0016-5107/91/3606-0044$03.00 GASTROINTESTINAL ENDOSCOPY Copyright © 1991 by the American Society for Gastrointestinal Endoscopy
Somatostatin prevents acute pancreatitis after pancreatic duct sphincter hydrostatic balloon dilation in patients with idiopathic recurrent pancreatitis Moises Guelrud, MD, Sonia Mendoza, MD Lourdes Viera, MD, Daniel Gelrud, MS Caracas, Venezuela
The purpose of this study was to determine whether prophylactic somatostatin infusion can prevent pancreatitis after hydrostatic balloon dilation of the pancreatic duct sphincter segment in 16 patients with idiopathic recurrent pancreatitis. This study demonstrated that prophylactic administration of somatostatin before, during, and after the procedure diminished the incidence and severity of acute pancreatitis. We recommend consideration of such prophylaxis in patients undergoing this procedure. (Gastrointest Endosc 1990;36:44-47)
Acute pancreatitis is a dreaded complication of endoscopic retrograde cholangiopancreatography (ERCP)l and endoscopic sphincterotomy.2-4 The incidence is 1 and 3%, respectively. When the pancreatic duct sphincter segment is manipulated with hydrostatic balloon dilators, the incidence of acute pancreatitis can be as high as 43%.5 Somatostatin, a tetradecapeptide first isolated from the hypothalamus,6 is a potent inhibitor of human pancreatic exocrine and endocrine secretion in vivo 7-9 and can be postulated as being of therapeutic value in the prevention of acute pancreatitis provoked by pancreatic sphincter dilation. The aim of the present study was to determine whether prophylactic somatostatin infusion can prevent pancreatitis after hydrostatic balloon dilation of the pancreatic duct sphincter segment in patients with idiopathic recurrent pancreatitis. MATERIALS AND METHODS Subjec~s
Patients were selected from those referred because of recurrent attacks of acute pancreatitis. Their initial diagnostic workup consisted of appropriate laboratory tests, Received February 10, 1990. For revision June 7, 1990. Accepted July 16, 1990. From the Gastroenterology Department, Hospital General del Oeste, M.S.A.S. Los Magallanes, Catia, Caracas, Venezuela. Reprint requests: Moises Guelrud, MD, Policlinica Metropolitana, Urb. Caurimare, Caracas, Venezuela.
44
upper gastrointestinal radiography and endoscopy, upper abdominal ultrasonography, ERCP, and examination of CCK-OP stimulated bile for cholesterol crystals. The study group consisted of 16 patients, 13 women and 3 men, ranging in age from 20 to 61 years. All had more than two episodes of acute pancreatitis in the preceding 6 months, with elevated serum amylase and lipase activity of at least three times the normal values. In none of the patients was there history of systemic disease that might cause pancreatitis, and none had evidence of calculus biliary tract disease or marked distortion of the pancreatic duct evident by ERCP. In some cases there was slight dilation of the pancreatic duct with delayed drainage. All patients had abnormally elevated pressure of the sphincter of Oddi (SO). In all patients, endoscopic manipulation was performed at least 1 month after the last attack of pancreatitis and was similar in both groups. The study was approved by the Human Research Review Committee of the hospital, and informed consent was obtained from all participants. SO manometry
Subjects were examined with an Olympus JF-1T sideviewing endoscope (Olympus Corporation of America, Lake Success, N.Y.) after a 14-hr fast. Diazepam, 10 mg intravenously, was given when sedation was required. Pressure recording was accomplished using a triple-lumen catheter (Wilson Cook Medical, Winston-Salem, N.C.). Each lumen was attached to an external Cobe CDX-2 transducer (Cobe Laboratories, Lakewood, Colo.) and connected to a 4-channel Sandhill DMS-A recorder (Sandhill, Littleton, Colo.). The recording channels were constantly perfused with bubble-free water at a rate of 0.25 ml/min by a minimally GASTROINTESTINAL ENDOSCOPY
compliant hydraulic-capillary infusion system (Arndorfer Medical Specialties, Greendale, Wise.). The catheter was passed through the biopsy channel of the duodenoscope. Lodgment in the common bile duct (CBD) was verified by aspiration of bile. The catheter was then slowly withdrawn in I-mm increments until a highpressure zone was located, the elevated pressure being then recorded, pausing 3 min or longer at each station where maximum activity was present. Aspiration of crystal-clear liquid indicated that the catheter was in the pancreatic duct. The duration of recording was shorter, pausing 1 to 2 min at each station where maximum activity was present. After each ductal and pull-through recording, duodenal pressure was measured as a zero reference. Pressure measurements from the several channels usually differ, one being higher than the others. We chose to study the tracing with the highest pressure. Three pull-throughs were done to ensure that the recording was not an artifact. The reported maximal pressure represented the mean of highest single pressure in each of 3 pull-throughs. Basal SO pressure was calculated by subtracting the duodenal pressure (zero reference) from the baseline SO pressure reading between phasic waves. Before endoscopic spincterotomy, basal SO pressure was obtained from the CBD segment of the sphincter. After endoscopic sphincterotomy, the pancreatic duct was then selectively cannulated, and the same procedure was repeated to obtain pancreatic duct pressure. All tracings were coded and read blindly without knowledge of the patients identification. Basal manometric values obtained previouslylO in 50 healthy volunteers in our laboratory showed a mean basal SO pressure of 14.8 ± 6.3 mm Hg (mean ± SD) with a range of 4 to 30 mm Hg and a mean basal pancreatic duct sphincter pressure of 17.3 ± 5.8 mm Hg, with a range of 8 to 26 mm Hg. Abnormally elevated SO basal pressure in our laboratory is 35 mm Hg or greater, which represents 3 SD of the mean. Endoscopic sphincterotomy
This procedure was performed in all 16 patients. After the papilla was identified in the usual manner, the bile duct was entered with a 4-cm wire sphincterotome. Cannulation into the bile duct was confirmed by injection of contrast medium through the sphincterotome. Diathermy was applied to the wire portion of the cutting probe, and the oral prominence of the papilla was incised cephalad. No complications were encountered. Endoscopic hydrostatic balloon dilation
A diagnostic pancreatogram was performed, after which a coiled-spring wire guide (0.035 inch diameter) was inserted through the cannula into the pancreatic duct. While monitoring all exchanges under fluoroscopic control, the cannula was withdrawn over the wire which had been advanced to maintain its position. Once the cannula was removed, the balloon catheter (5 F in diameter, 180 em in length, with a balloon 2-cm long and 6-mm wide when fully distended (Microvasive, Milford, Mass.), was placed over the guide wire and advanced through the instrument into the pancreatic duct, its position being confirmed by radiopaque markers. The balloon was distended with a 50% solution of contrast medium, thus allowing fluoroscopic monitoring. VOLUME 37, NO.1, 1991
The fully distended balloon was held in posjtion for 3 min exerting pressures of 75 psi before being deflated. Sequence of procedures
On the first day of study a diagnostic ERCP was first performed. On a subsequent day, SO manometry was performed, then followed by endoscopic sphincterotomy. After 2 weeks to allow healing, pancreatic duct sphincter manometry was repeated, following which pancreatic sphincter hydrostatic balloon dilation was performed. Somatostatin infusion
Patients were randomized into two groups by a numeric system developed by chance. Each group consisted of eight patients in whom intravenous somatostatin (Serono, Rome, Italy) infusion at a dose of 250 ~g/hour and intravenous placebo (normal saline) infusion were administered in a double-blind manner. Infusion was started 1 hour prior to dilation and maintained for a total of 12 hour. The two groups were similar in relation to age, sex, and basal SO pressures. Routine clinical measures and standard laboratory tests showed no significant changes when data before and after treatment were compared. No side effects of somatostatin or saline infusion were reported. Statistical analysis
Pressure values were expressed as the mean ± SE. Significance of differences between mean values was analyzed using Student's t test for paired variates. Fisher's exact test was used for the analysis of the differences in the incidence of pancreatitis between the two study groups.
RESULTS All of the 16 patients had elevated basal SO pressures from the CBD segment (48.8 ± 2.7 mm Hg) before endoscopic sphincterotomy. The basal pancreatic duct sphincter pressure (54.8 ± 2.5 mm Hg) was higher, without statistical significance, than the CBD segment pressure obtained before endoscopic sphincterotomy. There was no change in the basal pancreatic duct sphincter pressure (52.5 ± 2.9 mm Hg) after endoscopic sphincterotomy. In the control group (saline infusion), six patients developed acute pancreatitis (Fig. 1) defined as upper abdominal pain with epigastric tenderness and at least 3-fold increase over normal values of serum amylase and lipase. In three of these patients, pancreatitis was clinically severe. Two patients exhibited hyperamylasemia without clinical pancreatitis. In the somatostatin infusion group, two patients developed mild pancreatitis (Fig. 2). In the remaining six patients, hyperamylasemia was observed but without symptoms of acute pancreatitis. The differences were statistically significant with a p < 0.01.
DISCUSSION Complications incident to endoscopic sphincterotomy have been reported to occur in 8 to 10% of 45
0.9% SALINE
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24
preventing acute pancreatitis in the experimental animal may be ineffective in treating pancreatitis in humans. One explanation for this difference may be related to the time of administration of the drug. In the experimental animal, drugs usually are given in anticipation of induced pancreatitis, while in humans, drugs are administered only after pancreatitis is in progress. Somatostatin, a substance known to decrease pancreatic secretion, is postulated to more effectively suppress pancreatitis if it is given prophylactically to a patient at risk. This condition pertains to patients undergoing balloon dilation of the pancreatic duct sphincter segment. The total cost of somatostatin infusion was $360, an amount extremely low compared with the total cost of hospitalization and medical care due to acute pancreatitis. The use of somatostatin pertains only to this specific procedure, and the result of this study can not be extrapolated to less invasive biliary endoscopy procedures where the incidence of pancreatitis without prophylaxis is much lower. However, prophylactic somatostatin administration has been recommended to prevent postoperative pancreatic complications in patients undergoing ERCP and pancreatic surgeryY-13 Recently, it has been shown 14 that octreotide, a somatostatin analogue, may inhibit sphincter of Oddi motility in the prairie dog. This effect may be beneficial in reducing intrapancreatic duct pressure and may contribute in preventing pancreatitis. In the present study, prophylactic administration of somatostatin before, during, and after the procedure diminished the incidence and severity of acute pancreatitis consequent to hydrostatic balloon dilation of the pancreatic duct sphincter segment. We recommend consideration of such prophylaxis in patients undergoing this procedure. ACKNOWLEDGMENTS
Figure 2. Serum amylase values before and after somatostatin infusion. Two patients (big circles) developed acute pancreatitis.
The authors thank Dr. William S. Haubrich for reviewing the manuscript.
patients. 2- 4 The incidence of acute pancreatitis varies between 1 and 3%, and is higher yet in patients with papillary stenosis. In a survey of 25 centers in West Germany,4 it was found that of 7585 endoscopic sphincterotomies in patients with choledocholithiasis, 77 patients (1.01%) developed acute pancreatitis. However, in 813 patients with papillary stenosis, 28 patients (3.4%) had consequent acute pancreatitis. When the pancreatic duct sphincter segment is manipulated with a balloon dilator, the rate of acute pancreatitis is even higher. In 16 patients in whom pancreatic duct sphincter dilation was performed, 7 patients (43 %) developed acute pancreatitis. 5 It is well known that drugs shown to be effective in
1. Bilbao MK, Dotter CT, Lee TG, Katon RM. Complications of endoscopic retrograde cholangiopancreatography: a study of 10,000 cases. Gastroenterology 1976;70:314-20. 2. Geenen JE, Vennes JA, Silvis SE. Resume of a seminar on endoscopic retrograde sphincterotomy. Gastrointest Endosc 1981;27:31-8. 3. Cotton PB, Vallon AG. British experience with duodenoscopic sphincterotomy for removal of bile duct stones. Br J Surg 1981;68:373-5. 4. Seifert E. Endoscopy and biliary disease. In: Blumgart LH, ed. The biliary tract. London: Churchill Livingstone, 1982:61-81. 5. Guelrud M, Mendoza S, Viera L. Idiopathic recurrent pancreatitis and hypercontractil sphincter of Oddi. Treatment with endoscopic sphincterotomy and pancreatic duct dilation [Abstract]. Gastroenterology 1986;90:1443. 6. Brazeau P, Vale W, Burgus R, et al. Hypothalamic polypeptide that inhibits the secretion of immunoreactive pituitary growth hormone. Science 1973;179:77-9. 7. Dollinger HC, Raptis S, Pfeiffer EF. Effects of somatostatin on
REFERENCES
46
GASTROINTESTINAL ENDOSCOPY
8. 9. 10. 11.
exocrine and endocrine pancreatic function stimulated by intestinal hormones in man. Horm Metab Res 1976;8:74-8. Hanssen LE, Hanssen KF, Myren J. Inhibition of secretin infusion in man. Scand J GastroenteroI1977;12:391-4. Lin TM, Evans DC, Shaar CJ, Root MA. Action of somatostatin on stomach, pancreas, gastric mucosal blood flow, and hormones. Am J Physiol 1983;244:G40-5. Guelrud M, Mendoza S, Rossiter G, Villegas MI. Sphincter of Oddi manometry in healthy volunteers. Dig Dis Sci 1990;35:3846. Tulassay Z, Papp J, Koranyi L, et al. Effect of somatostatin on
VOLUME 37, NO.1, 1991
metabolic changes following ERCP. Wien Klin Wochenschr 1982;94:261-5. 12. Borsch G, Bergbaner M, Nebel W, et al. Effect of somatostatin on amylase level and pancreatitis rate following ERCP. Med Welt 1984;35:109-12. 13. Roncoroni L, De Bernardinis M, Violi V, et al. Effect ofperioperative somatostatin administration of sphincteroplasty-induced increase of amylase. Am J Gastroenterol 1986;81:432-5. 14. Ahrendt SA, McGuire GE, Lillemoe KD, et al. Somatostatin inhibits sphincter of Oddi motility. Gastroenterology 1990;98:A242.
47
Somatostatin prevents acute pancreatitis after pancreatic duct sphincter hydrostatic balloon dilation in patients with idiopathic recurrent pancreatitis Moises Guelrud, MD, Sonia Mendoza, MD Lourdes Viera, MD, Daniel Gelrud, MS Caracas, Venezuela
The purpose of this study was to determine whether prophylactic somatostatin infusion can prevent pancreatitis after hydrostatic balloon dilation of the pancreatic duct sphincter segment in 16 patients with idiopathic recurrent pancreatitis. This study demonstrated that prophylactic administration of somatostatin before, during, and after the procedure diminished the incidence and severity of acute pancreatitis. We recommend consideration of such prophylaxis in patients undergoing this procedure. (Gastrointest Endosc 1990;36:44-47)
Acute pancreatitis is a dreaded complication of endoscopic retrograde cholangiopancreatography (ERCP)l and endoscopic sphincterotomy.2-4 The incidence is 1 and 3%, respectively. When the pancreatic duct sphincter segment is manipulated with hydrostatic balloon dilators, the incidence of acute pancreatitis can be as high as 43%.5 Somatostatin, a tetradecapeptide first isolated from the hypothalamus,6 is a potent inhibitor of human pancreatic exocrine and endocrine secretion in vivo 7-9 and can be postulated as being of therapeutic value in the prevention of acute pancreatitis provoked by pancreatic sphincter dilation. The aim of the present study was to determine whether prophylactic somatostatin infusion can prevent pancreatitis after hydrostatic balloon dilation of the pancreatic duct sphincter segment in patients with idiopathic recurrent pancreatitis. MATERIALS AND METHODS Subjec~s
Patients were selected from those referred because of recurrent attacks of acute pancreatitis. Their initial diagnostic workup consisted of appropriate laboratory tests, Received February 10, 1990. For revision June 7, 1990. Accepted July 16, 1990. From the Gastroenterology Department, Hospital General del Oeste, M.S.A.S. Los Magallanes, Catia, Caracas, Venezuela. Reprint requests: Moises Guelrud, MD, Policlinica Metropolitana, Urb. Caurimare, Caracas, Venezuela.
44
upper gastrointestinal radiography and endoscopy, upper abdominal ultrasonography, ERCP, and examination of CCK-OP stimulated bile for cholesterol crystals. The study group consisted of 16 patients, 13 women and 3 men, ranging in age from 20 to 61 years. All had more than two episodes of acute pancreatitis in the preceding 6 months, with elevated serum amylase and lipase activity of at least three times the normal values. In none of the patients was there history of systemic disease that might cause pancreatitis, and none had evidence of calculus biliary tract disease or marked distortion of the pancreatic duct evident by ERCP. In some cases there was slight dilation of the pancreatic duct with delayed drainage. All patients had abnormally elevated pressure of the sphincter of Oddi (SO). In all patients, endoscopic manipulation was performed at least 1 month after the last attack of pancreatitis and was similar in both groups. The study was approved by the Human Research Review Committee of the hospital, and informed consent was obtained from all participants. SO manometry
Subjects were examined with an Olympus JF-1T sideviewing endoscope (Olympus Corporation of America, Lake Success, N.Y.) after a 14-hr fast. Diazepam, 10 mg intravenously, was given when sedation was required. Pressure recording was accomplished using a triple-lumen catheter (Wilson Cook Medical, Winston-Salem, N.C.). Each lumen was attached to an external Cobe CDX-2 transducer (Cobe Laboratories, Lakewood, Colo.) and connected to a 4-channel Sandhill DMS-A recorder (Sandhill, Littleton, Colo.). The recording channels were constantly perfused with bubble-free water at a rate of 0.25 ml/min by a minimally GASTROINTESTINAL ENDOSCOPY
compliant hydraulic-capillary infusion system (Arndorfer Medical Specialties, Greendale, Wise.). The catheter was passed through the biopsy channel of the duodenoscope. Lodgment in the common bile duct (CBD) was verified by aspiration of bile. The catheter was then slowly withdrawn in I-mm increments until a highpressure zone was located, the elevated pressure being then recorded, pausing 3 min or longer at each station where maximum activity was present. Aspiration of crystal-clear liquid indicated that the catheter was in the pancreatic duct. The duration of recording was shorter, pausing 1 to 2 min at each station where maximum activity was present. After each ductal and pull-through recording, duodenal pressure was measured as a zero reference. Pressure measurements from the several channels usually differ, one being higher than the others. We chose to study the tracing with the highest pressure. Three pull-throughs were done to ensure that the recording was not an artifact. The reported maximal pressure represented the mean of highest single pressure in each of 3 pull-throughs. Basal SO pressure was calculated by subtracting the duodenal pressure (zero reference) from the baseline SO pressure reading between phasic waves. Before endoscopic spincterotomy, basal SO pressure was obtained from the CBD segment of the sphincter. After endoscopic sphincterotomy, the pancreatic duct was then selectively cannulated, and the same procedure was repeated to obtain pancreatic duct pressure. All tracings were coded and read blindly without knowledge of the patients identification. Basal manometric values obtained previouslylO in 50 healthy volunteers in our laboratory showed a mean basal SO pressure of 14.8 ± 6.3 mm Hg (mean ± SD) with a range of 4 to 30 mm Hg and a mean basal pancreatic duct sphincter pressure of 17.3 ± 5.8 mm Hg, with a range of 8 to 26 mm Hg. Abnormally elevated SO basal pressure in our laboratory is 35 mm Hg or greater, which represents 3 SD of the mean. Endoscopic sphincterotomy
This procedure was performed in all 16 patients. After the papilla was identified in the usual manner, the bile duct was entered with a 4-cm wire sphincterotome. Cannulation into the bile duct was confirmed by injection of contrast medium through the sphincterotome. Diathermy was applied to the wire portion of the cutting probe, and the oral prominence of the papilla was incised cephalad. No complications were encountered. Endoscopic hydrostatic balloon dilation
A diagnostic pancreatogram was performed, after which a coiled-spring wire guide (0.035 inch diameter) was inserted through the cannula into the pancreatic duct. While monitoring all exchanges under fluoroscopic control, the cannula was withdrawn over the wire which had been advanced to maintain its position. Once the cannula was removed, the balloon catheter (5 F in diameter, 180 em in length, with a balloon 2-cm long and 6-mm wide when fully distended (Microvasive, Milford, Mass.), was placed over the guide wire and advanced through the instrument into the pancreatic duct, its position being confirmed by radiopaque markers. The balloon was distended with a 50% solution of contrast medium, thus allowing fluoroscopic monitoring. VOLUME 37, NO.1, 1991
The fully distended balloon was held in posjtion for 3 min exerting pressures of 75 psi before being deflated. Sequence of procedures
On the first day of study a diagnostic ERCP was first performed. On a subsequent day, SO manometry was performed, then followed by endoscopic sphincterotomy. After 2 weeks to allow healing, pancreatic duct sphincter manometry was repeated, following which pancreatic sphincter hydrostatic balloon dilation was performed. Somatostatin infusion
Patients were randomized into two groups by a numeric system developed by chance. Each group consisted of eight patients in whom intravenous somatostatin (Serono, Rome, Italy) infusion at a dose of 250 ~g/hour and intravenous placebo (normal saline) infusion were administered in a double-blind manner. Infusion was started 1 hour prior to dilation and maintained for a total of 12 hour. The two groups were similar in relation to age, sex, and basal SO pressures. Routine clinical measures and standard laboratory tests showed no significant changes when data before and after treatment were compared. No side effects of somatostatin or saline infusion were reported. Statistical analysis
Pressure values were expressed as the mean ± SE. Significance of differences between mean values was analyzed using Student's t test for paired variates. Fisher's exact test was used for the analysis of the differences in the incidence of pancreatitis between the two study groups.
RESULTS All of the 16 patients had elevated basal SO pressures from the CBD segment (48.8 ± 2.7 mm Hg) before endoscopic sphincterotomy. The basal pancreatic duct sphincter pressure (54.8 ± 2.5 mm Hg) was higher, without statistical significance, than the CBD segment pressure obtained before endoscopic sphincterotomy. There was no change in the basal pancreatic duct sphincter pressure (52.5 ± 2.9 mm Hg) after endoscopic sphincterotomy. In the control group (saline infusion), six patients developed acute pancreatitis (Fig. 1) defined as upper abdominal pain with epigastric tenderness and at least 3-fold increase over normal values of serum amylase and lipase. In three of these patients, pancreatitis was clinically severe. Two patients exhibited hyperamylasemia without clinical pancreatitis. In the somatostatin infusion group, two patients developed mild pancreatitis (Fig. 2). In the remaining six patients, hyperamylasemia was observed but without symptoms of acute pancreatitis. The differences were statistically significant with a p < 0.01.
DISCUSSION Complications incident to endoscopic sphincterotomy have been reported to occur in 8 to 10% of 45
0.9% SALINE
w
2000
(/J
< ..J
> ~
::;:
co: 400
::;: a:
::l
UJ
(j)
200
(H-g~~S) PRE
3
6
12
24
preventing acute pancreatitis in the experimental animal may be ineffective in treating pancreatitis in humans. One explanation for this difference may be related to the time of administration of the drug. In the experimental animal, drugs usually are given in anticipation of induced pancreatitis, while in humans, drugs are administered only after pancreatitis is in progress. Somatostatin, a substance known to decrease pancreatic secretion, is postulated to more effectively suppress pancreatitis if it is given prophylactically to a patient at risk. This condition pertains to patients undergoing balloon dilation of the pancreatic duct sphincter segment. The total cost of somatostatin infusion was $360, an amount extremely low compared with the total cost of hospitalization and medical care due to acute pancreatitis. The use of somatostatin pertains only to this specific procedure, and the result of this study can not be extrapolated to less invasive biliary endoscopy procedures where the incidence of pancreatitis without prophylaxis is much lower. However, prophylactic somatostatin administration has been recommended to prevent postoperative pancreatic complications in patients undergoing ERCP and pancreatic surgeryY-13 Recently, it has been shown 14 that octreotide, a somatostatin analogue, may inhibit sphincter of Oddi motility in the prairie dog. This effect may be beneficial in reducing intrapancreatic duct pressure and may contribute in preventing pancreatitis. In the present study, prophylactic administration of somatostatin before, during, and after the procedure diminished the incidence and severity of acute pancreatitis consequent to hydrostatic balloon dilation of the pancreatic duct sphincter segment. We recommend consideration of such prophylaxis in patients undergoing this procedure. ACKNOWLEDGMENTS
Figure 2. Serum amylase values before and after somatostatin infusion. Two patients (big circles) developed acute pancreatitis.
The authors thank Dr. William S. Haubrich for reviewing the manuscript.
patients. 2- 4 The incidence of acute pancreatitis varies between 1 and 3%, and is higher yet in patients with papillary stenosis. In a survey of 25 centers in West Germany,4 it was found that of 7585 endoscopic sphincterotomies in patients with choledocholithiasis, 77 patients (1.01%) developed acute pancreatitis. However, in 813 patients with papillary stenosis, 28 patients (3.4%) had consequent acute pancreatitis. When the pancreatic duct sphincter segment is manipulated with a balloon dilator, the rate of acute pancreatitis is even higher. In 16 patients in whom pancreatic duct sphincter dilation was performed, 7 patients (43 %) developed acute pancreatitis. 5 It is well known that drugs shown to be effective in
1. Bilbao MK, Dotter CT, Lee TG, Katon RM. Complications of endoscopic retrograde cholangiopancreatography: a study of 10,000 cases. Gastroenterology 1976;70:314-20. 2. Geenen JE, Vennes JA, Silvis SE. Resume of a seminar on endoscopic retrograde sphincterotomy. Gastrointest Endosc 1981;27:31-8. 3. Cotton PB, Vallon AG. British experience with duodenoscopic sphincterotomy for removal of bile duct stones. Br J Surg 1981;68:373-5. 4. Seifert E. Endoscopy and biliary disease. In: Blumgart LH, ed. The biliary tract. London: Churchill Livingstone, 1982:61-81. 5. Guelrud M, Mendoza S, Viera L. Idiopathic recurrent pancreatitis and hypercontractil sphincter of Oddi. Treatment with endoscopic sphincterotomy and pancreatic duct dilation [Abstract]. Gastroenterology 1986;90:1443. 6. Brazeau P, Vale W, Burgus R, et al. Hypothalamic polypeptide that inhibits the secretion of immunoreactive pituitary growth hormone. Science 1973;179:77-9. 7. Dollinger HC, Raptis S, Pfeiffer EF. Effects of somatostatin on
REFERENCES
46
GASTROINTESTINAL ENDOSCOPY
8. 9. 10. 11.
exocrine and endocrine pancreatic function stimulated by intestinal hormones in man. Horm Metab Res 1976;8:74-8. Hanssen LE, Hanssen KF, Myren J. Inhibition of secretin infusion in man. Scand J GastroenteroI1977;12:391-4. Lin TM, Evans DC, Shaar CJ, Root MA. Action of somatostatin on stomach, pancreas, gastric mucosal blood flow, and hormones. Am J Physiol 1983;244:G40-5. Guelrud M, Mendoza S, Rossiter G, Villegas MI. Sphincter of Oddi manometry in healthy volunteers. Dig Dis Sci 1990;35:3846. Tulassay Z, Papp J, Koranyi L, et al. Effect of somatostatin on
VOLUME 37, NO.1, 1991
metabolic changes following ERCP. Wien Klin Wochenschr 1982;94:261-5. 12. Borsch G, Bergbaner M, Nebel W, et al. Effect of somatostatin on amylase level and pancreatitis rate following ERCP. Med Welt 1984;35:109-12. 13. Roncoroni L, De Bernardinis M, Violi V, et al. Effect ofperioperative somatostatin administration of sphincteroplasty-induced increase of amylase. Am J Gastroenterol 1986;81:432-5. 14. Ahrendt SA, McGuire GE, Lillemoe KD, et al. Somatostatin inhibits sphincter of Oddi motility. Gastroenterology 1990;98:A242.
47
