Endoscopy 2011; 43(3): 230-232
DOI: 10.1055/s-0030-1256219
Editorial

© Georg Thieme Verlag KG Stuttgart · New York

After all these years of SOD and endotherapy – how far have we come? The role of endoscopic treatment for acute recurrent pancreatitis (ARP) with sphincter of Oddi dysfunction (SOD)

D.  Tan1 , S.  Sherman1
  • 1Department of Gastroenterology and Hepatology, Indiana University Medical Center, Indianapolis, Indiana, USA
Further Information

Publication History

Publication Date:
01 March 2011 (online)

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The etiology of acute pancreatitis can be determined in the majority of patients. Alcohol and gallstones account for 60 % – 90 % of cases. Other causes include hypertriglyceridemia, hypercalcemia, drug reactions, trauma, genetics, neoplasia, surgery, endoscopic retrograde cholangiopancreatography (ERCP), etc. However, despite a careful history, physical examination, laboratory testing, and radiological evaluation, 10 % – 30 % of cases will have no obvious etiology and will be labeled as idiopathic acute pancreatitis (IAP) [1] [2] [3]. Patients with recurrent episodes of IAP are classified as having idiopathic acute recurrent pancreatitis (IARP). A structural cause for IARP will be found in the majority of patients who are further investigated with endoscopic ultrasound (EUS), ERCP with sphincter of Oddi manometry (SOM), bile crystal analysis (for those with the gallbladder in situ), and magnetic resonance imaging/cholangiopancreatography. The literature shows that sphincter of Oddi dysfunction (SOD) is the most frequent cause of IARP. Using ERCP with SOM as the gold standard for diagnosis, SOD has been manometrically documented in 15 % – 72 % of such patients [4] [5] [6] [7] [8] [9] [10] [11].

The pathogenesis of SOD relates to either an anatomic obstruction at the sphincter of Oddi caused by fibrosis and/or inflammation, or to a functional (”dyskinetic”) obstruction caused by sphincter muscle spasm. This results in elevation of pancreatic sphincter pressure and has been shown to correlate with increased intrapancreatic ductal pressure, presumably playing a role in the pathogenesis of pancreatitis [12]. However, elevated pancreatic basal sphincter of Oddi pressure and concomitant elevated pancreatic duct pressure are found in patients with pain only and no prior evidence of pancreatitis, arguing that it is not the sole determinant of pancreatitis.

Previous studies in which biliary (BES), pancreatic (PES) or dual biliary and pancreatic sphincter ablation (DES) were performed surgically [6] [13] [14] or endoscopically [9] [10] [15] [16] [17] [18] [19] [20] [21] for IARP due to SOD have shown a decreased incidence of future attacks of pancreatitis, and it appears that pancreatic SOD plays a role in the pathogenesis of recurrent attacks even if it was not the original cause. In recent years endoscopic therapy has become the treatment of choice over surgery for SOD. The decision on whether to perform BES alone, PES alone or DES was based on results of the SOM findings and/or the discretion of the physician in both the retrospective and prospective studies. Overall data in these studies seem to suggest that DES resulted in a lower recurrence rate compared with BES or PES ablation alone.

References

Stuart ShermanMD 

Division of Gastroenterology and Hepatology
Indiana University School of Medicine

550N University Boulevard
UH 4100
Indianapolis
Indiana
USA

Fax: +1-317-9681066

Email: ssherman@iupui.edu