Gallstones formation

Biliary sludge A deposit of tiny stones or crystals made up of cholesterol, calcium bilirubinate, and other calcium salts. The cholesterol and calcium bilirubinate crystals in biliary sludge can lead to gallstone formation. 

The Role of Bile Acids in Cholesterol-Rich Gallstone Formation... 

This profile of changes was comparable to that seen in patients with conventional cholesterol gallstone disease, the only difference being that, as a result of OT, the chemistry probably developed in days or weeks, as opposed to months or years in the case of spontaneous gallstone formation. ... 

The Adverse Effects of Increased Proportions of DCA in Bile on Cholesterol Gallstone Formation... 

There are multiple ways by which an increase in the percentage DCA in bile may pre-dispose to cholesterol gallstone formation. Carulli et al. showed that DCA-rich bile induces biliary cholesterol hyper-secretion when compared with other bile acids (Graph 8.6). This is likely to be due to the greater hydro-phobicity and detergent efiect of DCA, which would be able to solubilise the lipids in the canalicular cell wall more readily. It may well explain why there have been linear relationships demonstrated between the percentage DCA in bile and (i) the mole percentage cholesterol and (ii) the cholesterol saturation index in bile. This may also explain why there is a link between the... 

In London, the Guy s Hospital group d wished to see if they could extrapolate validly from OT-treated acromegalic patients to those with sporadic gallstone disease. They also wished to study further the mechanism whereby prolongation of colonic transit might influence DCA metabolism, biliary cholesterol secretion and saturation, and therefore the risk of cholesterol gallstone formation. To study this, Thomas et developed a working hypothesis... 

Unlabeled Uses Prophylaxis of liver transplant rejection, treatment of alcoholic cirrhosis, biliary atresia, chronic hepatitis, gallstone formation, sclerosing cholangitis... 

Cholesterol is a vital component of the human body. It stabilizes cell membranes and is the precursor of bile acids, vitamin D, and steroid hormones. The body s cells can synthesize cholesterol when needed, but excess cholesterol cannot be broken down and must be excreted from the body through the bile into the small intestine. When imbalances occur, cholesterol can accumulate in the gallbladder promoting gallstone formation. Cholesterol accumulation in the bloodstream (hypercholesterolemia) can cause atherosclerotic plaques to form within artery walls. 

All fibrates can cause an increase in the cholesterol saturation of bile. An increase in gallstone formation has been reported. This is a class effect. The fibrates may cause altered LFTs, including GGT and ALP. Use of a fibrate may make it difficult to distinguish between hepatotox-icity and worsening cholestasis. 

Pravastatin is the statin of choice in this patient as it is least likely to accumulate, is hydrophilic, and is not highly protein bound. The starting dose should be low and should be increased cautiously. Monitoring of LFTs is required. Colestyramine and colestipol may be considered and may help the patient s pruritus. Niacin and acipimox could be used if the pruritus does not worsen. The fibrates should be avoided because of the risk of gallstone formation. Ezetimibe could be considered alone. 

Caroli-Bosc FX, Le GP, Pugliese P, et al. (2001) Role of fibrates and HMG-CoA reductase inhibitors in gallstone formation epidemiological study in an unselected population. Dig Dis Sci 46 540-544. 

Uhler ML, Marks JW, Voigt BJ, et al. (1998) Comparison of the impact of transdermal versus oral oestrogens on biliary markers of gallstone formation in postmenopausal women. / Clin Endocrinol Metab 83 410-414. 

Alvaro, D., Angelico, M., Gandin, C., Corradini, S.G., Capocaccia, L. Physico-chemical factors predisposing to pigment gallstone formation in liver cirrhosis. X Hepatol. 1990 10 228 -234... 

A possible consequence of bile acid abnormalities and cholestasis associated with ciclosporin is the development of cholelithiasis in liver transplant patients when the donor has pre-existing susceptibihty for cholesterol gallstone formation or abnormalities of bile composition. 

Portincasa, P. et al. (1995) Cholesterol gallstone formation in man and potential treatments of the gallbladder motility defect. Scand.J. Gastroenterol., Suf l. 212, 30,63-78. 

After his return to Denmark in 1946, he concentrated his research on vitamin K, vitamin E, fats, cholesterol, and nutritional studies in relation to gallstone formation. 

B-Sitosterol - Recent reports demonstrated the efficacy of P-sitosterol in lowering plasma LDL-C in patients with Type II hyperlipoproteinemia. "" 3-Sitosterol obtained from tall oil was found to be effective at 3 g/day, a dose substantially lower than that required with older preparations. However, in juvenile Type II hyperlipoproteinemia, 3-sitosterol lowered LDL-C by only 6% but, in addition, decreased HDL-C by 15% thus, 3-sitosterol was not recommended for the treatment of hypercholesterolemia in children." A potential problem with 3-sitosterol is the increased risk of gallstone formation, in view of the finding of Increased saturation index of bile in patients given 3 g/day of plant sterols. ... 

Gallbladder inflammation (cholecystitis) usually presents with acute abdominal pain (colic) with radiation to the right shoulder. The normal composition of bile is about 5% cholesterol, 15% phosphatidylcholine, and 80% bile salt in a micellar liquid form. Increased cholesterol from high-fat diets or genetic conditions can upset the delicate micellar balance, leading to supersaturated cholesterol or cholesterol precipitates that cause gallstone formation. Removal of the gallbladder is a common treatment for this painful condition. 

Eighty percent of gallstones in the Western world are a result of cholesterol precipitation from the bile, a condition known as cholelithiasis. The pathogenetic mechanism of gallstone formation usually involves a culmination of... 

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