TY - JOUR
T1 - Why does somatostatin cause gallstones?
AU - Ahrendt, Steven A.
AU - McGuire, Gretchen E.
AU - Pitt, Henry A.
AU - Lillemoe, Keith D.
N1 - Funding Information:
From the Department of Surgery, The Johns Hopkins School of Medicine, and the Surgical Service, Baltimore Veterans Administration Medical Center, Baltimore, Maryland. Supported in part by Grant R29.DK 41889 from the National Institutes of Health, Bethesda, Maryland, and a research grant from the Veterans Administration, Washington, DC.
PY - 1991/1
Y1 - 1991/1
N2 - Long-term administration of the somatostatin analogue, octreotide, is complicated by gallstone formation. Somatostatin is known to inhibit hepatic bile secretion and gallbladder emptying. However, the effect of octreotide on gallbladder bile composition remains unknown. Therefore, we tested the hypothesis that octretide would alter hepatic bile composition and cause gallbladder stasis, thereby increasing gallbladder bile solute concentrations. Fourteen control prairie dogs received daily saline injections, whereas 10 animals received 1 μg of octreotide subcutaneously three times per day for 5 days. Cholecystectomy and common bile duct cannulation were then performed. Octreotide increased hepatic bile concentrations of bilirubin monoglucuronide (p <0.05), total bilirubin (p <0.05), and total protein (p <0.01). Rsa, an index of gallbladder stasis, was decreased (p <0.01) in the octreotide group. Gallbladder bile total calcium (p <0.05), bilirubin monoglucuronide (p <0.05), total bilirubin (p <0.01), total protein (p <0.05), and total lipids (p <0.05) were increased in the octreotide group. Animals receiving octreotide also had decreased hepatic (p <0.05) and gallbladder (p <0.001) bile pH. No differences in cholesterol saturation index were observed. These data suggest that in the prairie dog, octreotide (1) alters hepatic bile composition, (2) causes gallbladder stasis, and (3) increases gallbladder bile calcium, bilirubin, protein, lipid, and hydrogen ion concentrations. We conclude that octreotide causes alterations in gallbladder bile composition that increase the likelihood of cholesterol and calcium bilirubinate precipitation.
AB - Long-term administration of the somatostatin analogue, octreotide, is complicated by gallstone formation. Somatostatin is known to inhibit hepatic bile secretion and gallbladder emptying. However, the effect of octreotide on gallbladder bile composition remains unknown. Therefore, we tested the hypothesis that octretide would alter hepatic bile composition and cause gallbladder stasis, thereby increasing gallbladder bile solute concentrations. Fourteen control prairie dogs received daily saline injections, whereas 10 animals received 1 μg of octreotide subcutaneously three times per day for 5 days. Cholecystectomy and common bile duct cannulation were then performed. Octreotide increased hepatic bile concentrations of bilirubin monoglucuronide (p <0.05), total bilirubin (p <0.05), and total protein (p <0.01). Rsa, an index of gallbladder stasis, was decreased (p <0.01) in the octreotide group. Gallbladder bile total calcium (p <0.05), bilirubin monoglucuronide (p <0.05), total bilirubin (p <0.01), total protein (p <0.05), and total lipids (p <0.05) were increased in the octreotide group. Animals receiving octreotide also had decreased hepatic (p <0.05) and gallbladder (p <0.001) bile pH. No differences in cholesterol saturation index were observed. These data suggest that in the prairie dog, octreotide (1) alters hepatic bile composition, (2) causes gallbladder stasis, and (3) increases gallbladder bile calcium, bilirubin, protein, lipid, and hydrogen ion concentrations. We conclude that octreotide causes alterations in gallbladder bile composition that increase the likelihood of cholesterol and calcium bilirubinate precipitation.
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U2 - 10.1016/0002-9610(91)90381-M
DO - 10.1016/0002-9610(91)90381-M
M3 - Article
C2 - 1987853
AN - SCOPUS:0025975298
SN - 0002-9610
VL - 161
SP - 177
EP - 183
JO - The American Journal of Surgery
JF - The American Journal of Surgery
IS - 1
ER -