Clinical Trial Details
— Status: Completed
Administrative data
| NCT number |
NCT01717599 |
| Other study ID # |
4-2012-0466 |
| Secondary ID |
|
| Status |
Completed |
| Phase |
N/A
|
| First received |
|
| Last updated |
|
| Start date |
August 29, 2012 |
| Est. completion date |
August 28, 2013 |
Study information
| Verified date |
May 2021 |
| Source |
Yonsei University |
| Contact |
n/a |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Interventional
|
Clinical Trial Summary
Pancreatitis is one of the major complications of ERCP. It has been shown that NSAIDs are
potent inhibitors of phospholipase A2, activity which is increased in pancreatitis. The only
one study with IM diclofenac showed reduction of post-ERCP pancreatitis without SOD
(sphincter of Oddi dysfunction) by subgroup analysis in small study population. Therefore the
investigators must need large scaled randomized control study including of SOD.
Description:
The study described in this report will be approved by the ethics committee of Yonsei
University School of Medicine, Seoul, Korea. Between July 2012 and February 2013, 380
patients fulfilled the inclusion criteria, 380 of whom were included in the final analysis.
Consecutive patients were recruited for the study who presented to the Yonsei University
Medical Center with variable symptom or cause for ERCP older than 20years. Patients were
excluded from study participation if they had a contraindication for diclofenac, including
patients with recently diagnosed peptic ulcer disease or active/recent gastrointestinal
hemorrhage within 4 weeks, renal failure(Cr > 1.4), those who had taken an NSAID during the
preceding week(ASA 325 mg daily or less acceptable), those who developed acute pancreatitis
during the 2 weeks before ERCP, those with a history of chronic calcific pancreatitis or
allergy to aspirin or NSAID, and those who did not agree to participate in the study.
Additionally, if state of patients was intrauterine pregnancy or breast feeding mother, they
were excluded. Entry to the study was restricted to patients advised to have endoscopic
retrograde cholangiography with or without pancreatography for extrahepatic cholestasis
and/or impaired liver function tests.
The patients received 90 mg IM diclofenac available in our hospital immediately after ERCP at
recovery room. Patients were observed in the recovery room for at least 90 minutes after the
procedure. Patients in whom abdominal pain developed during this observation period were
admitted to the hospital (or for current inpatients, kept in the hospital). Decisions
regarding evaluation of complications after the procedure and in-hospital care were left to
the discretion of the endoscopist and clinical-service staff members, who were unaware of
study-group assignments.
Patients who were discharged after an uneventful ERCP were contacted by telephone within 5
days to capture delayed occurrence of the primary end point. Patient demographics, risk
factors, ERCP procedural elements, and follow-up data were recorded on standardized
data-collection forms by an investigator or coordinator who was unaware of study-group
assignments. The intramuscular route was selected on the basis of available small sized data
suggesting that intramuscular NSAIDs are effective in preventing post-ERCP pancreatitis,
perhaps owing to more rapid and complete bioavailability than with oral administration. (1)
At the end of each procedure, the researchers recorded the details of the maneuvers
performed, including the total time of the procedure, the number of attempts at cannulation,
the number of pancreatic duct cannulations, the final diagnosis, and whether a
sphincterotomy, a needle-knife papillotomy, or stent placement were performed. We did not use
pancreatic duct stenting for prevention of pancreatitis. Patients were sedated with IV
midazolam and IV continuous infusion of propofol under monitoring by anesthesiologist during
whole time of procedure. Xylocaine spray was used as a local anesthetic. Serum amylase was
determined 4 hours after ERCP.
If the 4-hours serum amylase level was < 3 times the upper normal limit and there was no
clinical evidence of acute pancreatitis at that time, patients were allowed free oral fluids
and a diet. If the 4- hours serum amylase level was > 3 times the upper normal limit and the
patient exhibited pain or nausea and vomiting, then the patient was kept fasting and IV
crystalloid fluids with opiate analgesics were prescribed. The following 24 hours blood tests
were repeated for serum amylase and the patients were interviewed and examined for clinical
evidence of acute pancreatitis.
Acute pancreatitis was defined as serum amylase at least three times the upper limit of
normal range 24hours after the procedure associated with new or increased upper abdomen or
epigastric pain, back pain, and epigastric tenderness and hospitalization or prolongation of
existing hospitalization for at least 2 nights. Patients with persistent signs and symptoms
of pancreatitis after 48 hours underwent contrast-enhanced computed tomography.
Pancreatitis was graded as mild, moderate, or severe. The severity was determined according
to consensus guidelines, with mild post-ERCP pancreatitis resulting in a hospitalization of
≤3 days, moderate post-ERCP pancreatitis resulting in a hospitalization of 4-10 days, and
severe post-ERCP pancreatitis resulting in a hospitalization of > 10 days, or leading to the
development of pancreatic necrosis or pseudocyst, or requiring percutaneous or surgical
intervention.
Sphincter of Oddi dysfunction (SOD) was defined according following Classification. Biliary
type I SOD was defined as biliary-type abdominal pain, liver enzyme elevation, and common
bile duct dilation > 9mm. Biliary type II SOD was defined as biliary-type abdominal pain and
either abnormal liver enzymes or a dilated bile duct. Biliary type III SOD was defined as
biliary-type pain without any other objective findings. Pancreatic type I SOD was defined as
pancreatic-type pain and a dilated pancreatic duct and elevated pancreatic enzymes, or
recurrent acute pancreatitis. Type II pancreatic SOD was defined as pancreatic-type pain and
a dilated pancreatic duct or elevated pancreatic enzymes. Type III pancreatic SOD was defined
as pancreatic-type pain alone.
The instruments used were cannula, sphincterotome, guidewire, and stone basket (Olympus,
Japan).
Adverse events were defined as reported previously. Any cases of post-ERCP pancreatitis,
other complications of the procedure, and adverse events that were potentially attributable
to the study drug were reported to the local institutional review board and the data and
safety monitoring board. These reportable adverse events were gastrointestinal bleeding,
perforation, infection, renal failure, allergic reaction, myocardial infarction,
cerebrovascular accident, and death.
