THE EFFECT OF PLASMA LOW-DENSITY-LIPOPROTEIN APHERESIS ON THE HEPATICSECRETION OF BILIARY LIPIDS IN HUMANS

Background-The liver is a key organ in the metabolism of cholesterol i n humans. It is the only organ by which substantial amounts of cholest erol ape excreted from the body, either directly as free cholesterol i nto the bile or after conversion to bile acids. The major part of chol esterol synthesis in the body occurs in the liver. Cholesterol is also taken up by the liver from plasma lipoproteins. The relative contribu tions of newly synthesised cholesterol and plasma lipoprotein choleste rol to bile acid synthesis and biliary cholesterol secretion, respecti vely, are not known in detail. Aims-To determine how a rapid lowering of plasma low density lipoprotein (LDL) and very low density lipoprote in (VLDL) cholesterol influences the biliary secretion rates of choles terol and bile acids in patients with cholesterol gallstones and compl ete biliary drainage. In this model with a completely interrupted ente rohepatic circulation, the secretion of bile acids equals the new synt hesis of bile acids in the liver. Patients-Eight patients with common bile duct stones of cholesterol type undergoing conventional cholecyst ectomy and choledocholithotomy. Methods-At operation a balloon occluda ble Foley catheter attached to a T tube was inserted into the bile duc t with the balloon placed just past the distal limb of the T tube. The T tube was allowed to drain the bile externally. One week after the o peration the Foley catheter balloon was inflated, creating complete bi liary drainage. Twelve hours following the inflation plasma LDL aphere sis was carried out for two hours. Bile was collected for 15 minute pe riods starting one hour before the apheresis and ending two hours afte r its termination. During the collection of bile, plasma lipids were a nalysed on several occasions. Results-The plasma level of LDL choleste rol decreased by 26% from (mean (SEM)) 2.19 (0.29) to 1.63 (0.17) mmol /l during the LDL apheresis while high density lipoprotein (HDL) chole sterol in plasma was unaffected. During LDL apheresis apolipoprotein B containing lipoproteins bind to the column, causing a significant dec rease of not only plasma LDL but also of VLDL cholesterol. The secreti on rate of bile acids decreased significantly by 31% from 131 (38) to 90 (16) mu mol/15 minutes (p=0.045). The output of phospholipids also decreased by 19%. The biliary secretion rate of cholesterol was not, h owever, affected by the plasma LDL apheresis. Conclusions-The results suggest that, in patients with cholesterol gallstones and complete bil iary drainage, lowering of plasma LDL and VLDL cholesterol reduces the biliary secretion rate-synthesis-of bile acids without affecting the biliary secretion rate of cholesterol.