چکیده (انگلیسی):

Background/Objectives: Our aim was to investigate the calcium content of
different gallstone compositions and the pathogenic mechanisms of calcium carbonate
gallstones.
Methods: Between August 2001 and July 2007, gallstones from 481 patients, including 68
calcium carbonate gallstones, were analyzed for total calcium content. Gallbladder bile
samples from 33 cases and six controls were analyzed for pH, carbonate anion level, freeionized
calcium concentration and saturation index for calcium carbonate.
Results: Total calcium content averaged 75.6 %, 11.8 %, and 4.2 % for calcium carbonate,
calcium bilirubinate and cholesterol gallstones. In 29.4 % of patients, chronic and/or intermittent
cystic duct obstructions were caused by polypoid lesions in the neck region and 70.6 %
were caused by stones. A total of 82 % of patients had chronic low-grade inflammation of
the gallbladder wall and 18.0 % had acute inflammatory exacerbations. In the bile, we found
the mean pH, mean carbonate anion, free-ionized calcium concentrations, and mean saturation
index for calcium carbonate to be elevated in comparison to controls.
Conclusion: From our study, we found chronic and/or intermittent cystic duct obstructions and
low-grade GB wall inflammation lead to GB epithelium hydrogen secretion dysfunction.
Increased calcium ion efflux into the GB lumen combined with increased carbonate anion presence
increases SI_CaCO3 from 1 to 22.4. Thus, in an alkaline milieu with pH 7.8, calcium
carbonate begins to aggregate and precipitate.