Cholecystokinin Prophylaxis of Parenteral Nutrition-Induced Gallbladder Disease

Effect of the prokinetic agent, erythromycin, in the richardson ground squirrel model of cholesterol gallstone disease

“…38 Reducing 39-41 or eliminating 9,10 the residence time of bile salts in the gallbladder and/or accelerating small intestinal transit 8 promotes bile salt secretion, reduces the CSI, and might have a role in preventing stone formation both in humans and in animal models. 24,[39][40][41] Conceivably, erythromycin treatment might have decreased the absorption of cholesterol, perhaps through very rapid intestinal transit. This does not appear to have occurred, because serum cholesterol levels were markedly elevated in both the erythromycin-and the placebo-treated groups on the highcholesterol diet.…”

Biliary motility.

“…156 One interpretation of the evidence that implicates altered biliary motility in the aetiology of gall stone formation is that gall bladder activity must be maintained in a tight narrow band between overactivity reducing the bile acid pool with consequent lithiasis,' '2-1' and underactivity causing stasis and gall stone precipitation. '35-156 Furthermore, as argued earlier, a reduction in the rate of turnover of the efterohepatic circulation of bile acids is associated with reduced hepatic bile acid secretion, so on balance we support the view that decreased biliary motility rather than increased biliary motility is the aetiological event in cholelithiasis.…”

Management of patients with a short bowel

“…There are many therapies proposed to prevent the formation of gallstones. Cholecystokinin (CCK) injections have been successful [173] . Periodic pulsed infusions of amino acids or small amounts of enteral feed stimulate endogenous CCK release, cause gallbladder contraction and thus prevent gallbladder stasis [174] .…”