In the formation of
gallstone diseases, there are numerous genes, that are held responsible for liver disorders primarily and diseases of bile flow and bile formation, modification of lipid metabolism
diabetes mellitus,
obesity, glutene sensitive enteropathy,
Crohn-disease,
Down syndrome, Gucher syndrome,
cystic fibrosis as well as haematological disorders and state following ileum resection. In the development of these,
bacterial infections, inflammatory reactions,
metal element power and
free radicals play an important role.
Fatty acids,
lipid oxides, diene conjugates and other lipid peroxidation products are moving from the liver to the bile, and they initiate primer and secondary
free radical reactions in the bile duct and gallbladder. The
inflammation processes in the gallbladder wall produce
free radicals. The free
bilirubin content of the bile behaves pro- and
antioxidant molecules. The ambivalent property of free
bilirubin, which is detected concentration in the gallbladder bile -- from microsomal leakage or as a consequence of bacterial deglucuronidation -- increases the
free radical reactions in the gallbladder. The
gallstone formation of free
bilirubin with
metal ions, primarily Ca ++
ions makes
calcium hydrogen bilirubinate in the bile.
Calcium ions can react with
fatty acids and hereby modify the bile viscosity. The
lipids, free
bilirubin and
metal elements are all components in stone formation.
Antioxidants, concerning their derivates or molecules, medicines, which increase
antioxidant property can influence the bile composition or inhibit the
gallstone formation on several levels.