild pancreatitis. Hyperamylasemia was associated more frequently with procedure duration greater than 60 minutes ( P<.001) and insertion depth greater than 25 cm ( P<.013). CONCLUSIONS: The incidence of hyperamylasemia after anterograde DBE is common and particularly associated with longer procedure time and insertion depth. The cumulative incidence of pancreatitis was 3%. We recommend the avoidance of both unnecessarily lengthy procedures and deep insertion distances in patients who undergo anterograde DBE.

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AIM: To assess the efficacy of allopurinol to prevent hyperamylasemia and pancreatitis after endoscopic retrograde cholangiopancreatography (PEP). METHODS: One hundred and seventy patients were enrolled and randomized to two groups: a study group (n = 85) who received 300 mg of oral allopurinol at 15 h and 3 h before endoscopic retrograde cholangiopancreatography (ERCP) and a control group (n = 85) receiving an oral placebo at the same times. Main Outcome Measurements included serum amylase levels and the number severity of the episodes of pancreatitis. Serum amylase levels were classified as normal (< 150 IU/L) or hyperamylasemia (> 151 IU/L). Episodes of PEP were classified following Ranson's criteria and CT severity index. RESULTS: Gender distribution was similar between groups. Mean age was 53.5 +/- 18.9 years for study group and 52.8 +/- 19.8 years for controls. Also, the distribution of benign pathology was similar between groups. Hyperamylasemia was more common in the control group (P = 0.003). Mild PEP developed in two patients from the study group (2.3%) and eight (9.4%) from control group (P = 0.04), seven episodes were observed in high-risk patients of the control group (25%) and one in the allopurinol group (3.3%, P = 0.02). Risk factors for PEP were precut sphincterotomy (P = 0.02), pancreatic duct manipulation (P = 0.002) and multiple procedures (P = 0.000). There were no deaths or side effects. CONCLUSION: Oral allopurinol before ERCP decreased the incidences of hyperamylasemia and pancreatitis in patients submitted to high-risk procedures.

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BACKGROUND: Acute pancreatitis (AP) represents the main complication after endoscopic retrograde cholangiopancreatopgraphy (ERCP) and appears in 1% to 10% of the cases. The incidence increases in patients with opacification and instrumentation of pancreatic duct and it varies according to the indications of the procedure and the intervention performed. Risk factors for this complication include history of pancreatitis, difficult canulation, pancreatic acinar opacity, Oddi sphincter hypertension and sphincterotomy. OBJECTIVE: Evaluate the efficacy of rectal indometacine to reduce the incidence of hyperamylasemia and AP post-ERCP. METHODS AND MATERIALS: Control clinical trial simple blind perfomed between June and December of 2004. One hundred seventeen patients were included in the study. They were randomly assigned in two groups: 1) study group (n = 61, 52%), 100 mg of rectal indomethacin was administered 2 hours previous to the procedure and, 2) control group (n = 56, 47.8%) received placebo (glycerine suppository). Hyperamylasemia was diagnosed with levels > 151 U/L and AP with levels > 600 U/L and characteristically abdominal pain. RESULTS: Gender distribution was of 79 (67.5%) women and 38 (32.5%) men. Mean age was of 54.2 +/- 18.8 years for the study group and 50.1 +/- 18.1 years for the control group. After ERCP, 12 patients (10.2%) of the study group and 19 (16.2%) of control group presented hyperamylasemia (p = 0.09). AP was present in 3 patients (2.5%) in the study group and 8 patients (6.8%) of the control group (p = NS). There was no mortality in our study. CONCLUSION: The use of 100 mg of rectal indomethacine previous to ERCP decreases the risk of hyperamylasemia and AP. However, these differences did not reach statistical significance, probably because a greater sample of patients was needed.

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The objective of the present study was to determine the efficacy of prophylactic administration of gabexate for the prevention of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis, hyperamylasemia and pancreatic pain. Patients scheduled for ERCP were randomized into two groups in a double-blind manner: the patients in the gabexate group were treated with continuous intravenous infusion of 300 mg gabexate dissolved in 500 mL Ringer's solution at 111 mL/h, starting 30 min before the endoscopic maneuvers and continuing up to 4 h after them; placebo group patients were treated only with Ringer's solution also starting 30 min before the endoscopic maneuvers and continuing up to 4 h. Data for 193 patients were analyzed. The incidence of post-ERCP pancreatitis was 3 patients (3.1%) in the gabexate group and 10 (10.5%) in the placebo group (P = 0.040). The incidence of hyperamylasemia was 33 patients (33.7%) in the gabexate group and 42 (43.7%) in the placebo group (P = 0.133). The incidence of pancreatic pain was 15 patients (15.3%) in the gabexate group and 28 (29.5%) in the placebo group (P = 0.018). The results suggest that a 4.5-h infusion of gabexate (for a total of 300 mg) could prevent post-ERCP pancreatitis and pancreatic pain.

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The objective of the present study was to determine the efficacy of prophylactic administration of gabexate for the prevention of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis, hyperamylasemia and pancreatic pain. Patients scheduled for ERCP were randomized into two groups in a double-blind manner: the patients in the gabexate group were treated with continuous intravenous infusion of 300 mg gabexate dissolved in 500 mL Ringer's solution at 111 mL/h, starting 30 min before the endoscopic maneuvers and continuing up to 4 h after them; placebo group patients were treated only with Ringer's solution also starting 30 min before the endoscopic maneuvers and continuing up to 4 h. Data for 193 patients were analyzed. The incidence of post-ERCP pancreatitis was 3 patients (3.1 percent) in the gabexate group and 10 (10.5 percent) in the placebo group (P = 0.040). The incidence of hyperamylasemia was 33 patients (33.7 percent) in the gabexate group and 42 (43.7 percent) in the placebo group (P = 0.133). The incidence of pancreatic pain was 15 patients (15.3 percent) in the gabexate group and 28 (29.5 percent) in the placebo group (P = 0.018). The results suggest that a 4.5-h infusion of gabexate (for a total of 300 mg) could prevent post-ERCP pancreatitis and pancreatic pain.

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Hyperamylasemia has been reported in more than 65% of patients with severe leptospirosis, and the true diagnosis of acute pancreatitis is complicated by the fact that renal failure can increase serum amylase levels. Based on these data we retrospectively analyzed the clinical and histopathological features of pancreas involvement in 13 cases of fatal human leptospirosis. The most common signs and symptoms presented at admission were fever, chills, vomiting, myalgia, dehydratation, abdominal pain and diarrhea. Trombocytopenia was evident in 11 patients. Mild increased of AST and ALT levels was seen in 9 patients. Hyperamylasemia was recorded in every patient in whom it was measured, with values above 180 IU/L (3 cases). All patients presented acute renal failure and five have been submitted to dialytic treatment. The main cause of death was acute respiratory failure due to pulmonary hemorrhage. Pancreas fragments were collected for histological study and fat necrosis was the criterion used to classify acute pancreatitis. Histological pancreatic findings were edema, mild inflammatory infiltrate of lymphocytes, hemorrhage, congestion, fat necrosis and calcification. All the patients infected with severe form of leptospirosis who develop abdominal pain should raise the suspect of pancreatic involvement.

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