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Background: Endoscopic pancreatic sphincterotomy has been touted as effective therapy for chronic pancreatitis and unexplained abdominal pain resulting from pancreatic sphincter dysfunction. Although short-term data are encouraging, there are no reports on how these patients fare beyond the first few months. Methods: We performed a retrospective review of records on all patients who had pancreatic sphincterotomy during a 4-year period between August 1992 and November 1996. Chronic pancreatitis was diagnosed by pancreatography. Patients were evaluated for symptomatic response to pancreatic sphincterotomy and clinical improvement was defined as greater than 50% reduction in the magnitude of pain. Results: Fifty-five patients had pancreatic sphincterotomy including patients with (n = 40) and without (n = 15) chronic pancreatitis. After a median follow-up of 16 months, 60% of all patients reported improvement of pain scores (3.6 ± 3.4 vs. 8.8 ± 1.8; p Conclusions: In a subgroup of patients with pancreatic sphincter dysfunction, endoscopic pancreatic sphincterotomy results in significant sustained clinical improvement. (Gastrointest Endosc 2000;52:15-9.)

Major papilla pancreatic sphincter dysfunction, a variant of sphincter of Oddi dysfunction, causes pancreatitis or pancreatic-type pain. Endoscopic manometry as performed at endoscopic retrograde cholangiography is the most commonly used method to identify sphincter dysfunction. Noninvasive testing, such as secretin-stimulated ultrasound analysis of duct diameter, is less reliable and of relatively low sensitivity. Two-thirds of patients with sphincter of Oddi dysfunction have elevated pancreatic basal sphincter pressure. Patients with suspected or documented sphincter of Oddi dysfunction may respond to biliary sphincterotomy alone, but warrant evaluation of their pancreatic sphincter if symptoms persist after therapy. Whether such pancreatic and biliary sphincters should be treated at the first treatment session is controversial. Pancreatic sphincterotomy is associated with a complication rate very similar to that of biliary sphincterotomy except that the pancreatitis rate is two- to fourfold higher. Prophylactic pancreatic stenting diminishes such pancreatitis by approximately 50%.

To date, endoscopic manometry is the best method for evaluating the function of the sphincter. Sphincter of Oddi manometry (SOM) remains the gold standard to correctly diagnose the sphincter of Oddi dysfunction (SOD) and stratify therapy. Several dynamic abnormalities relating to the intensity, frequency, and propagation of sphincter contractions have been described. However, their clinical use generally has been abandoned in favor of basal sphincter pressure alone, because this measurement is stable over time, and has stronger interobserver reliablility, reproducibility on repeating testing, and is associated with the responsiveness to therapy. A significant elevated risk of pancreatitis was attributed to the technique. The risk of pancreatitits associated with manometric evaluation of the pancreatic sphincter is markedly reduced when manometry is performed with continous aspiration from the pancreatic duct via one of the 3 catheter lumens. This section reviews indications, conscious sedative drugs, techniques, and the appropriate interpretations of SOM.

연락처: 김호각, 705-718, 대구시 남구 대명4동 3056-6 대구가톨릭대학교 의과대학 내과학교실 Tel: (053) 650-4041, Fax: (053) 624-3281 E-mail: hgkim@cu.ac.kr Correspondence to: Ho Gak Kim, M.D. Department of Internal Medicine, Catholic University of Daegu School of Medicine, 3056-6, Daemyeong 4-dong, Nam-gu, Daegu 705-718, Korea Tel: +82-53-650-4041, Fax: +82-53-624-3281 E-mail: hgkim@cu.ac.kr Fig. 1. Contrast-enhanced CT finding of the patient. Pancreas was normal looking without edema, peripancreatic infiltration, or fluid collection. 췌장 오디 괄약근 기능 이상

Sphincter of Oddi dysfunction (SOD) is a clinical entity caused by a primary motility alteration of either the biliary or the pancreatic sphincter. SOD is a rare condition that has been scarcely reported in children. Most of the reported literature has been in children with idiopathic recurrent pancreatitis. These children are treated endoscopically by dual sphincterotomy of the pancreatic and common duct sphincters. However, the safety and efficacy of sphincter of Oddi manometry and sphincterotomy in the pediatric population await further study.

To facilitate pancreatic stone retrieval, four patients with chronic pancreatitis and pancreatic stones underwent endoscopic pancreatic sphincter balloon dilation (EPSBD) rather than pancreatic sphincterotomy. Extracorporeal shock wave lithotripsy combined with endoscopic removal was carried out in three patients. Stone removal following EPSBD was completely successful in all four patients. Patients showed no severe complications during the dilation procedure. In one patient, to prevent pancreatitis, an endoscopic nasopancreatic drain was placed for 1 week after EPSBD. Compared with pancreatic sphincterotomy, EPSBD can be performed safely in patients with chronic pancreatitis to assist in the extraction of pancreatic duct stones. Use of the EPSBD procedure in cases of chronic pancreatitis provides a useful approach to improve endoscopic clearance of pancreatic duct stones.

The incidence of pancreatic ductographic abnormalitites (PDA) in patients with normal and abnormal pancreatic orifice manometry is not known. AIM: Evaluate the incidence of (PDA) in patients with clinically suspected SOD who undergo pancreatic manometry (PSOM). METHOD: The MUSC GI Trac data base was reviewed for consecutive patients with clinically suspected SOD who had successful unequivocal PSOM between 2/94 and 11/99. Patients with pancreas divisum, prior pancreatic duct or orifice therapy, and failed/inadequate pancreatic ductography were excluded from analysis. The ductographic findings of duct dilatation, duct irregularity and irregular side branch changes, were compared individually and as a group with the findings of PSOM. PSOM was performed using a standard 5 F aspirating catheter (Wilson-Cook,Winston-Salem, NC) and PSH diagnosed if the mean pressure from two leads was >40 mmHg. RESULTS: Of 833 patients (mean age 46.3 yrs, range 16-86yrs., M/F 218/615), 429 (52%) had abnormal PSOM (ie PSH) and 431 (52%) had at least one PDA. At least one PDA was present in 248/429 (58%) of patients diagnosed with PSH, and 45% (181/402) with no PDA had PSH (p

Background: Endoscopic biliary sphincterotomy in sphincter of Oddi dysfunction (SOD) patients has a high risk of post-ERCP pancreatitis. It is hypothesized that this high complication rate is due to residual pancreatic sphincter hypertension. Aim: To decrease the pancreatitis rate of SOD patients after biliary sphincterotomy by injecting botulinum toxin into the residual pancreatic sphincter. This is technically simpler and involves less pancreatic manipulation than pancreatic stent placement. Methods: All patients undergoing ERCP with manometry for suspicion of biliary SOD where asked to participate in this study. Manometry was performed to obtain baseline biliary and pancreatic sphincter pressures with at least two pull-through recordings. Patients with normal basal pressures (less than 40 mmHg) were excluded. Those with elevated pressures were randomized to receive botulinum toxin vs. sham saline injection after the biliary sphincterotomy. Fifty units of botulinum toxin was delivered via sclerotherapy needle as two 25 U injections of 0.25cc each into the pancreatic sphincter in the botulinum toxin therapy group. For those in the sham arm, 0.50cc of saline was injected into the duodenal lumen via sclerotherapy needle. All patients were assessed 24 hours post-procedure for complications. Results: Between 2/12/99 and 11/30/99 a total of 57 patients were referred for ERCP with manometry for suspected SOD. Fifty-one consented to participate in the protocol. Thirteen had elevated baseline pressures and were randomized. Six received botulinum toxin injection and 7 were randomized to sham injection. A total of 4 (57%) patients in the sham group developed procedure-induced pancreatitis as compared to 2 (33%) in the botulinum toxin group (NS). No differences were observed in the severity of pancreatitis between the groups. Conclusions: In the small number of patients studied to date, no definite conclusion can be made about the effect of botulinum toxin injection on the pancreatitis rate of SOD patients following biliary sphincterotomy.

BACKGROUND: PSH can persist after BSx. There is little information regarding the clinical symptom response to BSx and PSx in patients with PSH. AIM: Evaluate the effect of PSx on symptoms in patients with persistent PSH after prior BSx. METHODS: Patients with prior sphincter of Oddi dysfunction (SOD) treated initially with BSx and who had persistent PSH were analyzed. Clinical data were evaluated for the subsequent endoscopic therapy (if any). All patients were contacted by telephone to evaluate symptom response to their most recent endoscopic therapy. Manometry was performed with a standard perfused, aspirating catheter and SOD diagnosed if the mean pressure form two leads was ≥ 40 mmHg. Persistent PSH was documented by pancreatic manometry immediately after BSx and prior to PSx at a subsequent procedure. Patients who had normal pancreatic manometry were excluded from analysis. RESULTS: 42 patients (mean age 53 yrs, range 21-83 yrs , M:F=9/39) underwent isolated BSx in the setting of PSH. Of these 21 (50%) patients returned with persistent symptoms and underwent PSx. Patients were interviewed regarding symptom response at a mean of 39 months ( range 6.8-53months) after their most recent endoscopic intervention. Of the 21 patients who only had BSx as their most recent therapy (i.e. untreated PSH), 13 (62%) reported resolution of pain/symptoms, 6 (29%) reported improvement of symptoms and 2 (9%) reported no change in symptoms. Of the 21 patients who returned after BSx with persistent symptoms and who underwent PSx to treat PSH, 3 (14%) reported resolution of symptoms,11 (52%) reported improved symptoms, 6 (29%) reported no change and 1 (5%) reported worsening symptoms. After initial BSx, post-ERCP pancreatitis occurred in 4/21 (19%) patients who subsequently returned with symptoms, compared to 1/21 (5%) (NS) in patients who did not receive subsequent PSx. CONCLUSIONS: 1] Pancreatic sphincterotomy can improve symptoms in 66% of patients with prior biliary sphincterotomy but persistent PSH and symptoms. 2] However, a significant portion of patients (45%) with persistent PSH immediately after biliary sphincterotomy report symptom improvement without pancreatic sphincterotomy. This suggests that BSx alone may provide adequate symptom relief in some patients. Further study is needed to identify which patients with PSH would benefit from pancreatic sphincterotomy in addition to biliary sphincterotomy.

The first case of obstructive jaundice secondary to a chronic afferent loop obstruction has been reported. The cause of the obstructed afferent loop was found to be a carcinoma of the gastric pouch occurring 25 years after surgery for peptic ulcer disease. The failure to develop any evidence of pancreatitis despite marked dilatation of the biliary tree and gall bladder suggests the existence of an independent functioning pancreatic sphincter, perhaps the sphincter of Boyden.

The pancreas was one of the last organs to receive the critical attention of early anatomists and physiologists; but since Langerhans described it histologically in 1869, its anatomy and physiology have been the subject of close scrutiny. The pancreatic sphincter mechanism, however, which normally should allow pancreatic secretion to flow into the duodenum and prevent reflux of bile or duodenal contents into the pancreatic ducts, has been difficult to study. Consequently, its physiological functions and the factors that control these functions are largely enigmatic.