TY - JOUR
T1 - Role of gallbladder mucus in the pathogenesis of cholesterol gallstones
AU - Doty, Jeffrey E.
AU - Pitt, Henry A.
AU - Kuchenbecker, Stephen L.
AU - Porter-Fink, Vicki
AU - DenBesten, Lawrence W.
N1 - Funding Information:
From the Surgical Service, Veterans Administration Medical Center, Sep-ulveda. and the department of Surgery. Uniwrsii of Califomia, Los Angeles, California. This work was supported by a Veterans Administration Research Grant.
PY - 1983/1
Y1 - 1983/1
N2 - Recent observations indicate that the hepatic secretion of lithogenic bile, gallbladder mucus hypersecretion, and gallbladder stasis are all critical factors in the pathogenesis of cholesterol gallstones. Using the prairie dog gallstone model, we investigated the interaction of these factors and the sequence in which they develop. The results of this study indicated that (1) gallbladder bile mucus concentration is elevated before cholesterol precipitation and increases progressively with the formation of cholesterol crystals, (2) cystic duct resistance increases in the presence of cholesterol crystals, and (3) agglomerates of cholesterol crystals, but not fine, sonicated crystals increase cystic duct resistance. We conclude that these alterations trigger a self-perpetuating cycle of mucus hypersecretion, cholesterol crystallization, and gallbladder stasis which culminates in the formation of cholesterol gallstones.
AB - Recent observations indicate that the hepatic secretion of lithogenic bile, gallbladder mucus hypersecretion, and gallbladder stasis are all critical factors in the pathogenesis of cholesterol gallstones. Using the prairie dog gallstone model, we investigated the interaction of these factors and the sequence in which they develop. The results of this study indicated that (1) gallbladder bile mucus concentration is elevated before cholesterol precipitation and increases progressively with the formation of cholesterol crystals, (2) cystic duct resistance increases in the presence of cholesterol crystals, and (3) agglomerates of cholesterol crystals, but not fine, sonicated crystals increase cystic duct resistance. We conclude that these alterations trigger a self-perpetuating cycle of mucus hypersecretion, cholesterol crystallization, and gallbladder stasis which culminates in the formation of cholesterol gallstones.
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U2 - 10.1016/0002-9610(83)90166-6
DO - 10.1016/0002-9610(83)90166-6
M3 - Article
C2 - 6849496
AN - SCOPUS:0020691130
SN - 0002-9610
VL - 145
SP - 54
EP - 61
JO - The American Journal of Surgery
JF - The American Journal of Surgery
IS - 1
ER -